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TEXT-BOOK 


PRACTICAL  MEDICINE 


DESIGNED  rOK  THE  TJSE  OF 


STUDENTS  AND  PRACTITIONERS  OF  MEDICINE 


ALFRED  L.  LOOMIS,  M.D.,  LL.D., 

Pbopbssob  of  Pathology  and  Practicax  Medicine  in  the  Medical  Depaetilent  of  the  UNrrEB» 
siTT  OF  THE  City  of  New  Yobk  ;  Visiting  Phtsician  to  Bellbvtts  Hospital,  Etc. 


THIRD  EDITION. 


WITH  TWO  HUNDRED  AND  ELEVEN  ILLUSTRATIONS 


NEW    YOEK 

WILLIAM  WOOD  AND  COMPANY 

1885 


CoPTKIfiHT,    1884, 

By  WILLIAM  WOOD  &  COMPANY. 


PREFACE  TO  FIRST  EDITION. 


In  the  preparation  of  a  Text-book  of  Practical  Medicine,  my  experience 
as  a  medical  teacher  has  led  me  to  employ,  quite  extensively,  plates  illus- 
trating the  morbid  changes  and  objective  symptoms  of  disease. 

The  present  work,  both  in  text  and  illustration,  is  practically  a  revision 
and  an  elaboration  of  lectures  given  during  the  past  eighteen  years  in  the 
Medical  Department  of  the  University  of  the  City  of  New  York. 

I  have  avoided,  as  far  as  possible,  the  discussion  of  unsettled  questions, 
and  in  order  to  economize  space  have  made  reference  to  many  of  these  only 
in  brief  foot-notes. 

The  Classification  adopted  is  that  which  it  has  been  my  custom  to  fol- 
low in  teaching,  and  is  based  on  our  present  knowledge  of  the  etiology  of 
disease. 

It  is  well  known  that  many  diseases  present  very  different  types  in  differ- 
ent countries,  and  I  have  selected  for  description  those  types  commonly 
observed  by  the  American  physician; 

I  have  considered  only  those  diseases  which  come  strictly  within  the 
province  of  Practical  Medicine,  and  have  endeavored  to  indicate  the 
treatment  usually  followed  in  this  country. 

The  illustrations,  with  but  few  exceptions,  have  been  made  by  my  assist- 
ant, Dr.  Maurice  N.  Miller  (Instructor  in  the  Laboratory  of  Normal  and 
Pathological  Histology,  University  Medical  College).  The  microscopical 
drawings  were,  in  most  instances,  made  from  sections  prepared  in  the  Lab- 
oratory by  Dr.  Miller,  especially  for  this  work,  and  they  will,  I  believe, 
aid  in  the  appreciation  of  the  actual  morbid  processes  and  conditions. 

In  the  consultation  of  Authorities,  particularly  the  German  and  French, 
in  the  reading  of  the  proof,  and  in  the  preparation  of  the  Index,  I  have 
been  assisted  by  Dr.  Leigh  Hunt,  Assistant  Instructor  in  the  Pathological 
Laboratory  of  the  University. 

If  I  have  failed  to  give  credit — either  in  the  text  or  in  foot-notes — to 
those  from  whom  many  of  the  facts  stated  have  been  drawn,  it  has  been 
an  unintentional  omission. 

19  West  34th  Street,  New  York  City, 
July,  1884. 


PEEFACE  TO  THE  THIRD  EDITION. 


Five  months  after  the  publication  of  this  treatise  the  Author  has  been 
notified  by  the  Publishers  that  they  are  about  to  issue  a  Third  Edition. 

The  brief  period  allowed  for  revision  has  given  opportunity  only  to 
correct  typographical  errors,  and  to  make  important  verbal  changes  in  the 
text. 

The  Author  returns  his  sincere  acknowledgments  to  the  profession  for 
the  expressions  of  appreciation  which  his  labors  have  received. 

19  West  34th  Street, 
April  1st,  1885. 


CONTENTS. 


INTRODUCTION. 

INFLAMMATION. 

1. — Inflammation  of  Serous  Surfaces. 
2. — Inflammation  of  Mucous  Surfaces. 

(a)  Croupous  Inflammation  of  Mucous  Surfaces. 

(&)  Diphtheritic  Inflammation  of  Mucous  Surfaces, 

(c)  Ulceration  of  Mucous  Surfaces. 
3. — Parenchymatous  Inflammation. 
4. — Interstitial  Inflammation. 
5. — Fate  of  Pus Page  1-8 

SECTION   I. 
DISEASES  OF  THE  RESPIEATOEY  ORGANS. 

DISEASES  OP  THE  NASAL  PASSAGES. 

Acute  Coryza. — Chronic  Coryza. — Hypertrophic  Nasal  Cataerh. — Atrophic 
Nasal  Catarrh. — Oz^na 9-17 

DISEASES  OP  THE  LARYNX. 

Acute  Catarrhal  Laryngitis. — Chronic  Catarrhal  Laryngitis. —  Chronic 
Laryngitis  of  Phthisis. — Chronic  Laryngitis  of  Syphilis. — CEdema  Glotti- 
Dis. — Croupous  Laryngitis. — Laryngeal  Ulcers. — Neuroses  of  the  Larynx. 
— Tumors  of  the  Larynx 17-41 

BRONCHITIS. 

Acute  Catarrhal  Bronchitis. — Acute  Capillary  Bronchitis. — Chronic  Catar- 
rhal Bronchitis. — Croupous  or  Plastic  Bronchitis. — Bronchiectasis.  . .  41-69 

DISEASES  OP  THE  LUNGS  AND  PLEURA. 

Acute  Lobar  Pneumonia. — Lobular  Pneumonia. — Interstitial  Pneumonia. — 
Pulmonary  Hyperemia. — Pulmonary  (Edema. — Pulmonary  Infarction. — 
Pulmonary    Apoplexy,— Pulmonary    Gangrene. — Pulmonary    Collapse. — 


VI  CONTENTS. 

Pulmonary  Emphysema. — Parasitic  Diseases. — Morbid  Growths  in  the 
Lung  AND  Pleura. — Pleurisy,  {a)  Acute. — {h)  Sub-acute. — (c)  Suppurative. — 
(d)  Adhesive. — (e)  Cancer  of  the  Pleura. — (/)  Hydropneumothorax. — {g)  Hydro- 
thorax. — Qi)  Ecemothorax.) — Pulmonary  Phthisis,  (a)  Acute  Phthisis. — (&) 
Chronic  Phthisis. — (c)  Chronic  Fibrous  Phthisis. — (d)  Chronic  Tubercular 
Phthisis Page  70-207 


SECTION  II. 

DISEASES  OF  THE  DIGESTIVE  SYSTEM,  INCLUDING  DIS- 
EASES OF  THE  LIVER,  SPLEEN,  AND  PANCREAS. 

DISEASES  OP  THE  MOUTH. 

Stomatitis,  (a)  Catarrhal. — (5)  Follicular. — (c)  Gangrenous. — {d)  Ulcerative. — 
Thrush. — Diseases  of  the  Tongue,  (a)  Glossitis. — (J)  Camcer. — Paro- 
titis   208-219 

DISEASES  OP  THE  PHARYNX. 
Tonsilitis. — Inflammations. — Retropharyngeal  Abscess 219-224 

DISEASES  OP  THE  CESOPHAGUS. 
Inflammations. — Cancer 324-227 

DISEASES  OF  THE  STOMACH. 

Inflammations,  (a)  Acute. — (b)  Sub-acute. — (c)  Chronic. — {d)  Phlegmonous. — Dys- 
pepsia.— Cancer  and  Ulcer. — Neuroses. — H^matemesis. — Dilatation.  228-256 

DISEASES  OF  THE  INTESTINES. 

Enteritis. — Diarrhcea. — Cholera  Morbus. — Cholera  Infantum. — Dysentery. 
— Typhlitis  and  Perityphlitis. — Intestinal  Ulcers. — Intestinal  Hemor- 
rhage.  —  Intestinal  Obstkuction. — Waxy  Degeneration. — Cancer. — Rec- 
titis. — Intestinal  Parasites. — Intestinal  Colic. — Constipation. — Perito- 
nitis.— Ascites 257-336 

DISEASES  OP  THE  LIVER. 

HYPER.SMIA.  {a)  Active. — (5)  Passive. — Inflammations,  {a)  Interstitial  Hepatitis 
or  Cirrhosis. — (J)  Circumscribed  Hepatitis  or  Abscess. — (c)  Diffused  Hepatitis  or 
Acute  Yellow  Atrophy. — Perihepatitis. — Pylephlebitis.  — Degenerations. 
(a)  Amyloid. — (b)  Fatty. — (c)  Pigmentary. — {d)  Atrophic. — New  Growths  (a) 
Cancer. — (b)  Gummata. — (c)  Hydatids. — (d)  Tubercle. — Diseases  of  the  Gall- 
ducts  and  Gall-bladder. — Jaundice. — Functional  Derangements 337-409 

DISEASES  OP  THE  PANCREAS. 

Acute  Diseases. — Degenerations.  («)  Fatty. — (6)  Waxy. — Morbid  Growths 
(Cancer,  Tubercle,  etc.). — Cysts.— Calculi 410-413 


CONTENTS.  Vii 

DISEASES  OF  THE  SPLEEN. 

HYPERiEMiA. — Inflammation,  including  Embolism  and  Infarction. — Htpeeteo- 
PHY. — Degenerations. — Morbid  Growths. — Parasites Page  413-419 


SECTION  III. 

DISEASES  OF  THE   HEAET,   BLOOD-VESSELS,  AND   KID- 
NEYS. 

DISEASES  OP  THE  HEART. 

Pericarditis.  —  Endocarditis. — Valvular  Lesions.  —  Hypertrophy.  —  Dilata- 
tion.— Myocarditis. — Degenerations. — Atrophy.  —  Thrombosis. — Aneurism. 
— Morbid  Growths  and  Parasites. — Tuberculosis  op  the  Pericardium. — 
Neuroses.  — Hydropericardium.  — Pneumohydropekicardium.  —  Syphilitic 
Disease  of  the  Heart 420-510 

DISEASES   OF  THE  BLOOD-VESSELS. 

DISEASES  OF  THE  ARTERIES. 

Acute  Endarteritis  .  —  Chronic  Endarteritis. — Periarteritis.  —  Degenera- 
tions, (a)  Fatty.  —  (b)  Waxy.  —  (c)  Calcareous.  —  Syphilis.  —  Hypertrophy, 
Atrophy,  and  Narrowing 511-535 

DISEASES  OF  THE  VEINS. 
Acute  Phlebitis. — Chronic  Phlebitis.  — Dilatation 535-539 

DISEASES  OF   THE   KIDNEYS. 

THE  URINE. 
NoemaIj  Constituents. — Urinary  Sediments. — Acute  Uremia 539-543 

THE  KIDNEYS. 

BbnaXi  HYPERiEMiA. — Renal  HEMORRHAGE. — Bright's  DISEASES,  (a)  Parenchy- 
matous  Nephritis. — (b)  Interstitial  Nex>hritis. —  (c)  Amyloid  Degeneration. — 
Pyelitis. — Acute  Suppurative  Nephritis. — Hydronephrosis. — Cystic  Kid- 
ney.— Renal  Calculi — New  Growths  {Cancer,  etc.). — Parasites. — Perine- 
PHRiTic  Abscess. — Hematuria.— Chyluria. — Cystitis .543-607 

SECTION    IV. 
ACUTE  GENEEAL  DISEASES. 

MIASMATIC    CONTAGIOUS    DISEASES. 

Ttphoid  Fever. —  Yellow  Fever. — Cholera. — Diphtheria. —  Cerebro-spinai. 
Meningitis. — Septic^mla.. — Pyaemia.— Erysipelas. — Acute  Miliary  Tuber- 
culosis   609--710 


Vni  CONTENTS. 

ACUTE  CONTAGIOUS  DISEASES. 

Typhus  Fever. — Relapsing  Fever. — Small-pox. — ^Varicella. — Scarlet  Fever. — 
Measles. — German  Measles.  —  Miliary  Fever.  —  Influenza.  — Whooping- 
cough.— Hydrophobia Page  710-805 


MALARIAL  DISEASES. 

Intermittent    Fever. —  Remittent   Fever. — Continued    Malarial    Fever. — 
Pernicious  Fever. — Dengue  Fever.— Chronic  Malarial  Infection.  . .  .806-856 


SECTION  V. 

CHEONIO  GENERAL  DISEASES. 

Rheumatism.  —  Gout.  —  Diabetes. —  Anemia  . —  Chlorosis.  —  Progressive  Perni- 
cious Anemia. — Leucocyth^mia. — Pseudo-Leukemia.  — Addison's  Disease. — 
Ammonemia. —  Hemophilia. — Scurvy. —  Purpura. — Myxcedema. —  Scrofula. 
— Rickets. — ^Alcoholism. — Trichinosis. — Syphilis 856-923 


SECTION  VL 

DISEASES  OF  THE  NERVOUS   SYSTEM,  INCLUDING  DIS- 
EASES OF  THE  BRAIN,  SPINAL  CORD  AND  FUNG 
TIONAL  NERVOUS  DISEASES. 

GENERAL  SYMPTOMATOLOGY 
Op  Nervous  Diseases 925-830 

DISEASES   OP  THE  BRAIN. 

Cerebral  Hyperemia  {Active  or  Passive). — Cerebral  Anemia. — Meningitis. — 
Cerebral  Thrombosis  and  Embolism. — Cerebral  Softening. — Cerebral 
Apoplexy. — Abscesses  of  the  Brain. — Cerebral  Tumors. — Sclerosis  of  the 
Brain. — Hypertrophy  of  the  Brain 930-990 

DISEASES  OP  THE  SPINAL  CORD  AND  ITS  MENINGES. 

Spinal  Hyperemia. — Spinal  Meningitis. — Acute  Myelitis. — Chronic  Myelitis. — 
Non-inflammatory  Softening. — Acute  Bulbar  Paralysis. — Progressive 
Bulbar  Paralysis. — Infantile  Spinal  Paralysis. — Acute  Spinal  Paralysis 
OF  Adults. — Chronic  Anterior  Myelitis. — Progressive  Muscular  Atrophy. 
— Cerebro-spinal  Sclerosis. — Locomotor  Ataxia. — Spasmodic  Tabes  Dor- 
SALis. — Amyotrophic  Lateral  Sclerosis. — Pseudo-Hypertrophic  Paraly- 
sis.—Spinal  Apoplexy 990-1034 


CONTENTS.  IX 

FUNCTIONAL  DISEASES  OF  THE  NERVOUS  SYSTEM. 

Epilepsy.  —  Htstebia.  —  Hystebo-Epilepsy.  —  Catalepsy.  —  Neurasthenia.  — 
Chorea.— Sunstroke. — Spinal  Irritation. — Tetanus. — Facial  Paralysis. — 
Paralysis  Agitans. — Localized  Spasm  and  Paralysis. — Chronic  Lead 
Poisoning.  —  Chronic  Mercublalism.  — Vertigo.  —  Neuralgia.  —  Megrim. — 
Eclampsia. — Sea-sickness Page  1034-1079 


LIST  OF  ILLUSTEATIONS. 


Fie.  Paob 

1.  Inflammation  of  omentum i.  3 

2.  Epithelium  and  pus  cells  from  serous  inflammation 3 

3.  Inflammation  of  a  serous  membrane 5 

4.  Inflammation  of  a  mucous  membrane 6 

5.  Diphtheritic  inflammation  of  a  mucous  surface 7 

6.  Membrane  and  exudation  in  croupous  laryngitis 28 

7.  Position  of  vocal  cords  in  the  dift'erent  forms  of  laryngeal  paralysis 36 

8.  Multiple  papilloma  of  the  right  vocal  cord 39 

9.  The  trachea  laid  open  showing  same  tumor  as  seen  in  Pig.  8 39 

10.  Morbid  anatomy  of  acute  catarrhal  bronchitis 42 

11.  Physical  signs  of  bronchitis 44 

12.  Bronchial  wall  in  chronic  catarrhal  bronchitis 50 

13.  Various  forms  of  bronchiectasis 56 

14.  Mould  of  bronchi  in  sputum  of  plastic  bronchitis 58 

15.  Morbid  anatomy  of  first  stage  of  acute  lobar  pneumonia 70 

16.  Morbid  anatomy  of  second  stage  of  acute  lobar  pneumonia 71 

17.  Morbid  anatomy  of  second  stage  of  pleuro-pneumonia 72 

18.  Morbid  anatomy  of  third  stage  of  acute  lobar  pneumonia 73 

19.  Morbid  anatomy  of  purulent  infiltration 75 

20.  Temperature  record  in  acute  lobar  pneumonia  in  an  adult 82 

21.  Temperature  record  in  acute  lobar  pneumonia,  observations  every  sis  hours. .  83 

22.  Temperature  record  in  acute  lobar  pneumonia  ending  in  purulent  infiltration.  84 

23.  Physical  signs  of  the  three  stages  of  acute  lobar  pneumonia 91 

24.  Morbid  anatomy  of  lobular  pneumonia  102 

25.  Temperature  record  in  lobular  pneumonia  in  a  child 104 

26.  Morbid  anatomy  of  interstitial  pneumonia 109 

27.  Morbid  anatomy  of  brown  induration  of  the  lung 115 

28.  Hemorrhagic  infarctions 121 

29.  Morbid  anatomy  of  emphysema  of  the  lung 132 

30.  Cancer  of  lung  ~ 140 

31.  Hydatids  of  lung 145 

32.  Temperature  record  in  acute  pleurisy 147 

33.  Physical  signs  in  acute  pleurisy  with  a  small  amount  of  effusion 148 

34.  Physical  signs  in  pleurisy  with  effusion 154 

35.  Physical  signs  of  hydropneumothorax 167 

36.  Acute  phthisis ;  alveolus  filled  with  fibrin  and  cells 173 

37.  Acute  phthisis ;  alveolus  filled  with  cells 173 

38.  Coagulation -necrosis  in  acute  phthisis 174 

39.  Tubercle  bacilli  from  phthisical  sputum 175 

40.  Temperature  record  in  a  case  of  acute  phthisis 176 

41.  Morbid  anatomy  of  chronic  catarrhal  phthisis 179 

42.  Lung  cavity 180 

43 .  Chronic  fibrous  phthisis 181 

44.  Morbid  anatomy  of  anthracosis 182 


xii  LIST   OF   ILLUSTRATIONS. 

Fl3.  PABE 

45.  Chronic  tubercular  phthisis,  with  miliary  tubercles 183 

46.  Chronic  tubercular  phthisis  showing  tubercular  nodule 184 

47.  Physical  signs  of  iirst  stage  of  chronic  phthisis. 194 

48.  Physical  signs  of  cavities  in  third  stage  of  chronic  phthisis 195 

49.  Oidium  albicans 213 

50.  Stricture  of  the  oesophagus 225 

51.  Stomach  wall  in  sub-acute  gastritis 230 

52.  Mucous  membrane  and  stomach-tubules  in  chronic  gastritis 233 

53.  Sarcinge  ventriculi  from  vomit  of  chronic  gastritis 234 

54.  Cancer  of  pyloric  end  of  stomach 242 

55.  Perforating  ulcer  of  stomach 247 

56.  Dilatation  of  stomach 255 

57.  Acute  enteritis,  small  intestine  near  ileum 257 

58.  Acute  follicular  enteritis ;  transverse  colon  showing  ulceration 258 

59.  First  stage  of  acute  dysentery 272 

60.  Second  stage  of  acute  dysentery 273 

61.  Temperature  record  in  acute  dysentery 275 

62.  Tubercular  ulcers;   ileum 286 

63.  Intussusception  (intestinal  obstruction) 290 

64.  Head  of  taenia  solium  (tape-worm) 307 

65.  Mature  segment  of  taenia  solium 307 

66.  Head  of  taenia  saginata 308 

67.  Oxyuris  vermicularis  with  ovum;  and  ascaris  lumbrieoides 3l9 

68.  Passive  hepatic  hyperaemia 340 

69.  Interstitial  hepatitis 343 

70.  Interstitial  hepatitis,  same  as  Fig.  69:  more  highly  magnified 344 

71.  Circumscribed  suppurative  hepatitis  (pyaemic  abscesses) 350 

72.  Cells  from  a  lobule  in  acute  yellow  atrophy  of  the  liver 356 

73.  Amyloid  degeneration  of  the  liver 367 

74.  Three  intralobular  zones ;  waxy,  fatty  and  pigment  degenerations  of  the  liver.  368 

75.  Chronic  atrophy  of  the  liver 371 

76.  Fatty  infiltration  of  the  liver 373 

77.  Fatty  degeneration  of  the  liver 373 

78.  Pigmentary  degeneration  of  the  liver 375 

79.  Same  as  Fig.  78:  more  highly  magnified 376 

80.  Cancer  of  the  liver 379 

81.  Diagrammatic  enlargements  of  liver 381 

82.  Hydatids  of  liver  :  budding  vesicles 385 

83.  Hydatids  of  liver  :  head  of  echinocoecus 387 

84.  Gall-bladder  filled  with  calculi 401 

85.  Section  of  a  large  gall-stone  showing  layers 403 

86.  Crystals  of  cholesterin 403 

87.  Areas  of  splenic  enlargement  as  shown  by  percussion 416 

88.  Morbid  anatomy  and  physical  signs  of  sero-plastie  pericarditis 431 

89.  Physical  signs  of  pericarditis  with  eifusion 435 

90.  Changes  in  mitral  valve  in  diphtheritic  endocarditis 431 

91.  Changes  in  aortic  valves  in  diphtheritic  endocarditis 433 

93.  Section  of  aortic  valve  in  acute  endocarditis 438 

93.  Diagram  showing  mode  of  production  of  cardiac  murmurs 443 

94.  Diagram  showing  area  of  cardiac  murmurs 444 

95.  Vegetations  on  aortic  valves  in  aortic  obstruction 445 

96.  Sphygmographic  tracing  of  pulse  in  aortic  obstruction 446 

97.  Morbid  anatomy  of  aortic  insufficiency 448 

98.  Sphygmographic  ti-acing  of  pulse  in  aortic  regurgitation 450 

99.  Morbid  anatomy  of  mitral  stenosis 453 


LIST   OF   ILLUSTRATI0K8.  Xlll 

Fig.  Page 

100.  Mitral  orifice  showing  button-hole  slit  in  stenosis 454 

101.  Sphygmographic  tracing  of  pulse  in  mitral  stenosis 455 

102.  View  of  left  heart  in  mitral  regurgitation 458 

103.  Sphygmographic  tracing  of  pulse  in  mitral  regurgitation 460 

104.  Physical  signs  in  left  ventricular  hypertrophy 477 

105.  Physical  signs  in  right  ventricular  hypertrophy .    477 

106.  Section  of  heart  wall  in  acute  myocarditis 487 

107.  Teased  fibres  of  heart-muscle  in  fatty  degeneration  of  the  heart 491 

108.  Muscle-fibres  showing  fatty  infiltration  of  the  heart. ...   492 

109.  Chronic  endarteritis  :  "  atheroma  " 513 

110.  Diagrammatic  representation  of  formation  of  thrombi  and  emboli _    516 

111.  Re-establishment  of  circulation  by  anastomosis  after  embolism 518 

112.  Morbid  anatomy  of  spontaneous  arterial  aneurism 520 

113.  Hippuric  acid 530 

114.  Fat  globules  from  chylous  urine 531 

115.  Leucin  and  tyrosin 531 

116.  Uric  acid  crystals 532 

117.  Urate  of  soda 532 

118.  Urate  of  ammonia  crystals 532 

119.  Oxalate  of  calcium  crystals 533 

120.  Ammonio-magnesian,  or  triple  phosphate 533 

121.  Phosphate  of  calcium 533 

122.  Cystine 534 

123.  Epithelium  from  urinary  deposits 534 

124.  Blood  in  the  urine 535 

125.  Pus  in  the  urine 535 

126.  Epithelial  casts  in  the  urine 536 

127.  Hyaline  casts  in  the  urine 536 

128.  Granular  casts  in  the  urine 536 

129.  Fatty  casts  in  the  urine  536 

130.  Blood  casts  in  the  urine  536 

131.  Spermatozoa  in  the  urine 537 

132.  Torula  cerevisise ;  penicilium  glaucum ;  and  sarcinae  ventriculi 537 

133.  Section  from  Malpighian  pyramid  in  passive  renal  hypersemia 544 

134.  Hemorrhage  from  vascular  tuft  of  a  glomerulus  in  renal  hemorrhage 548 

135.  Renal  hemorrhage  and  renal  infarction 549 

136.  Cortex  of  kidney  showing  cloudy  swelling  in  acute  Bright's  disease 553 

137.  Cortex  of  kidney  showing  advanced  degenerative  changes  in  acute  Bright's 

disease 554 

138.  Cortex  of  kidney  in  chronic  parenchymatous  nephritis 563 

139.  Cortex  of  kidney  in  early  cirrhotic  Bright's 569 

140.  Cortex  of  kidney  in  advanced  cirrhotic  Bright's 570 

141.  Cortex  of  kidney  showing  commencing  waxy  changes 575 

142.  Medullary  portion  of  kidney  showing  advanced  amyloid  change 576 

143.  Arterio-capillary  fibrosis :  two  glomeruli  from  the  cortex  of  a  contracted  kidney.  585 

144.  Longitudinal  section  of  cystic  kidney 592 

145.  A  cyst  of  the  kidney:  epithelial  lining  shown 592 

146.  Renal  calculi :  an  embedded  mulberry  calculus 593 

147.  Mucous  surface  of  ileum  in  first  week  of  typhoid  fever 615 

148.  Mucous  surface  of  ileum  in  second  week  of  typhoid  fever 616 

149.  Mucous  surface  of  ileum  in  third  week  of  typhoid  fever 616 

150.  Enlarged  mesenteric  lymphatics  in  typhoid  fever 617 

151.  Temperature  record  in  typical  (mild)  typhoid  fever 627 

152.  Temperature  record  in  non-typical  typhoid  fever 628 

153.  Temperature  record  in  yellow  fever 655 


XIV  LIST   OF   ILLUSTRATIONS. 

Fig.  Page 

154.  Temperature  record  in  septiesemia 695 

155.  Metastatic  pysemic  abscesses  of  the  lung 697 

156.  Temperature  record  in  pyaemia 699 

157.  Temperature  record  in  a  case  of  facial  erysipelas 703 

158.  Temperature  record  in  a  case  of  acute  miliary  tuberculosis 708 

159.  Temperature  record  in  severe  typhus  fever 721 

160.  Temperature  record  in  a  case  of  relapsing  fever 742 

161.  Temperature  record  in  a  case  of  discrete  small-pox 749 

162.  Temperature  record  in  a  case  of  confluent  small-pox 753 

168.  Temperature  record  in  a  case  of  varioloid 763 

164.  Temperature  record  in  a  case  of  scarlatina 771 

165.  Temperature  record  in  a  case  or  measles 786 

166.  Temperature  record  in  a  ease  of  German  measles 793 

167.  Temperature  record  in  a  case  of  influenza 798 

168.  Fever  curve  in  quotidian    intermittent 811 

169.  Fever  curve  in  tertian  intermittent 812 

170.  Fever  curve  in  quartan  intermittent 812 

171.  Section  of  liver  from  a  case  of    remittent  fever 818 

172.  Temperature  record  in  remittent  fever 821 

178.  Temperature  record  in  a  case  of  continued  malarial  fever 880 

174.  Temperature  record  in  continued  malarial  fever.    (Septic  variety) 833 

175.  Temperature  record  in  pernicious  fever.     (Comatose  variety) 841 

176.  Temperature  record  in  pernicious  fever.     (Algid  variety 843 

177.  Temperature  record  in  a  severe  case  of  dengue  fever 850 

178.  Temperature  record  in  a  mild  case  of  acute  rheumatism 859 

179.  Temperature  record  in  a  fatal  case  of  acute  rheumatism 859 

180.  Deformity  from  articular  rheumatism.     (Hand) 866 

181.  Section  of  a  gouty  cartilage 871 

182.  Vertical  section  of  a  Malpighian  pyramid  in  gouty  nephritis 872 

183.  Deformity  from  gout.     (Hand) 874 

184.  Blood  from  a  case  of  leucocythsemia 891 

185.  Section  of  a  leucocytheemic  spleen 893 

186.  Encapsulated  trichinte  in  voluntary  muscle 916 

187.  Trichinae  with  calcareous  deposits  and  degeneration  of  the  capsule 916 

188.  Temperature  record  in  the  fourth  week  of  trichinosis 917 

189.  Acute  meningitis,  showing  also  intact  meninges 936 

190.  Temperature  record  in  a  case  of    acute  meningitis 937 

191.  Tubercular  meningitis : — tubercular  deposits  along  blood-vessels 944 

192.  Temperature  record  in  a  ease  of  tubercular  meningitis 945 

193.  Pachymeningitis  interna. — Vertical  section  of  skull  and  cerebral  meninges. . .  958 

194.  Cerebral  softening 960 

195.  Small  blood-vessel  from  a  focus  of  yellow  softening.    (Cerebral  thrombosis  and 

embolism) 961 

196.  Cerebral  apoplexy;  newly  formed  clot  in  the  left  optic  tract 964 

197.  Vertical  section  of  the  cerebrum 969 

198.  Fibroma  of  the  cerebellum 978 

199.  Diagi-am  showing  connective-tissues  of  medullated  nerve  structure 985 

200.  Sclerosis  of  the  brain 986 

201.  Acute  myelitis .- 996 

203.  Chronic  bulbar  paralysis 1003 

203.  Muscle  of  the  tongue  in  chronic  bulbar  paralysis  contrasted  with  normal 

muscle 1003 

204.  Section  of  spinal  cord  in  early  stage  of  infantile  spinal  paralysis 1006 

205.  Same  as  204  after  establishment  of  sclerotic  process 1006 

206.  Teased  fibres  from  abductor  poliicis  in  progressive  muscular  atrophy 1013 


LIST   OF   ILLUSTRATIONS.  XV 

Fig.  Pagk 

207.  Sketch  of  a  hand  in  progressive  muscular  atrophy 1013 

208.  Cerebro-spinal  sclerosis 1015 

209.  Regions  of  degenerative  changes  in  spinal  cord. — Diagrammatic. 1018 

210.  Locomotor  ataxia. — Section  of  cord  in  cervical  region 1019 

211.  Spinal  apoplexy : — clot  in  the  left  anterior  comu 1029 


A  TEXT-BOOK 


07 


PRACTICAL  MEDICINE. 


INFLAMMATION. 


According  to  the  older  writers  the  cardinal  symptoms  of  inflammation 
are  pain,  heat,  redness  and  swelling,  features  which  are  more  striking  in 
those  forms  of  inflammation  which  come  under  the  care  of  the  surgeon  than 
in  those  which  the  physician  is  called  upon  to  treat.  As  the  knowledge  of 
tissues  and  processes  became  more  detailed  and  complete,  and  as  the  hidden 
changes  underlying  these  grosser  ones  were  brought  to  light,  pathologists 
sought  to  discover  the  essence  of  the  inflammatory  process,  to  find  its  cause, 
and  to  determine  in  which  tissues  or  organs  th'e  primary  causative  change 
occurred.  The  history  of  the  theories  and  definitions  of  inflammation  is  a 
record  of  the  varying  importance  that  has  been  attached  to  one  or  another 
of  the  changes  observed.  Into  these  theories,  and  the  arguments  by  which 
they  have  been  in  turn  supported  and  assailed,  it  is  not  desirable  here  to 
enter.  It  will  be  sufficient  to  describe  the  changes  observed  in  the  tissues 
and  to  define  the  associated  terms  of  which  use  will  hereafter  be  made. 

Hyperaemia. — Except  in  the  non-vascular  tissues,  as  the  cornea  and 
cartilage,  the  earliest  change  observed  is  in  the  circulation,  and  this 
change  is  manifested  by  a  change  in  the  color  of  the  affected  part,  which 
becomes  red  and  congested.  This  redness  is  due  to  an  increase  of  the 
quantity  of  blood  in  the  part ;  at  first  the  hyperaemia  is  active,  that  is, 
blood  is  brought  to  the  part  and  passed  through  the  capillaries  in 
1 


INFLAMMATIOIT. 


larger  quantities  than  before  ;  but  it  may  become  passive,  a  condition  in 
•which,  while  the  quantity  of  blood  present  in  the  part  is  greater  than 
usual,  the  current  is  much  slower,  the  amount  which  actually  passes 
through  the  capillaries  in  a  given  time  being  less  than  normal ;  finally, 
this  retardation  of  the  flow  may  end  in  actual  arrest :  stasis.     That  hyper- 

aemia  is  only  an  accompaniment, 
and  not  the  essence,  of  inflammation 
is  shown  by  the  fact  that  the  hyper- 
semia  which  is  caused  by  section  of 
the  sympathetic  nerves  is  not  accom- 
panied by  the  other  symptoms  and 
changes  observed  in  inflammation. 

Exudation. — The  swelling  which 
has  been  mentioned  as  one  of  the 
four  cardinal  symptoms  is  due  main- 
ly to  the  presence  of  a  liquid  infil- 
trated through  the  tissues.  This 
liquid  comes  from  the  blood  by 
exudation  through  the  walls  of  the 
capillaries  ;  but  it  is  not  simply  the 
plasma  or  serum  of  the  blood ;  its 
chemical  composition  is  different,  it 
is  the  plasma  of  the  blood,  with  the 
addition  of  materials  furnished,  pre- 
sumably, by  the  elements  of  the 
tissues  which  it  bathes.  It  is  this 
addition    which     distinguishes    the 

F,  G.  Red  and^  white  corpuscles  from  Jmrsting  of   liquid  from  the  normal  iuices  of  the 

CCtDZllClTZSS 

H.  Exfoliated  epithelium,    x  300.  part,  or  from  that  of  oedema,  and 

which  makes  it  an  inflammatory  exudation. 

Cellular  Elements. — In  order  to  furnish  these  peculiar  constituents  to 
the  exudation,  the  cellular  elements  of  the  tissues  undergo  change  in  form 
and  nutrition.  The  chemical  interchanges  whicb  constitute  normal  nu- 
trition, and  which  are  carried  on  between  the  cells  of  the  tissues  and  the 
liquid  furnished  to  the  cells  by  the  blood,  are  modified  in  character  or 
extent,  and  the  cells  themselves  are  correspondingly  modified  in  form.  On 
the  one  hand,  the  cells  may  show  a  tendency  to  return  to  their  earlier 
embryonal  form,  to  become  swollen,  globular,  pale  and  succulent,  perhaps 
to  divide,  to  form  new  cells  by  proliferation  ;  on  the  other  hand,  the  exag- 
gerated activity  of  the  cell  may  prove  too  great  a  strain  upon  it,  and  it  dies 
or  becomes  disabled  by  passage  into  the  condition  known  as  fatty  degenera- 
tion. The  former  of  these  two  results  is  the  one  seen  most  commonly  in 
the  connective-tissue  framework  and  envelopes  of  the  various  parts  and 
organs,  and  the  latter  in  the  specific  cells  that  constitute  their  parenchyma. 

Suppuration. — Examination  of  fresh  normal  tissues  shows,  scattered 
through  them,  free  cells  which  closely  resemble  the  colorless  coi'puscles  of 
the  blood  and   lymph.      Like  them,  they  possess  the  power  of  amoeboid 


Fig.  1. 
Inflammation  of  tbe  Omentum. 

A.  Arteriole. 

B.  Venule. 

C.  Inflammatory  stasis  with  escape  of  blood  glob- 

ules. 

D.  Extravasated  blood  corpuscles. 

E.  Infiltration  of  connective-tissue  with  pus  coi'pus- 
cles. 


INFLAMMATION". 


movement,  of  rapidly  changing  their  shape  by  throwing  out  processes,  of 
moving  from  place  to  place  by  means  of  this  change  of  form,  and  of  multi- 
plying by  division.  They  are  called  "  wandering  cells,"  or  leucocytes, 
because  of  their  supposed  identity  with  the  colorless  corpuscles  of  the  blood. 
Under  normal  conditions  the  leucocytes  contained  within  the  blood-vessels 
may  occasionally  be  seen  to  pass  through  the  unbroken  wall  of  a  capillary 
by  means  of  this  power  of  amoeboid  movement  which  they  possess ;  when 
the  tissue  adjoining  the  capillary  is  inflamed,  the  number  of  cells  -''  migrat- 
ing "  through  its  wall  is  notably  increased.  Furthermore,  when  a  part  is 
inflamed  the  fixed  corpuscles  of  the  omnipresent  connective-tissue  swell, 
as  has  been  described,  and  give  rise 
by  proliferation  to  other  cells,  which 
cannot  be  distinguished  morphologi- 
cally from  the  normal  wandering  cells 
or  leucocytes.  When  these  cells  ac- 
cumulate in  great  numbers  (whether 
by  transformation  of  connective-tissue 
cells  or  by  migration  from  the  vessels) 
they  constitute  pus,  and  suppuration 
is  said  to  have  occurred.  The  process 
is  accompanied  by  more  or  less  de- 
struction of  tissue,  either  by  the  trans- 
formation of  the  cells  into  pus-cells, 
or  by  necrosis,  death  of  the  tissue 
In  consequence  of  pressure  or  of  modi- 
fication of  its  nutritive  conditions.  When  the  process  takes  place  upon  a 
free  surface  it  is  called  ulceration;  when  within  the  substance  of  an  organ, 
the  collection  is  called  an  abscess. 

Resolution  ;  Cicatrization.  — The  inflammatory  process,  as  thus  described, 
maybe  arrested  at  any  point.  If  the  irritation  is  slight  or  of  short  duration, 
if  the  change  has  not  progressed  to  the  point  of  tissue  destruction  and  for- 
mation of  pus,  the  withdrawal  of  the  prim.ary  cause  is  followed  by  a  dimi- 
nution of  the  swelling  and  congestion,  and  by  return  to  the  normal  state  ; — 
this  is  called  resolution.  When,  on  the  other  hand,  necrotic  changes  have 
taken  place  the  simple  arrest  of  the  inflammation  is  not  sufficient,  the  losses 
must  be  made  good,  the  destruction  repaired.  Thi^  is  cicatrization,  and  it 
is  accomplished  largely  by  cells  of  the  connective-tissue.  As  the  conditions 
become  more  favorable,  the  cells  newly  formed  by  proliferation  no  longer 
remain  stationary,  lose  their  vitality,  and  become  pus,  but  they  progress  in 
the  direction  of  a  normal  development  and  form  new  tissue.  The  irregular 
pink  granulations  seen  within  a  wound  or  upon  an  ulcerated  surface  are 
formed  of  masses  of  young  cells  crowded  with  capillary  loops  of  new  forma- 
tion. The  cells,  at  first  large,  soft,  finely  granular  and  Juicy,  become 
smaller  and  firmer,  and  the  intercellular  substance  increases  and  becomes 
fibrous.  If  the  inflammatory  process  has  taken  place  in  the  interior  of  an 
organ,  involving  only  a  small  portion  of  tissue,  and  has  stopped  short  of 
the  formation  of  a  distinct  collection  of  pus,  the  result  of  the  reparative 


Fig.  2. 
Desquamated  epithelia  audpus  cells  from  an  in- 
flamed serous  surface,     x  500. 


4  I^sTFLAMMATIOIS". 

process  is  a  mass  of  fibrous  connective-tissue,  a  cicatrix  ;  and  if  a  collection 
of  pus  has  actually  formed,  but  is  only  of  small  size,  the  pus  may  disappear 
by  liquefaction  of  its  cellular  elements  and  absorption.  If,  on  the  other 
hand,  a  larger  abscess  has  formed  and  has  been  opened,  its  cavity  becoming 
filled  by  the  granulatiens,  the  same  change  into  fibrous  tissue  follows,  and 
a  cicati'ix  is  again  the  result.  The  same  is  true  of  ulceration  of  a  free  sur- 
face, with  the  addition  that  the  surface  of  the  cicatrix  is  covered  by  a  layer 
of  epithelium  resembling  more  or  less  closely  the  original  layer  which  has 
been  destroyed  by  the  ulceration.  When  the  irritation  has  been  less  active 
but  more  prolonged,  and  has  perhaps  involved  an  entire  organ,  its  effect 
again  appears  in  an  increase  of  the  connective-tissue  of  the  part  involved ; 
but  the  consequences  of  this  increase  are  most  serious.  The  original  "  fixed 
cells"  of  the  connective-tissue  multiply  as  in  the  other  case  mentioned,  and 
develop  into  fully  formed  tissue,  and  the  amount  of  this  tissae  becomes  in 
consequence  much  greater  than  normal.  In  its  natural  evolution  it  retracts, 
and  by  its  quantity  and  its  retraction  it  presses  upon,  and  interferes  with 
the  nutrition  of  the  specific  cellular  elements  of  the  organ,  so  that  they  be- 
come less  fit  to  perform  their  functions.  This  change  is  called  induration 
or  cirrJiosisj  common  examples  are  cirrhosis  of  the  liver,  and  '^contracted 
kidney  "  or  interstitial  nephritis. 

INFLAMMATIOTSr    OF   FREE    SURFACES. 

First :  Serous  Surfaces. — The  most  common  form  of  inflammation  of  serous 
membranes  is  that  which  results  in  the  production  of  serum,  fibrin,  or  pus, 
in  variable  proportions ;  these  products  may  infiltrate  the  substance  of  the 
inflamed  membrane,  be  poured  out  upon  its  free  or  attached  surface,  or 
collect  in  cavities  lined  by  it.  The  first  change  in  this  inflammatory  pro- 
cess is  in  the  blood-vessels,  which  contain  more  than  their  normal  quantity 
of  blood,  and  it  is  from  the  blood  circulating  in  the  vessels  that  most  of  the 
characteristic  inflammatory  products  are  derived.  After  the  initial  hyper- 
gemia,  the  fibrinogen  of  the  exudation  comes  in  contact  with  the  fibrinoplas- 
tic  material  of  the  tissues  (there  being  a  ferment  present),  coagulation  takes 
place,  and  layers  of  fibrin  containing  few  or  many  cells  are  formed  on  the 
free  surface.  These  layers  are  called  pseudo-membranes,  or  coagulable 
lymph.  If  the  inflammation  occurs  in  a  membrane  whose  normal  conforma- 
tion makes  a  free  effusion  possible  (as  the  pleura  and  peritoneum)  some 
serum  is  always  present.  It  may  be  only  infiltrated  through  the  meshes  of 
the  tissues,  or  it  may  accumulate  at  some  point  as  a  sero-fibrinous 
collection.  When  leucocytes  are  present  in  great  numbers  the  exu- 
dation is  fibrino-purulent.  The  greater  the  intensity  of  the  inflammation, 
and  the  more  enfeebled  the  patient,  the  greater  is  the  liability  to  pus  forma- 
tion. In  certain  serous  inflammations  the  exudation  may  be  hemorrhagic  ; 
the  blood  may  come  from  a  ruptured  capillary  vessel,  or  the  coloring  matter 
of  the  blood  corpuscle  may  be  set  free  and  color  the  exudation  without 
vascular  lesion.  Such  inflammation  of  serous  membranes  may  end  in 
necrosis  or  in  resolution.     If  the  inflammation  is  intense,  and  stasis  occurs 


INFLAMMATIOX. 


throughout  a  wide  area  of  tissue,  it  will  result  in  necrosis.  Stasis  is  the 
expression  of  a  higher  degree  of  injury  than  that  which  exists  in  simple  in- 
flammation/ The  intensity  of  the  inflammation  determines  whether  the 
result  shall  be  a  return  to  the  normal  condition  or  a  destruction  of  tissue. 
An  uncomplicated  serous  inflammation  is  neither  reproductive  nor  infective. 
It  has  no  tendency  except  to  stop  as  soon  as  its  primary  cause  ceases  to  act. 
"When  resolution  occurs,  the  emigration  of  leucocytes  ceases,  the  serous 
fluid  disappears,  and  the  fibrin  and  the  cell  elements,  after  they  have 
undergone  molecular  change,  are  absorbed. 

A  second  variety  of  inflammation  of  serous  membrane  is  characterized  by 
the  production  of  new  connective-tissue  cells  either  with  or  without  a  sero- 
purulent  exudation.  It 
may  be  an  acute  or  chronic 
process.  The  inflamed 
membrane  becomes 
thickened,  and  there  is 
abundant  cell  develop- 
ment in  its  substance  and 
on  its  surface.  These  cells 
are  not  pus-cells,  but  are 
embryonic  cells  from  the 
fixed  cells  of  the  tissue. 
If  the  inflammatory  proc- 
ess is  prolonged,  or  if  the 
membrane  becomes  very 
much  thickened,  eleva- 
tions are  formed  on  the 
surface  of  the  membrane, 
and  thus  adhesion  takes 
place  between  opposing 
serous  surfaces,  or  the 
membrane  becomes  thick- 
ened and  indurated.  If 
bands  of  adhesion  form, 
they  have  the  appearance  of  delicate  membranes.  This  new  tissue  at  first 
is  exceedingly  rich  in  capillary  vessels,  which  are  distinguished  from  the 
normal  capillaries  of  the  membrane  by  their  large  calibre  and  thin  walls. 
As  the  new  tissue  contracts,  it  may  shut  oS  its  own  blood  supply,  and  then 
undergo  fatty  change  and  be  absorbed,  leaving  no  trace  of  its  existence. 

Second ;  Mucous  Surfaces. — Inflammation  affecting  mucous  membranes 
may  be  either  catarrhal  or  croupous.  Catarrhal  mucous  inflammations  are 
either  acute,  sub-acute,  or  chronic.     In   the  acute  variety  the   affected 


Fig.  3. 

Inflammation  of  Serous  Membrane. 

Viriical  section  of  irijlanud  diajjhragmatic  ■pleura. 

A.  Free  S'irface  coTered  wilh  jihnnoiis  exudation. 

B.  EndotJuTial  layer  with  cdh  chanqerl  an'!  displaced;  at  (a)  t?ie 
cells  are  seen-  detached,  icithin  the  exudation. 

C.  Sub-endothelial  tissue  loith  nvmerous  and  enlarged  blood- 
vessels, d  d  d. 

e  ee.   Lyiiiph  spaces,     x  250.     After  Thi&rf elder. 


1  If  inflammation  is  an  arrest  of  function,  and  ?)(7/ diversion  of  agents  of  nutrition  into  new  channels  of 
activity,  restoration  of  a  part  to  the  natural  state  must  he  as  simple  as  its  departure  from  it,  and  resolution 
of  inflammation  means,  either  that  tlie  temporarily  arrested  process  goes  on  again,  or  if  the  process  has 
proceeded  to  its  ultimate  issue  (deatli  of  the  affected  part),  that  the  destroyed  part  has  to  be  repaired,  not 
by  a  continuation  of  the  morbid  process,  but  simply  by  the  restitution  of  the  normal  condition. 


INFLAMMATION". 


mucous  membrane,  at  the  very  beginning  of  the  process,  is  congested  and 
drier  than  normal,  the  functional  activity  of  the  mucous  glands  being  di- 
minished. After  a  time  an  abnormal  quantity  of  mucus  is  poured  out  on 
its  surface,  the  result  of  an  increase  in  the  functional  activity  of  the  glands. 
This  mucus  may  be  thicker  or  thinner  than  normal,  and  may  have  an  acrid 
or  irritating  quality.  Mucous  exudations  do  not  coagulate,  but  adhere 
somewhat  closely  to  the  surface  of  the  inflamed  membrane  ;  these  changes 
are  accompanied  by  desquamation  of  the  superficial  epithelial  cells.  If  the 
catarrh  assumes  a  purulent  character  in  addition  to  the  above  changes,  the 
mucous  surface  assumes  a  darker  and  livid  hue,  and  pus-cells  are  developed 
both  in  the  mucous  membrane  and  in  the  deeper  substance.  The  amount 
of  pus  will  indicate  the  intensity  and  character  of  the  inflammation.  In 
some  cases  there  are  very  few  pus-cells,  in  others  the  quantity  of  pus  is  very 

large,  and  the  tissues  are  extensive- 
ly infiltrated ,  with  them.  In 
chronic  catarrh  the  blood-vessels 
of  the  inflamed  membrane  are 
either  increased  in  size  and  num- 
ber, or  they  are  less  numerous  and 
more  swollen  than  normal,  giving 
to  the  membrane  a  grayish  appear- 
ance. The  production  of  mucus 
will  be  increased  or  diminished, 
according  as  the  functional  activity 
of  the  mucous  glands  is  increased 
or  diminished.  When  it  is  dimin- 
ished, the  membrane  assumes  a 
"^  dry  and  shining  appearance.  The 
■^  stroma  of  the  affected  membrane 
may  be  hypertrophied  or  atro- 
phied. The  mucous  glands  may 
also  undergo  hypertrophy  or  at- 
rophy. If  their  ducts  become  ob- 
structed they  may  suffer  cystic 
change  :   superficial  erosions  some- 

Veriical  section  of  nasal  se2)timu  ,.  „  ^  ,      ■/]        "^-i 

a.  Pi/swrpvsdes  and  degenerating  epithelium  on  the  timeS   OCCUr  irom    a    rapid,  epitne- 

/;  ee  svrface- 

b.  Superficial  layers  of  epithelium. 
c-  Svb-epHliehal  tissue. 

In  the  submucous  tissue  beneath  the  last  ivill  be  seen — 
//.  !7  0-  Longitudinal  and  transversely  divided  arteries, 

increased  in  number  and  size. 
li  h.  Veins. 

i  i.  Portions  of  enlarged  mucous  glands, 
jj.  Gland  ducts. 

A  portion  of  the  cartilage  of  nasal  sej)tum  is  seen  at  (d), 
with  its  ijerichrondrium  (e). '  x  800.    After  Thierf elder. 


FiCx.  4. 
Inflammation  of  Mucous  Membrane. 


lial  desquamation. 

Croupous  Inflammation  of  Mucous 
Membranes. — In  croupous  inflam- 
mation, the  hypersemia  is  more 
intense  than  in  catarrhal,  so  that 
the  mucous  surface  usually  assumes 
a  dark  livid  color  and  becomes 
swollen  ;  soon  its  free  surface  is  covered  with  a  fibrinous  exudation,  which 
takes  the  place  of  the  epithelium,  and  lies  upon  the  subepithelial  structures 
in  the  form  of  a  network  or  in  irregular  masses.  Enclosed  in  its  meshes 
are  epithelial  and  pus-cells ;  it  varies  in  thickness  from  an   exceedingly 


IISTFLAMMATION". 


thin  semi-transparent  membrane  to  one  that  may  be  an  eighth  of  an  inch 
in  thickness.  This  membranous  exudation  may  be  limited  to  small 
patches,  or  extend  over  a  large  surface.  At  first  it  is  firm  in  consistency 
and  adheres  closely  to  the  tissues  which  it  covers  ;  afterward  it  becomes 
soft,  and  is  easily  separated  from  the  subjacent  membrane  ;  when  fully 
formed  it  may  be  cast  off  in  patches  or  shreds.  Its  separation  is  accom- 
plished by  the  returning  secretion  of  the  follicles,  which  have  been  ob- 
structed, as  well  as  by  the  serous  effusion  from  the  inflamed  surface.  It 
may  sometimes  undergo  fatty,  and  more  rarely  a  mucous  degeneration,  and 
so  become  a  fluid  resembling  mucus.  Generally  in  simple  croupous  in- 
flammation the  submucous  tissue  is  but  slightly  involved,  and  its  meshes 
are  rarely  infiltrated. 

Diphtheritic  Inflammation  of  Mucous  Surfaces. — By  some  this  is  regarded  as 
identical  in  character  with  croupous.  It  differs  from  it  in  a  more  intense 
hypersemia,  and  a  more  extensive  infiltration  of  the  affected  tissue.  The 
fibrinous  exudation  is  more  abundant  and  granular,  and  there  is  a  greater 
metamorphosis  of  the  epithelial  and  tissue  cells.  The  membranous  exuda- 
tion seems  to  be  a  part  of  the  mucous  and  sub-mucous  tissues,  and  cannot 
be  removed  without  the  loss  of  their  substance.  In  the  surface  exudation, 
and  in  the  infiltrated  tissues  underlying  it,  are  found  multitudes  of  bacteria, 
especially  the  micrococci.  When  the  mucous  and  sub-mucous  tissues  are 
so  infiltrated  as  to  cause  undue  pressure,  and  to  cut  off  their  nutritive  sup- 
ply>  the  affected  tissue  dies  and  sloughs  away.  Between  simple  croupous 
and  diphtheritic  exudation 
there  is  every  possible 
gradation.  Some  claim 
that  the  fibrinous  degen- 
eration of  the  epithelium 
cells  is  the  source  of  the 
diphtheritic  exudation ; 
nearly  all  agree  that  the 
primary  changes  are  epi- 
thelial. This  form  of 
inflammation  mnst  be  re- 
garded as  the  local  expres- 
sion of  a  constitutional 
affection. 

■Ulceration  of  Mucous  Sur- 
faces.— Necrotic  processes 
may  be  the  result  of  intense 
purulent  catarrhs  or  diph- 
theritic inflammations  of 
mucous  surfaces.  Super- 
ficial loss  of  substance  from 
rapid  epithelial  degeneration,  and  ulcers  formed  by  the  bursting  of  small  ab- 
scesses are  the  chief  varieties  of  necrosis,  except  in  those  catarrhal  inflamma- 
tions where  the  blood  supply  is  so  suddenly  and  completely  shut  off  that 


1  -^r?v3?!'.-;<is-5i'ife3y^.. 


Pig.  5. 
Diphtheritic  Inflammation  of  Mucous  Membranes. 
Vertical  section  of  the  uvula. 
The  exudation  {A)  is  seen  taking  place  of  the  epithelium,  (B),  and 

firmly  attached  to  the  siib-mucosa,  G. 
At  jD  are  seen  enlarged  blood-vessels  and  mucous  glands. 
E.  Muscular  layer. '   x  55.    After  Thierf elder. 


8  IKFLAMMATIOIS'. 

the  mucous  membrane  dies  in  bulk  and  sloughs  away  (as  in  acute  dysen- 
tery). Most  of  the  little  abscesses  that  produce  ulceration  of  mucous  sur- 
faces are  due  to  obstruction  of  the  follicles  and  lymph  structures  that 
lie  in  the  substance  of  the  membrane  ;  in  consequence  of  their  obstruction 
their  contents  degenerate,  an  abscess  is  formed,  and  an  ulcer  is  the  result. 

Parenchymatous  Inflammation. — In  parenchymatous  inflammation,  the 
cells  which  perform  the  functions  of  the  organ,  the  blood-vessels,  and  the 
stroma  are  in  a  greater  or  less  degree  involved  in  the  inflammatory  process  ; 
and  this  may  pursue  an  acute,  or  chronic  course.  In  a  mild  type  of  paren- 
chymatous inflammation  the  cells  are  enlarged,  granular,  and  opaque,  and 
their  functional  activity  is  increased,  the  blood-vessels  contain  more  than 
their  normal  quantity  of  blood,  and  the  stroma  is  infiltrated  with  serum. 
The  affected  organ  is  slightly  increased  in  bulk,  but  returns  to  its  normal 
size  if  the  inflammation  terminates  by  resolution.  If  the  inflammatory 
process  is  very  intense  and  prolonged,  the  cells  are  destroyed,  the  circula- 
tion is  checked  or  arrested,  and  the  stroma  is  extensively  infiltrated  with 
serum  and  pus.  The  inflamed  organ  is  greatly  increased  in  size,  assumes  a 
livid  or  purple  hue,  and  its  functional  activity  is  arrested.  In  chronic 
parenchymatous  inflammation  the  cells  undergo  fatty  degeneration  and 
disintegration.  The  walls  of  the  vessels  undergo  extensive  thickening,  their 
calibre  is  diminished,  and  they  may  be  obliterated.  The  stroma  is  in- 
creased by  the  development  of  new  tissue.  The  function  of  the  affected 
organ  is  impaired  and  never  returns  to  its  normal  condition,  as  the  result- 
ing changes  are  permanent. 

In  Interstitial  inflammation  the  connective-tissue  or  stroma  of  the  organ 
in  the  part  involved  is  affected.  If  the  inflammation  is  acute,  it  is  usually 
suppurative.  The  pus  formation  may  be  limited  to  small  areas,  or  it  may 
be  diffused.  When  the  pus-cells  are  few,  resolution  is  possible,  but  if  they 
are  numerous  and  infiltrate  a  large  area  of  the  organ,  abscesses  are  formed 
with  dense,  firm  walls.  If  the  inflammation  is  chronic,  it  ends  in  indura- 
tion and  cirrhosis,  by  the  formation  of  new  connective-tissue,  but  does  not 
form  pus.  The  new  tissue  corresponds  in  kind  to  the  original  stroma  of 
the  organ,  and  is  permanent.  The  affected  organ  never  returns  to  its  nor- 
mal condition. 

Fate  of  Pus. — Pus  may  undergo  absorption,  be  evacuated,  become  inspis- 
sated, or  undergo  caseous  transformation.  To  be  absorbed  it  must  undergo 
fatty  degeneration  and  become  converted  into  granular  matter ;  its  absorp- 
tion is  accomplished  by  the  lymphatics.  Its  evacuation  is  accomplished  by 
an  ulcerative  process,  established  in  the  tissues  which  contain  it.  "When 
it  has  been  converted  partly  into  fatty  and  partly  into  granular  matter,  it 
may  become  inspissated  by  the  absorption  of  its  liquid  portion  and  remain 
unchanged  for  a  long  period.  If  it  becomes  incapsulated,  it  changes  into 
caseous  matter  and  remains  as  a  cheesy  mass. 


SECTION    I. 
DISEASES   OF  THE   RESPIRATORY   ORGANS. 

In  considering  diseases  of  the  respiratory  tract,  I  shall  commence  with 

DISEASES   OP   THE   NASAL  PASSAGES. 

The  Medical  diseases  affecting  these  passages  may  be  included  under  the 
general  head  of  Nasal  Catarrhs,  for  nasal  catarrh  appears,  either  as  cause 
or  effect,  in  all  intra-nasal  diseases.  These  diseases  may  be  conveniently 
considered  in  the  following  order  : 

I.  Acute  Coryza.  III.  Hyjjertropliic  Nasal  Catarrh. 

II.   Chronic  Coryza.  IV.  Atro^phic  Nasal  Catarrh. 

V.   Ozmna. 

ACUTE    COEYZA. 

Acute  Coryza  is  an  acute  catarrhal  inflammation  of  the  nasal  mu- 
cous membrane  characterized  by  engorgement  and  tumefaction  of  the  tis- 
sues over  the  turbinated  bones.    It  is  commonly  called  "  cold  in  the  head." 

Morbid  Anatomy. — At  the  onset  of  the  affection,  the  anterior  portion  of 
the  nasal  mucous  membrane  is  markedly  congested,  its  normal  pink  and 
red  hue  being  replaced  by  a  bright  arterial  red,  while  the  inner  margins  of 
the  turbinated  tissues  assume  the  blue  color  of  intense  venous  engorgement. 
The  turbinated  tissues  are  tumefied  because  of  the  distension  of  the  venous 
spaces  with  blood.  Having  lost  their  normal  tonicity,  they  are  unable  to 
retract  and  reduce  the  turgescence.  The  distension  is,  after  a  time,  relieved 
by  an  exudation,  and  the  blood  gradually  resumes  its  natural  flow. 

Etiology. — Acute  coryza  may  result  from  momentary  reduction  of  the 
surface  temperature  by  chilling,  which  causes  an  unequal  distribution  of 
blood.  As  the  nasal  mucous  membrane  has  less  resistance  than  other  mu- 
cous surfaces,  its  inflammation  is  the  result.  It  may  also  be  occasioned  by 
external  irritants,  such  as  tobacco,  dust,  acrid  fumes  from  chemicals,  or  by 
direct  injury  ;  extensive  desiccation  of  the  nasal  mucous  membrane,  inspis- 
sated mucus,  and  foreign  bodies  may  also  cause  it. 

Symptoms.— An  acute  coryza  may  be  ushered  in  by  a  slight  chill.  It  is 
often  preceded  by  a  pricking  sensation  in  the  turbinated  tissues.  These 
structures  are  rendered  extremely  sensitive  by  the  intense  hyperaemia,  so 
that  sneezing  is  provoked  by  touching  them.  The  sudden  tumefaction 
accompanying  venous  engorgement  arrests  secretion  and  causes  an  uncom- 
fortable sensation  of  dryness  ;  this  is  somewhat  relieved  by  a  free  mucous 


10  DISEASES   OF   THE   EESPIRATORY    ORGANS. 

discharge,  which  in  a  short  time  becomes  miico-purulent.  The  accessory 
cavities  of  the  nose  may  become  involved,  producing  headache. 

Differential  Diagnosis. — A  j)ersistent  discharge,  caused  by  foreign  bodies 
in  the  nostrils,  may  be  mistaken  for  an  acute  catarrh.  Concealed  scrofu- 
lous and  syphilitic  ulcers,  with  co-existing  coryza,  cause  similar  symptoms, 
but  will  hardly  be  mistaken  for  it. 

Prognosis. — The  nostril  generally  returns  to  its  normal  condition  in  a 
few  days.  Eepeated  attacks  of  acute  coryza  may  result  in  permanent  struct- 
ural changes,  and  lead  to  a  chronic  nasal  catarrh.  The  ear,  lachrymal 
duct,  accessory  nasal  sinuses  and  cavities  may  secondarily  become  involved. 

Treatment. — An  effort  to  abort  the  disease  in  its  incipiency  may  be  made 
by  the  administration  of  ten  or  fifteen  grains  of  quinine,  given  alone,  or 
with  an  equal  quantity  of  bromide  of  sodium.  A  full  dose  of  opium  at  its 
very  onset  may  restore  the  vascular  equilibrium  and  abort  the  affection. 
Inhalations  of  ammonia,  carbolic  acid  and  alcohol,  the  vapor  of  solutions 
of  carbolic  acid  inhaled  through  a  cone,  and  fumes  of  iodine  and  cologne, 
inhaled  through  a  sponge,  often  relieve  the  engorgement  and  tension  of  the 
mucous  membrane  by  exciting  exudation.  Depletion  of  the  turbinated  tis- 
sues by  puncturing  them  with  sharp  needles,  relieves  the  turgescence  and 
iavors  their  retraction.  Spraying  of  the  parts  reduces  the  congestion  by 
chilling  the  turgid  tissues,  and  gives  comfort  and  hastens  recovery  by  re- 
moving acrid  discharges.^  Chloride  of  sodium,  bicarbonate  of  soda  and 
borax  (two  grains  to  the  oz.  of  water)  make  efficient  cleansing  solutions. 

CHRONIC    CORYZA. 

{Chronic  Nasal  Catarrh.) 

Chrokic  Cortza  is  a  chronic  catarrhal  inflammation  of  the  nasal 
mucous  membrane  characterized  by  an  excessive  and  persistent  discharge 
of  mucus. 

Morbid  Anatomy. — There  is  intense  and  persistent  congestion  of  the  nasal 
mucous  membrane  without  pronounced  tumefaction  of  the  deeper  tissues 
covering  the  turbinated  bones.  The  abnormal  cell  production  is  not 
accompanied  by  a  marked  increase  of  the  sub-mucous  cellular  tissues. 
A  continuous  discharge  of  watery  mucus  generally  escapes  anteriorly. 
Inspissation  of  the  mucus  seldom  occurs,  as  the  nares  are  constantly  moist. 
Excoriation  of  the  lips  and  integument  about  the  nostril  is  often  caused  by 
the  action  of  the  acrid  discharges. 

Etiology. — Constant  watery  mucous  discharges  are  sometimes  caused  by 
the  lodgment  of  foreign  bodies  in  the  nostril.  It  is  frequently  observed  in 
young  women  having  a  constitutional  tendency  to  catarrh.  Cachectic 
children  readily  acquire  the  disease.  An  irritating  atmosphere  or  abnor- 
mally moist  or  impure  air  may  develop  it. 

Symptoms. — Annoying  paroxyms  of  sneezing  are  of  frequent  though  not 
invariable  occurrence.     A  burning  sensation  of  the  anterior  nasal  orifices  is 

i  Delano's,  Goodyear's,  or  Ricliardsou's  hand  atomizers  are  best  for  this  purpose. 


HYPERTROPHIC    NASAL   CATARRH.  11 

often  complained  of.  Discomfort  is  sometimes  caused  by  the  excoriation 
resulting  from  the  acrid  discharges. 

Differential  Diagnosis. — Failure  to  find  a  foreign  body  in  the  nasal  pas- 
sages will  proTC  tliat  the  discharge  is  not  caused  by  mechanical  irritation. 
Absence  of  ulceration  demonstrates  the  catarrhal  nature  of  the  affection. 
The  chronicity  of  the  complaint  and  freedom  from  nasal  oTjstruction  dis- 
tinguish it  from  acute  coryza.  The  distinctive  feature  of  hypertrophic 
nasal  catarrh,  thickening  of  the  intra-nasal  tissue,  does  not  occur  in  chronic 
coryza.  In  hypertrophic  nasal  catarrh  the  secretions  usually  flow  pos- 
teriorly. Concentration  and  inspissation  of  the  nasal  mucus  rarely  occur 
in  chronic  coryza. 

Treatment. — The  nares  should  be  first  thoroughly  cleansed,  the  acrid 
discharge  being  best  removed  by  means  of  syringes  and  sprays.^  Weber's 
nasal  douche  is  convenient  for  cleansing.  Solutions  of  bicarbonate  of 
soda,  boracic  acid,  and  chloride  of  sodium,  five  to  ten  grains  to  the  ounce 
of  water  may  be  employed,  the  fluid  always  being  warmed  before  using. 

Alkaline  solutions  may  be  thrown  into  the  nasal  cavities  by  means  of 
atomizers.  After  the  nares  have  been  thoroughly  cleansed,  it  is  well  to  use 
astringents.  They  should  be  applied  in  the  form  of  sprays.  Of  these, 
ferric  alum,  five  grains  to  the  ounce  of  water,  sulphate  of  zinc,  and  tartaric 
acid,  three  grains  to  the  ounce  of  water,  are  the  most  efiicient.  Iodoform, 
applied  by  means  of  Ely's  powder-blower,  acts  as  a  local  anaesthetic,  and 
sometimes  affords  great  relief.  Vaseline  and  benzoated  oxide  of  zinc  oint- 
ment may  be  employed  to  protect  the  margins  of  the  nostril  and  heal 
excoriations.  Constitutional  vices  and  tendencies  should  be  corrected  by 
appropriate  treatment.  The  general  health  should  be  improved  by  tonics 
and  an  out-of-door  life. 

HYPEETROPHIC    ISTASAL    CATARRH. 

{Chronic  Naso-Pliaryngeal  Catarrh.) 

Hypertrophic  Nasal  Catarrh  is  a  chronic  catarrhal  inflammation, 
characterized  by  hypertrophy  of  the  turbinated  tissues  and  intra-nasal 
mucous  membrane. 

Morbid  Anatomy. — The  nasal  mucous  membrane  is  in  a  constant  state  of 
engorgement,  especially  the  soft  turbinated  structures,  whose  cavernous 
sinuses  are  so  distended  as  to  interfere  with  free  nasal  respiration.  Hyper- 
trophic changes  are  most  extensive  in  the  loose  turbinated  tissues ;  the 
hypertrophy  is  due  to  the  general  increase  of  the  soft  turbinated  structures. 
Permanent  dilatation  of  the  turbinated  blood  cavities  takes  place,  with  con- 
sequent loss  of  "  turbinated  erection."     Localized  thickening  of  the  tissues 

*  Dobell's  is  an  efficacious  cleansing  solution,  viz.: 

'^    Carbolic  acid gr.  j. 

Bicarbonate  of  soda 

Borax iia  gr.  v. 

Glycerine 3j. 

Water 5j. 

in. 


12  DISEASES   OF   THE   EESPIEA.TOEY   ORGAifS. 

over  the  septum,  with  deviation  of  this  structure,  is  of  common  occurrence. 
The  nasal  mucus,  with  epithelial  debris,  being  retarded  in  its  escape  by  the 
thickened  mucous  membrane,  inspissates  and  accumulates  in  the  nostril. 
The  turbinated  hypertrophies  have  a  light  pink  hue  ;  when  complicated  by 
acute  coryza  they  vary  in  color  from  arterial  red  to  a  venous  blue. 

Etiology. — This  disease  sometimes  results  from  repeated  attacks  of  acute 
coryza.  The  constant  irritation  caused  by  a  deviated  septum,  pressing 
upon  the  turbinated  tissues  or  nasal  mucous  membrane,  frequently  gives 
rise  to  it.  Distortion  of  tlie  nasal  gutter  from  deflection  of  the  septum, 
with  consequent  accumulation  of  mucus,  always  develops  it.  The  growth 
of  gelatinous  polypi  is  encouraged  by  the  abnormal  vascularity,  and  the 
irritation  they  produce  intensifies  the  affection.  The  dust  of  cities,  facto- 
ries, and  certain  occupations  act  as  excitants.  Damp  localities,  irregu- 
lar living,  insufficient  clothing,  and  prolonged  exposure  to  cold  and  wet, 
also  predispose  to  it. 

Symptoms. — The  symptoms  of  this  affection  are  usually  due  to  turbinated 
enlargement  and  accumulated  secretions.  Thick,  tenacious  mucus  collects 
in  the  nostrils,  and  small  masses  drop  into  the  pharynx,  and  thence 
pass  into  the  larynx,  producing  irritation,  coughing  and  retching.  The 
nostrils  may  be  permanently  or  temporarily  occluded.  Hearing  is  impaired, 
either  by  extension  of  the  catarrhal  processes,  or  collapse  of  the  Eustachian 
tube  from  suction  induced  by  nasal  stenosis.  Obstinate  sneezing,  head- 
ache, suffusion  of  the  eyes,  or  the  ordinary  symptoms  of  cold  in  the  head, 
may  occur  as  the  result  of  acute  exacerbations.  The  pressure  exercised  by 
the  thickened  tissues  sometimes  produces  persiitent  neuralgia.  Nasal  ste- 
nosis, combined  with  laryngeal  irritation,  may  develop  symptoms  resem- 
bling spasmodic  astlima. 

Differential  Diagnods. — The  chronicity  of  the  affection  will  prevent  it  from 
being  mistaken  for  an  acute  coryza.  A  careful  examination  will  show 
whether  the  disease  is  simple,  or  dependent  upon  the  presence  of  foreign 
bodies  or  growths.  The  mistake  of  confounding  turbinated  hypertro|)hies 
with  gelatinous  polypi  may  be  avoided  by  comparing  the  gelatinous  appear- 
ance, mobility,  and  clear  contour  of  the  polypus,  with  the  fleshy  hue,  firm 
attachment,  and  irregular  shape  of  the  hypertrophied  turbinated  tissues. 

Prognosis. — The  cure  of  hypertropliic  nasal  catarrh  depends  upon  the 
general  health,  the  nature  of  the  structural  changes,  and  the  complications. 
Patients,  otherwise  in  good  health,  who  have  acquired  the  disease  from 
prolonged  exposure,  may  be  permanently  relieved  by  a  change  of  climate, 
after  the  removal  of  the  nasal  obstruction.  The  part  played  by  a  deviated 
nasal  septum,  in  chronic  nasal  catarrh,  is  joronounced,  and  its  excision  is 
as  much  called  for  as  the  removal  of  a  foreign  body.  Turbinated  hyper- 
trophies obstruct  nasal  drainage  and  respiration,  and  provoke  and  continue 
the  disease  which  produced  them.  There  are  cases  in  which  the  simple 
excision  of  the  offending  structures,  by  removing  the  cause  of  the  disease 
and  restoring  normal  respiration,  circulation  and  drainage,  effects  a  cure. 
When  the  health  is  much  impaired,  with  a  tendency  to  profuse  catarrhal 
discharges,  and  with  great  distortion  of  the  interior  of  the  nostril,  the 


ATROPHIC    NASAL    CATARRH.  13 

prognosis  is  unfavorable.     More  or  less  relief,  however,  can  be  afforded  in 
all  cases. 

Treatment. — The  treatment  of  hypertrophic  nasal  catarrh  consists  in  the 
restoration  of  the  symmetry  of  the  nasal  chambers,  and  the  local  cleansmg 
of  the  part,  with  the  prolonged  local  use  of  certain  medicinal  agents. 
Caustics  and  cutting  instruments  are  now  employed  to  remove  obstructions 
and  restore  drainage  and  nasal  respiration.  The  exfoliation  produced  by 
cauterization  with  chromic  acid  and  nitrate  of  silver  slowly  reduces  intra- 
nasal hypertrophies.  They  may  be  used  when  the  tissues  are  easily  acces- 
sible. The  platinum  knife,  made  incandescent  by  the  galvanic  current,  is 
extensively  used  to  diminish  hypertrophied  tissues.  It  acts  either  by 
eschar  and  cicatricial  contraction,  or  by  excision.  Grlacial  acetic  acid,  ap- 
plied by  means  of  Bosworth's  nasal  applicator,  forms  an  eschar  which  can 
be  easily  limited,  and  immediately  neutralized  by  an  alkaline  spray.  Tur- 
binated hypertrophies  and  gelatinous  polypi  can  be  safely  removed  by  the 
cold  wire,  with  Jarvis'  Ecraseur.  After  the  removal  of  the  hypertrophied 
tissues,  Dobell's  solution,  or  the  bicarbonate  or  chloride  of  sodium,  may  be 
employed  to  cleanse  the  parts  ;  the  addition  of  an  antiseptic  like  carbolic 
or  salicylic  acid,  or  the  permanganate  of  potash,  is  often  of  service. 
Nasal  washes  are  most  effective  when  employed  with  the  post-nasal  syringe. 
Cleansing  can  be  practised  by  the  patient,  by  means  of  Warner's  nasal 
douche.  Astringents  should  only  be  used  after  thorough  cleansing.  They 
are  usually  applied  by  means  of  sprays.  Insufflations  of  boracic  acid  and 
iodoform  are  sometimes  advantageously  .employed.  Insufflation  should 
only  be  practised  with  powder-blowers  working  on  the  Ely  principle. 

ATROPHIC    ]SrASAL    CATARRH. 

{Dry  Nasal  Catarrh.) 

Atrophic  Nasal  Catarrh  is  a  chronic  catarrhal  inflammation  re- 
sulting in  atrophy  and  desiccation  of  the  nasal  mucous  membrane. 

Morbid  Anatomy. — The  nasal  cavities  are  very  much  enlarged  from  atro- 
phy of  the  soft  and  osseous  turbinated  structures.  The  mucous  membrane 
becomes  thin,  and  loses  part  of  its  epithelium  and  some  of  its  mncous 
glands ;  and  there  is  an  unnatural  dryness  of  the  nasal  and  naso-pharyngeal 
mucous  membrane  from  deficient  glandular  secretion.  Crusts  of  decom- 
posing mucus  adhere  to  the  turbinated  ridges,  and  occupy  the  sinuosities 
of  the  nostrils. 

Etiology. — This  disease  is  local  in  character.  It  may  be  brought  on  by 
rapid  absorption  of  moisture  from  the  nasal  mucous  membrane,  hence  the 
frequency  of  its  occurrence  in  persons  continually  subjected  to  the  desiccat- 
ing influence  of  a  dry  or  dusty  atmosphere.  Occupations  which  favor  this 
desiccation,  as  wood-turning,  soldering,  milling,  cigar-making,  develop  the 
affection.  It  is  sometimes  associated  with  a  hypertrophic  nasal  catarrh, 
and  in  such  cases  probably  owes  its  existence  to  a  local  modification  of  the 
catarrhal  processes  by  which  the  inflammatory  activity  is  largely  expended 


14  DISEASES    OF    THE    KESPIEATORY    ORGA]S'S. 

upon  the  glandular  follicles.  Accumulation  of  the  nasal  mucus  is  favored 
by  the  destruction  of  the  cilia  of  the  epithelium.  The  prolonged  contract- 
ing effect  of  inspissating  nasal  mucus  promotes  progressive  atrophy  of  the 
soft  tissues  and  bones. 

Symptoms.— There  is  usually  entire  loss  of  the  sense  of  smell ;  a  feeling 
of  fullness  in  the  nose  is  sometimes  complained  of,  the  sensation  resembling 
that  produced  by  a  foreign  body.  Neuralgia  and  dull  frontal  headache  are 
often  present.  An  annoying  fetor,  not  an  invariable  occurrence,  results 
from  the  decomposition  of  retained  nasal  secretions.  Obstructed  nasal 
respiration  from  accumulation  or  lodgment  of  crusts  causes  much  discom- 
fort. Tenderness  and  extreme  sensitiveness  of  the  mucous  membrane  may 
follow  the  detachment  of  the  incrustations. 

Differential  Diagnosis. — The  glazing  and  desiccation  of  the  surface  demon- 
strate the  existence  of  dry  catarrh;  its  chronicity  will  distinguish  the  affec- 
tion from  the  temporary  dryness  of  an  acute  catarrhal  inflammation. 
Accumulations  of  crusts,  with  the  co-existing  musty  stencii,  are  often  associ- 
ated with  the  atrophic  changes.  In  the  advanced  stages  the  unnatural 
roominess  of  the  nares  from  general  shrinkage  of  the  soft  and  osseous 
structures  is  a  distinguishing  feature  of  the  affection. 

Prognosis. — The  disease  does  not  perceptibly  shorten  life.  Beneficial  re- 
sults, or  comj)lete  restoration  of  the  glandular  function,  may  be  obtained  by 
careful  stimulation.  An  artificial  supply  of  moisture  relieves  the  dryness 
and  promotes  a  return  of  the  normal  secretion.  Antiseptic  cleansing  pre- 
vents decomposition,  and  removes  a  disagreeable  feature  of  the  disease.  Loss 
of  tissue  from  atrophy  of  the  soft  and  solid  structures  is  permanent.  Be- 
lief of  the  dryness,  nasal  obstruction,  offensive  odor,  and  general  discomfort 
is  always  possible. 

Treatment. — Thorough  cleansing  with  alkaline  solutions  should  be  prac- 
tised to  remove  nasal  incrustations.  Dobell's  solution  or  carbolized  water 
rendered  alkaline  by  the  addition  of  soda  or  potash,  as  recommended  for 
hypertrophic  nasal  catarrh,  should  be  thrown  into  the  nasal  cavities  by 
means  of  the  post-nasal  syringe.  At  first  it  may  be  necessary  to  remove  the 
crusts  by  mechanical  means.  Cleansing  should  be  practised  daily  by  the 
patient.  Warner's  douche  may  be  used  for  this  purpose.  Accumulation 
and  inspissation  of  the  nasal  mucus  are  effectually  prevented.  The  painful 
spots  sometimes  produced  by  detachment  of  crusts  are  best  treated  by  the 
application  of  iodoform.  Fluid  cosmoline  or  melted  vaseline  thrown  into 
the  nostril  by  an  atomizer  will  prevent  the  reformation  of  catarrhal  crusts. 
As  the  sensibility  of  the  mucous  membrane  is  largely  obliterated  by  the 
atrophic  changes,  stimulating  powder  may  be  employed  to  provoke  secre- 
tion, and  thus  promote  the  discharge  of  the  accumulated  debris.  When 
there  is  marked  general  constitutional  impairment,  change  of  climate  or 
occupation  may  be  advisable,  with  the  administration  of  tonics  and 
alteratives. 


OZ^NA.  15 

{Fetid  Nasal  Catarrh.) 

The  term  Oz^ita  is  applied  to  necrotic  and  ulcerative  processes  in  the 
uose  and  its  neighboring  cavities,  accompanied  by  fetor  due  to  putrefaction. 

Morbid  Anatomy. — The  thick  mucus,  dry  crusts,  and  peculiar  processes  of 
atrophic  catarrh  are  discoverable  in  catarrhal  ozaena  of  the  nasal  cavity; 
muco-purulent  secretions  are  imprisoned  beneath  the  dried  follicles  of  mu- 
cus adhering  to  the  turbinated  ridges  and  interspaces,  and  then  undergo 
decomposition.  When  associated  with  the  disease  of  the  accessory  cavities, 
the  ethmoidal  cells,  the  sphenoidal  sinuses,  and  the  antrum  of  Highmore, 
there  is  continually  or  intermittently  a  discharge  of  glutinous  offensive 
muco-pus.  In  antral  ozgena  there  usually  exists  a  chronic  catarrhal  inflam- 
mation of  the  mucous  membrane  lining  the  maxillary  sinus  with  a  constant 
formation  of  muco-purulent  matter.  The  tertiary  ulcers  of  syphilitic 
ozaena  progress  rapidly,  eroding  the  soft  tissues,  denuding  the  turbinated 
bones,  and  inducing  necrosis.  Their  favorite  situation  is  upon  the  carti- 
lage of  the  septum.  Perforation  of  the  nasal  septum  by  syphilitic  ulcera- 
tion is  of  common  occurrence.  In  scrofulous  ozgena  the  mucous  membrane 
may  be  ulcerated,  or  an  accessory  cavity  may  be  involved  in  an  asthenic 
catarrhal  inflammation  ;  when  it  is  catarrhal  in  character,  a  peculiar  bluish 
viscid  discharge  may  be  discovered  oozing  from  the  cavity  or  sinus 
involved. 

Etiology. — The  ozsena  of  atrophic  catarrh  is  due  to  the  decomposition  of 
secretions  which  adhere  to  the  mucous  membrane.  When  the  ethmoidal 
cells'  or  sphenoidal  sinuses  are  involved,  the  offensive  odor  is  due  to  de- 
composition of  pent-up  muco-purulent  matter.  Antral  ozaena  may  origi- 
nate in  the  catarrhal  inflammation  set  up  by  a  tooth  projecting  into  the 
antrum.  .  Catarrh  of  the  antrum  may  also  result  from  the  extension  of  in- 
flammation to  it  from  the  nares.  Syphilitic  ozaena  may  be  caused  by  osteitis, 
or  by  fetid  catarrh  and  decomposing  debris  of  ulcers.  It  maybe  associated 
with  disease  of  the  pneumatic  nasal  cavities.  JSTecrosed  bone  acts  as  an 
irritant,  provoking  and  keeping  up  the  fetid  discharges.  Scrofulous  ozaena 
may  originate  in  an  ulcer  or  in  catarrh  of  the  accessory  nasal  cavities. 
Ozaena  is  seldom  produced  by  the  decomposition  of  retained  secretions  in 
hypertrophic  nasal  catarrh. 

Symptoms. — In  the  ozaena  of  atrophic  catarrh,  the  patient  is  seldom 
disturbed  by  the  odor,  as  he  is  unable. to  distinguish  odors.  When  the 
disease  implicates  a  cavity,  the  sufferer  is  usually  painfully  aware  of  the 
ozaenous  taint.  The  detachment  of  incrustations  may  be  followed  by  slight 
or  alarming  hemorrhage.  Violent  retching  or  vomiting  may  be  caused  by 
the  passage  of  loosened  crusts  into  the  pharynx.  The  constant  effort  to 
free  the  nostril  from  incrustations  proves  extremely  wearisome  ;  a  dull 
headache  is  often  associated  with  disease  of  the  sinuses,  its  location  being 
determined    by  the  situation  of  the  cavity.     Ulcerative  ozaena  is  seldom 


16  DISEASES    OF    THE    EESPIRATORT    ORGAJSTS. 

accompanied  by  acute  pain.  Occasional  burning  sensations  and  severe 
headache  are  its  only  painful  symptoms. 

Differential  Diagnosis. — The  ozsena  of  atrophic  catarrh  is  diagnosticated  by 
the  rules  already  given  for  the  diagnosis  of  that  affection.  Failure  to  find 
a  source  for  ozaena  in  the  nasal  cavity,  discovery  of  the  peculiar  fetid  dis- 
charge already  described  as  trickling  from  the  superior  meatus,  the  condi- 
tion being  usually  unilateral,  are  evidences  of  the  existence  of  ozsena  of  the 
sphenoidal  sinus  or  ethmoid  cells.  Antral  ozaena  is  easily  recognized  by 
the  source  of  the  discharge  and  the  situation  of  the  pain.  Non-ulcerative 
strumous  or  syphilitic  ozsena  is  usually  confined  to  the  accessory  nasal 
cavities.  The  scrofulous  diathesis  and  history  or  manifestations  of  syphilis 
determine  its  nature.  In  the  ulcerative  ozaena  of  syphilis  the  ulcers  resem- 
ble similar  lesions  in  other  parts  of  the  respiratory  tract.  Their  edges  are 
ragged,  and  the  red  areola  encircling  the  ulcer  fades  away  into  the  surround- 
ing normal  or  congested  mucous  membrane.  There  is  often  a  puffiness  and 
infiltration  of  the  tissues  about  the  sore.  In  the  ulcerative  ozsena  of  scrof- 
ula the  edges  of  the  ulcer  are  usually  smooth  and  red,  occasionally,  how- 
ever, they  are  pale.  The  ulcer  and  areola  are  clearly  defined  in  the  pale 
ansemic  membrane.  Pale  granulations,  or  a  spongy  mucous  membrane,  may 
surround  the  margin  of  the  ulcer.  Its  chronicity,  the  enlarged  cervical 
glands,  cachexia,  and  general  evidences  of  strumous  diathesis,  establish  the 
nature  of  the  ulcer.  Perforation  of  the  septum  from  constant  removal  of 
scabs,  with  consequent  abrasion,  should  not  be  confounded  with  the  ravages 
of  specific  disease. 

Prognosis. — The  prognosis  as  regards  life  is  almost  always  favorable.  The 
conditions  determining  the  course  of  atrophic  nasal  catarrh  apply  also  to 
the  ozsena  complicating  this  afl:ection.  Scrofulous  catarrhal  ozsena  of  the 
sphenoidal  sinuses  and  ethmoidal  cells  is  dependent  up^n  the  general  health, 
and  may  persist  for  months,  or  even  years.  Syphilitic  non-ulcerative 
ozsena  is  more  amenable  to  treatment  than  the  scrofulous.  Antral  ozsena, 
due  to  simple  catarrhal  inflammation  or  the  presence  of  irritants,  responds 
to  proper  anti-syphilitic  treatment.  The  cure  or  relief  of  syphilitic  or 
scrofulous  ulcerative  ozsena  depends  upon  the  healing  of  these  ulcers. 
When  the  disease  depends  upon  the  presence  of  dead  or  dying  bone  its 
removal  will  often  produce  a  cure. 

Treatment. — The  treatment  recommended  for  an  atrophic  nasal  catarrh 
relieves  also  the  ozsena  complicating  this  affection.  When  the  disease  is 
confined  to  the  accessory  cavities  it  is  only  possible  to  remove  the  discharges 
as  they  accumulate  by  means  of  Dobell's  solution,  or  any  of  the  antiseptic 
alkaline  washes  recommended  for  hypertrophic  or  atrophic  nasal  catarrh. 
The  patient  can  accomplish  m.uch  in  this  direction  by  faithfully  using 
Warner's  nasal  douche.  Careful  applications  of  powder  made  with  an  Ely 
powder-blower  prove  beneficial.  Its  odor  may  be  disguised  by  tincture  of 
musk,  tonga  bean,  or  the  aromatic  essential  oils.  Antral  catarrh  due  to  a 
dead  tooth,  or  misplaced  filling,  may  require  the  removal  of  an  upper  molar 
and  perforation  of  the  alveolus.  Superficial  syphilitic  ulcers  when  within 
reach  are  readily  healed  by  local  applications  of  chromic  acid,  or  of  nitrate 


ACUTE    CATAREHAL    LARYNGITIS.  17 

of  silver  fused  upon  a  probe.  The  same  local  treatment  does  not  apply  to 
the  deep  syphilitic  ulcers.  Iodoform  frequently  applied  gives  the  best 
results  in  the  treatment  of  this  form.  Local  applications  should  be  always 
preceded  by  careful  cleansing  by  means  of  sprays  or  the  syringe.  Specific 
constitutional  medication  should  be  combined  with  the  local  treatment.  It 
prevents  the  recurrence  of  the  syphilitic  lesions  and  materially  hastens  cica- 
trization. In  the  deep  ulcers  rapidly  increased  doses  of  iodide  of  potassium, 
with  or  without  mercury,  are  required  to  facilitate  healing.  Local  stimula- 
tion does  not,  as  a  rule,  benefit  scrofulous  ulcers,  on  account  of  their  low 
vitality  ;  the  cleansing  and  iodoform  treatment  is  preferable.  Cod-liver  oil 
emulsions,  hypophosphites,  iron,  nutritious  diet,  with  the  usual  hygienio 
observances,  constitute  the  general  treatment.  The  removal  of  dead  or 
dying  bone  may  hasten  healing  or  complete  the  cure. 

DISEASES    OF    THE    LARYNX. 

Laryngeal  affections  may  be  primary  or  secondary  ;  primary ,  when  the 
larynx  is  first  affected,  and  the  affection  is  local;  secondary,  when  the 
laryngeal  disease  occurs  as  a  complication,  and  depends  upon  some  morbid 
state  of  the  general  system.  I  shall  consider  them  under  the  following 
heads  : 

I.  Acute  Catarrhal  Laryngitis.  V.  (Edema  Glottidis. 

II.   Chronic  Catarrhal  Laryngitis.  VI.  Croupous  Laryngitis, 

III.  Chronic  Laryngitis  of  Phthisis.  VII.  Laryngeal  Ulcers. 

IV.  Chronic  Laryngitis  of  Syphilis.        VIII.  Neuroses  of  the  Larynx. 

IX.  Tumors  of  the  Larynx. 

The  most  important  to  the  general  practitioner  in  this  list  are  the  inflam- 
mations. 

ACUTE    OATAEEHAL    LAEYIifGITIS. 

Acute  Catarrhal  Laryngitis  is  an  acute  inflammation  of  the  mucous 
membrane  of  the  larynx,  which  gives  only  the  products  of  a  catarrhal 
inflammation.  It  may  occur  at  any  age,  and  be  mild  or  severe  in  type ; 
the  severity  varies  in  proportion  to  the  extent  that  the  submucous  areolar 
tissue  of  the  larynx  participates  in  the  morbid  processes. 

Morbid  Anatomy. — The  anatomical  changes  which  take  place  in  this 
affection  are  characterized  by  redness,  swelling  and  softening  of  the  laryn- 
geal mucous  membrane ;  its  surface,  at  first  dry,  the  function  of  the 
mucous  glands  being  arrested,  is  soon  coated  with  mucus  which  contains 
epithelial  and  pus-cells.  When  the  deeper  tissues  are  affected,  the  in- 
flammatory products  accumulate  beneath  the  mucous  membrane,  in  its 
substance  and  upon  its  surface,  causing  tumefaction  of  the  parts,  which  in 
this  situation  is  attended  with  danger.  On  the  other  hand,  when  the  in- 
flammatory process  is  superficial,  and  all  the  products  are  upon  the  surface 
of  the  membrane,  there  is  little  danger.  At  the  post-mortem  examination 
there  is  often  less  redness  and  swelling  of  the  laryngeal  membrane  than  were 
2 


18  DISEASES    OF    THE    EESPIRATOET    ORGANS. 

observed  during  life,  owing  to  the  richness  of  this  mucous  membrane  in 
elastic  tissue.  The  redness  and  swelling  are  due  to  hypersemia  and  infil- 
tration of  the  mucous  membrane.  The  mucous  follicles  may  be  so  en- 
larged as  to  be  recognizable  by  the  naked  eye,  and  each  may  yield  on  pres- 
sure a  drop  of  muco-pus.  The  mucus  is  their  natural  secretion  greatly  in- 
creased in  amount,  containing  pus-cells  and  swollen  epithelial  cells.  If  the 
follicle  continues  to  suppurate,  it  is  destroyed,  leaving  a  small  depression 
or  ulcer.  This  inflammation  usually  runs  a  rapid  course,  yet  in  some 
cases  it  becomes  chronic.  It  may  produce  superficial  erosions,  it  may  also 
be  accompanied  by  ecchymoses  of  the  membrane,  and  an  escape  of  blood  in 
the  secretions ;  it  is  then  said  to  be  hemorrhagic,  and  the  hemorrhage  is 
due  to  rupture  of  capillary  vessels.  Again,  in  some  cases  it  is  limited  to  a 
portion  of  the  larynx,  more  especially  to  the  epiglottis  ;  then  it  is  usually 
associated  with  inflammation  of  the  mouth,  fauces  and  pharynx.  The 
danger  in  this  form  of  laryngitis  is  due  not  only  to  the  submucous  inflam- 
mation, but  also  to  the  spasm  of  the  glottis,  which  the  infiltration  causes, 
partly  by  reflex  action,  partly  by  direct  irritation  of  the  adductor  muscles 
of  the  vocal  cords. 

Etiology. — Badly  nourished  cachectic  subjects,  rather  than  the  strong  and 
healthy,  are  predisposed  to  acute  catarrhal  laryngitis  ;  those  constantly  ex- 
posed to  changes  of  temperature  in  the  open  air  are  less  liable  to  be  affected 
with  it  than  those  who  are  rarely  subjected  to  such  exposures.  There  is 
also  a  peculiar  vice  of  constitution  that  renders  certain  persons  especially 
liable  to  catarrhal  inflammation,  and  consequently  predisposes  them  to 
attacks  of  catarrhal  laryngitis.  Among  the  exciting  causes  of  this  affection 
may  be  named  chilling  of  the  surface  by  exposure  to  wet  and  cold,  par- 
ticularly that  of  the  neck  and  feet.  Mechanical  violence  to  the  larynx,  in- 
halations of  irritating  vapors  and  acrid  liquids  may  give  rise  to  the  most 
intense  laryngeal  catarrh. 

Laryngitis  may  also  be  developed  secondarily  during  the  course  of  the 
exanthematous  fevers,  typhus  fever,  diphtheria,  syphilis,  and  phthisis;  not 
infrequently  it  is  the  result  of  the  extension  of  inflammation  from  parts 
adjacent  to  the  larynx,  as  in  tonsillitis,  erysipelas,  etc.  Acute  bronchitis  is 
usually  attended  by  a  mild  form  of  acute  laryngeal  catarrh. 

Symptoms. — The  symptoms  that  attend  the  development  of  acute  ca- 
tarrhal laryngitis  vary  with  the  extent  and  severity  of  the  inflammatory 
process  ;  it  usually  comes  on  insidiously,  and  a  very  mild  laryngeal  catarrh 
may  suddenly  become  very  severe.  Usually  at  first  there  is  soreness  of  the 
throat,  accompanied  by  a  sense  of  constriction,  or  a  tickling  sensation  with 
a  tendency  to  cough  ;  the  larynx  is  tender  on  pressure,  there  is  difficulty  in 
swallowing,  which  becomes  more  and  more  marked  as  the  disease  pro- 
gresses ;  to  this  is  soon  added  difficulty  of  breathing.  The  character  of  the 
respiration  varies  with  the  seat  of  the  inflammation.  If  it  is  confined  ex- 
:clusively  to  the  upper  portion  of  the  larynx,  as  it  often  is  at  its  onset,  the 
difficulty  will  be  with  inspiration  only,  which  will  be  prolonged  and  accom- 
panied with  stridor ;  if  the  lining  membrane  of  the  whole  larynx  is  involved, 
and  the  calibre  of  the  larynx  becomes  contracted  from  cedematous  infiltra- 


ACUTE    CATAEKHAL    LAEYNGITIS.  19 

tion  and  spasmodic  approximation  of  the  vocal  cords,  there  will  be  difficulty 
with  both  inspiration  and  expiration,  and  both  will  be  protracted  and 
wheezing ;  in  severe  cases  the  patient  will  be  unable  to  lie  down.  There  is 
a  harsh  stridulous  cough,  with  (at  first)  little  or  no  expectoration  ;  if  there 
is  any,  it  is  tenacious  ;  later  it  may  become  thick,  purulent  and  abundant. 
The  voice  is  hoarse  or  is  reduced  to  a  whisper.  These  local  symptoms  are 
accompanied  by  a  flushed  face,  a  hot,  dry  skin,  the  temperature  often  rising 
to  105°  F.  The  pulse  is  frequent  and  hard  in  character.  In  severe  cases,  as  the 
disease  advances,  both  acts  of  respiration  become  more  and  more  labored,  the 
cough  more  and  more  metallic  in  character,  the  patient's  distress  increases, 
symptoms  of  imperfect  aeration  of  the  blood  are  developed,  the  countenance 
becomes  pale  and  anxious,  or  livid.  During  the  exacerbations  caused  by 
spasm  of  the  laryngeal  muscles,  suffocation  seems  imminent ;  in  the  inter- 
vals the  patient  becomes  drowsy,  the  vesicular  murmur  over  both  lungs  is 
feeble  or  inaudible,  the  capillary  circulation  is  obstructed,  the  lips  and 
nails  become  blue,  a  cold  perspiration  breaks  over  the  surface,  the  respira- 
tory sounds  become  gasping  in  character,  and  finally  delirium  and  coma 
close  the  scene. 

As  soon  as  the  characteristic  symptoms  are  manifest,  a  laryngoscopic 
examination  will  show  the  mucous  membrane  of  the  larynx  to  be  of  a 
bright  red  color ;  if  the  case  is  severe,  cedema  soon  appears,  the  parts 
being  red,  swollen  and  semi-transparent.  The  tumefaction  will  be  most 
marked  on  the  ventricular  folds,  which  may  entirely  conceal  from  view 
the  vocal  bands  ;  this  redness  and  tumefaction  may  extend  into  the 
trachea,  or  may  be  confined  to  the  mucous  membrane  of  the  larynx  and 
free  borders  of  the  epiglottis.  Death  may  occur  in  a  few  hours  or  it  may 
be  delayed  five  or  six  days  ;  it  is  caused  either  by  a  complete  closure  of  the 
rima  glottidis  from  tumefaction  of  the  mucous  and  submucous  tissues,  or 
the  patient  struggles  on  with  obstructed  respiration  and  dies  from  pulmon- 
ary or  cerebral  congestion  and  cedema.  If  death  takes  place  suddenly,  it  is 
caused  by  the  combined  effects  of  oedematous  swelling  and  spasm  of  the 
glottis.  When  fatal,  its  course  is  usually  rapid  and  severe  ;  when  recovery 
takes  place,  it  is  mild  in  character,  and  extends  over  a  period  of  seven  or 
eight  days. 

Differential  Diagnosis. — The  affections  which  may  be  confounded  with 
acute  catarrh  of  the  larynx,  are  croupous  laryngitis,  dipMlieria,  cedema  of 
tTie  larynx,  spasmodic  asthma,  hysterical  laryngeal  spasm,  and  thoracic 
aneurism.  In  very  young  children  it  is  often  impossible  to  distinguish 
between  catarrhal  laryngitis  and  croupous  laryngitis  ;  but  when  the  laryn- 
goscope can  be  used,  the  presence  or  absence  of  false  membrane  decides  the 
question.  The  history  of  the  attack,  the  accompanying  constitutional 
symptoms,  and  a  careful  laryngoscopic  examination,  will  enable  one  readily 
to  distinguish  between  the  laryngeal  symptoms  of  acute  laryngitis  and 
those  of  diphtheria,  cedema  glottidis,  or  laryngeal  spasm  ;  while  a  physical 
examination  of  the  thorax  determines  the  existence  or  the  non-existence  of 
spasmodic  asthma  and  thoracic  aneurism. 

Prognosis. — ^Age  is  the  most  important  element  in  prognosis.    In  young 


go  DISEASES    OP    THE    KESPIEATOEY   OEGAKS. 

children  this  disease  is  always  attended  with  danger  ;  in  adults  the  danger 
depends  upon  the  amount  of  oedema  present.  The  tendency,  even  in 
severe  cases,  is  to  recovery.  In  those  that  tend  to  a  fatal  termination, 
when  death  is  imminent  it  may  be  averted  by  the  performance  of  tracheotomy. 
There  is  always  danger  that  tlie  inflammation  will  extend  into  the  trachea, 
and  lead  to  a  bronchitis  or  pneumonia. 

Treatment. — When  active  febrile  symptoms  are  present  in  the  early 
stage  of  acute  catarrhal  laryngitis,  occurring  as  a  primary  disease  in  a 
strong,  robust  adult,  venesection  to  syncope  may  be  of  service  ;  bat  if  the 
symptoms  which  indicate  imperfect  aeration  of  the  blood  are  present,  or  if 
the  laryngitis  is  a  secondary  affection,  venesection  is  not  only  useless  but 
does  positive  harm.  There  is  no  reliable  evidence  that  local  depletion  by 
leeches,  the  application  of  blisters,  or  the  internal  administration  of  an- 
timony or  calomel,  has  any  power  to  arrest  the  progress  or  alleviate  any 
of  the  distressing  symptoms  of  this  disease.  It  has  been  claimed  that  when 
the  disease  involves  but  a  small  portion  of  the  larynx,  the  direct  applica- 
tion of  a  solution  of  nitrate  of  silver,  eighty  or  even  ninety  grains  to  the 
ounce,  to  the  inflamed  portion,  by  means  of  a  sponge,  camel's-hair  brush, 
or  with  a  laryngeal  nebulizer,  speedily  relieves  the  dyspnoea  and  ameli- 
orates the  general  symptoms.  Few,  however,  have  the  requisite  skill  and 
experience  in  topical  medication  of  the  larynx  to  make  such  applications 
efficaciously,  or  at  least  to  accomplish  what  is  claimed  for  them.  Most 
practitioners  would  do  much  more  harm  than  good  were  they  to  attempt  to 
make  such  applications. 

For  the  successful  management  of  this  disease,  a  warm,  moist  and 
uniform  temperature  is  essential ;  the  temperature  of  the  apartment 
should  never  be  allowed  to  fall  below  76°  F.  When  the  submucous 
areolar  tissue  is  either  not  at  all  or  only  slightly  involved,  vapor  inhala- 
tions unquestionably  give  the  greatest  relief,  and  have  greater  power  m 
arresting  the  inflammatory  process  than  all  other  local  measures ;  they  should 
be  commenced  early  and  perseveringly  continued.  The  internal  remedy  which 
seems  to  have  the  greatest  power  in  controlling  this  disease,  if  its  adminis- 
tration is  commenced  early,  is  the  sulphate  of  quinine  ;  it  must  be  given 
in  large  doses.  During  the  first  twenty-four  hours  hue7ity  grains  may  be 
given  to  a  child  three  years  of  age  suffering  with  a  severe  form  of  acute 
laryngeal  catarrh.  If  the  inflammatory  process  is  not  arrested  by  the  com- 
bined action  of  these  remedies,  oedema  is  almost  sure  to  follow,  and  the 
parts  should  be  freely  scarified  ;  in  the  adult  this  may  be  readily  done  with 
a  laryngeal  lancet  by  the  aid  of  the  laryngoscope.  Should  this  treatment 
fail  or  be  impossible,  and  should  the  dyspnoea  be  of  a  threatening  character, 
and  the  signs  of  imperfect  aeration  of  the  blood  be  well  marked,  tracheotomy 
must  not  be  delayed  ;  many  lives  have  been  lost  by  too  long  delaying  this 
operation.  For  the  successful  management  of  acute  laryngitis,  rest  to  the 
larynx  is  all  important. 


SIMPLE    CHRONIC    CATARRHAL    LARYNGITIS.  21 


SIMPLE    CHEOISTIC    CATAERHAL   LARYTTGITIS. 

This  is  essentially  a  chronic  inflammation  of  the  lining  membrane  of  the 
larynx,  the  submucous  tissue  being  slightly  involved.  When  once  estab- 
lished its  tendency  is  to  remain  stationary.  Like  the  acute,  it  may  be 
general  or  partial. 

Morbid  Anatomy. — When  the  disease  is  fully  developed  the  mucous  sur- 
face of  the  larnynx  is  always  more  or  less  coated  with  mucus  or  pus.  Its 
tissue  is  dark  colored,  sometimes  of  a  grayish  red  or  bluish  hue,  owing  to 
previous  ecchymosis ;  it  may  be  either  softer  or  firmer  than  natural ;  the 
mucous  glands  are  large  and  prominent,  the  submucous  tissue  is  thickened, 
and  the  vocal  bands  may  eibher  become  relaxed  or  stiffened,  and  hence  vi- 
brate less  than  in  health.  Paresis  of  certain  laryngeal  muscles  may  result 
from  the  thickening  and  infiltration.  When  the  trachea  is  involved,  the 
portion  of  the  mucous  membrane  covering  its  rings  is  reddened,  while 
the  intermediate  portions  are  of  a  dark  gray  color. 

Etiology. — This  affection  may  occur  as  a  primary  disease,  or  as  a  sequela 
of  a  mild  form  of  acute  laryngitis  ;  not  infrequently  it  is  the  result  of'  the 
extension  of  a  pharyngeal  inflammation  in  those  who  constantly  use  the 
voice  in  public  speaking  or  singing.  It  constitutes  the  chief  morbid  con- 
dition in  what  is  termed  "clergyman's  sore-throat."  It  is  frequently 
secondary  to  a  chronic  nasal  catarrh — the  catarrhal  process  extending  from 
the  nasal  passages.  The  constant  inhalation  of  irritating  particles  may  be 
a  cause  of  chronic  laryngitis  ;  but  it  most  frequently  occurs  as  an  accom- 
paniment of  other  affections,  as  syphilis,  pulmonary  phthisis,  and  laryngeal 
morbid  growths.  When  it  occurs,  as  it  frequently  does,  in  phthisical  or 
syphilitic  subjects,  it  is  described  as  laryngeal  phthisis,  and  syphilitic  laryn- 
gitis. The  variety  which  is  the  result  of  the  extension  of  a  follicular 
pharyngitis,  is  sometimes  separately  described  as  chronic  glandular 
laryngitis,  but  it  does  not  differ  from  simple  laryngeal  catarrh,  except 
that  in  it  the  minute  racemose  glands  are  principally  affected.  The  sudden 
development  of  the  larynx  in  males  which  takes  place  at  puberty  is  often 
attended  by  a  mild  form  of  chronic  laryngeal  catarrh.  In  every  variety  of 
chronic  bronchitis,  especially  that  occurring  in  old  age,  there  is  more  or 
less  chronic  laryngeal  catarrh, — in  many  instances  the  laryngeal  catarrh  is 
secondary  to  the  bronchitis. 

Symptoms. — The  symptoms  of  chronic  catarrhal  laryngitis  are  altogether 
local  in  character.  The  most  characteristic  are  the  changes  which  occur 
in  the  voice  ;  in  some  it  is  hoarse  and  husky,  in  other  cases  the  patient  is 
only  able  to  speak  in  a  husky  whisper.  The  voice  is  most  often  reduced  to 
a  whisper  in  the  dry  variety  of  laryngeal  catarrh.  Accompanying  or  pre- 
ceding the  vocal  changes,  there  is  a  hoarse,  stridulous  cough,  with  more  or 
less  abundant  muco-purulent,  or  purulent  expectoration  ;  not  infrequently 
the  expectoration  is  streaked  with  blood,  and  of  a  fetid  odor.  Inspiration 
and  expiration  are  more  or  less  impeded,  and  are  often  accompanied  by  a 
whistling  or  stridulous  sound,  and  moist  rdles  can  usually  be  heard  over 


22  DISEASES    OF    THE    RESPIRATORY    ORGANS. 

the  larynx.  There  is  often  soreness  and  tenderness  of  the  laryngeal  carti- 
lages when  pressed  laterally  or  backward  against  the  spine.  In  some  cases, 
the  act  of  swallowing  fluids  or  solids  is  attended  with  no  inconvenience  ; 
in  other  cases  it  excites  spasm  of  the  glottis,  and  thus  occasions  fits  of  dis- 
tressing dyspnoea.  If  constitutional  symptoms  exist,  they  are  due  to  sym- 
pathetic irritation,  and  are  in  no  way  characteristic  of  the  disease.  The 
principal  danger  is  from  chronic  laryngeal  oedema,  but  this  is  of  exceed- 
ingly rare  occurrence.  The  laryngoscopic  appearances  correspond  to  those 
changes  already  described  under  the  head  of  morbid  anatomy  of  the  dis- 
ease. The  laryngeal  mucous  membrane  is  of  a  deep  red  color,  verging  on 
purple.  The  change  in  color  is  most  marked  over  the  vocal  cords  and  ary- 
tenoid cartilages  ;  sometimes  the  larynx  has  the  appearance  of  being  very 
much  dilated,  at  other  times  it  is  apparently  contracted.  The  mucous 
surface  may  be  covered  over  with  a  muco-purulent  secretion,  or  may  pre- 
sent a  dry  and  shining  appearance  ;  the  enlarged  orifices  of  the  glands  may 
be  seen  as  pale  specks  on  the  congested  membrane,  or  as  red  circles  stud- 
ding a  pale  membrane.  In  addition  to  these  more  common  appearances, 
more  or  less  extensive  thickening  and  papillary  excrescences  are  sometimes 
visible. 

Differential  Diagnosis. — The  diagnosis  of  chronic  laryngitis  is  readily  made; 
the  changes  in  the  voice  at  once  direct  the  attention  to  the  larynx,  and 
the  laryngoscope  will  determine  the  nature,  extent  and  exact  seat  of  the 
disease.  Prom  the  general  and  local  symptoms,  chronic  laryngitis  may  be 
confounded  with  laryngeal  growths  and  nervous  affections  of  the  larynx, 
but  a  careful  laryngoscopical  examination  will  correct  any  error.  Phthis- 
ical and  syphilitic  laryngitis  may  be  distinguished  from  simple  catarrhal 
laryngitis  by  the  presence  of  ulcers,  by  a  careful  physical  examination  of 
the  lungs,  and  by  the  history  of  the  patient.  If  both  phthisis  and  syphilis 
can  be  excluded,  however  extensive  the  disease,  it  must  be  regarded  as  of 
primary  origin. 

Prognosis. — The  prognosis  in  this  affection  depends  on  its  pathological 
associations.  All  forms  of  simple  chronic  laryngitis,  unless  complicated, 
may  he  recovered  from  ;  at  least,  it  rarely,  if  ever,  leads  to  a  fatal  termina- 
tion. It  is  always  difficult,  however,  and  sometimes  impossible  to  cure 
chronic  laryngitis  in  old  people. 

Treatment. — The  most  efficient  agents  in  the  treatment  of  this  variety  of 
laryngitis  are  local  applications,  within  the  larynx,  to  the  parts  affected. 
These  topical  applications  may  be  made  at  the  time  of  a  laryngoscopical 
examination,  either  by  means  of  a  sponge  or  camel's-hair  hrush  carried 
within  the  larynx,  by  the  inhalation  of  vapor  impregnated  with  some  vol- 
atile substance,  or  in  the  form  of  nebulized  liquids.  The  most  certain  and 
most  satisfactory  method  is  the  use  of  atomized  liquids,  applied  by  means 
of  the  laryngeal  spray — the  mechanical  chilling  produced  by  the  spray  adds 
to  the  efficiency  of  the  astringent  solutions.  Sponges  and  brushes  are  apt 
to  irritate,  and  produce  hypergemia  of  the  larynx.  When  local  applications 
are  to  be  used  for  a  long  time,  mild  astringent  solutions  are  preferred. 
A  solution  of  alum,  perchloride  of  iron,  tannin,  or  the  sulphate  of  zinc. 


CHROKIC    CATAREH    OF   THE   LARYNX   IJST    PHTHISIS.  23 

from  one  to  twenty  grains  to  the  ounce  of  water,  may  be  used.  If  the  ap- 
plications are  made  directly  to  the  diseased  tissues,  and  sufficiently  often, 
it  matters  Tery  little  what  astringent  solution  is  used.  When  the  laryn- 
geal secretion  is  excessive,  the  local  application  of  turpentine  sometimes 
does  good.  For  steam  inhalations,  a  few  drops  of  oil  of  creosote,  oil  of 
pine,  or  oil  of  juniper,  added  to  half  a  pint  of  water  at  a  temperature  of 
150°  F.,  may  be  employed.  Neither  the  steam  nor  spray  inhalations  should 
be  continued  more  than  five  minutes  at  a  time  ;  they  may  be  repeated  three 
or  four  times  during  the  twenty-four  hours.  A  solution  of  carbolic  acid 
(two  grains  to  an  ounce  of  water),  either  as  a  spray  or  as  a  steam  inhala- 
tion, may  be  used  with  benefit  in  cases  where  the  laryngeal  secretion  has  a 
fetid  odor.  In  such  cases  the  nares  should  be  carefully  examined,  and  the 
passage  of  offensive  nasal  discharges  into  the  larynx  should  be  prevented. 
In  addition  to  the  local  treatment,  the  jaatient  must  be  removed  from  all 
sources  of  laryngeal  irritation.  The  vocal  organs  must  have  perfect  rest ; 
the  patient,  if  possible,  should  change  climate,  removing  to  such  as  he  finds 
best  suited  to  his  individual  case  ;  as  a  rule,  a  warm,  dry  atmosphere  best 
agrees  with  this  class  of  patients. 

Tlie  constitutional  treatment  of  each  patient  Avill  be  governed  by  his 
general  condition,  and  the  pathological  relations  of  the  laryngitis.  The 
general  hygiene  of  the  patient  should  always  be  carefully  regulated. 


CHEOlSriC    CATAEEH    OF   THE   LAETNX   EST   PHTHISIS. 

Simple  catarrhal  laryngitis  associated  with  pulmonary  phthisis  is  often 
modified  by  the  phthisical  cachexia,  and  degenerates  into  what  is  called  la- 
ryngeal pMliisis. 

Morbid  Anatomy. — The  laryngeal  structure,  sympathizing  with  the  general 
impairment  of  nutrition,  is  pale  in  the  earlier  stage  of  the  affection.  As 
the  inflammatory  and  tissue  changes  advance,  the  mucous  membrane  be- 
comes irregularly  vascular  and  of  a  peculiar  ashy-red  hue,  but  its  tissues 
become  progressively  thickened.  A  pear-shaped  enlargement  over  the 
mucous  membrane  which  covers  the  arytenoid  cartilage  is  a  characteristic 
feature  of  pronounced  laryngeal  phthisis.  The  epiglottis  in  the  catarrhal 
stage  of  the  affection  is  often  enlarged  and  shaped  like  a  turban.  The  sub- 
mucous tissues  become  infiltrated  with  small  cells.  These  cells  show  a 
tendency  to  cluster  and  form  cheesy  centres,  thus  paving  the  way  to  the 
development  of  tubercular  ulcers.  (Edema  from  serous  transudation  within 
the  loose  mucous  tissue  often  occurs.  Later,  localized  abrasions  occur 
where  the  tissues  are  in  contact,  or  at  points  where  the  friable  tissues  are  in 
constant  motion.  The  ulcerative  stage  may  become  pronounced,  and 
superficial  sores  of  an  ashy-gray  hue  occur  at  points  most  favorable  for 
their  development.  These  ulcers  may  enlarge  by  coalescence  or  individual 
extension  until  a  large  portion  of  the  ventricular  bands,  vocal  cords,  and 
epiglottis  becomes  involved.  They  often  advance  in  depth,  descending  the  . 
laryngeal  skeleton  and  eroding  the  cartilages;  the  roughened  structures  are 


24  DISEASES   OF  THE  EESPIKATOEY  OKGANS. 

constantly  covered  with  the  tenacious  muco-purulent  diseharges  which 
come  from  the  lungs,  or  are  excited  by  the  intense  local  irritation. 

Etiology. — The  phthisical  peculiarity  of  the  inflammation  receives  its 
impress  from  the  pulmonary  disease.  Constant  hawking  or  coughing,  pro- 
voked by  the  passage  of  the  irritating  discharges  over  the  laryngeal  struct- 
ure, and  the  constant  movement  of  the  parts,  favor  the  development  of 
the  laryngeal  complication.  The  local  and  general  cachexia,  with  at- 
tendant impaired  nutrition,  modifies  the  nature  and  course  of  the  catarrhal 
processes. 

Symptoms. — The  early  subjective  symptoms  are  generally  those  of  a  modi- 
fied chronic  laryngitis,  associated  with  constitutional  manifestations  of 
pulmonary  phthisis.  The  respiration  may  be  hurried  or  embarrassed. 
Hoarseness  or  complete  aphonia  is  produced  by  the  structural  changes,  and 
the  irritating  discharges  excite  distressing  paroxysms  of  coughing.  Painful 
deglutition  is  induced  by  counter-pressure  of  the  inflamed  or  thickened 
abraded  mucous  membrane,  the  disturbance  of  elevated  ulcers,  or  the  fric- 
tion of  food.  A  harassing  nervous  cough  exists  in  the  ulcerative  stage  of 
the  affection.  The  patient  hesitates  to  take  food  on  account  of  the  pain 
caused  by  the  passage  of  the  bolus.     This  hastens  the  general  emaciation. 

Differential  Diagnosis. — The  peculiar  pyriform  thickening  over  the  aryte- 
noid prominence  distinguishes  the  hypertrophic  from  simple  chronic 
catarrhal  laryngitis.  The  ashy-gray  hue,  irregular  vascularity,  and  gray 
infiltrated  vocal  cords  can  readily  be  contrasted  with  the  bright  inflam- 
matory redness  of  the  laryngeal  structures  seen  in  simple  catarrhal  laryn- 
gitis. The  non-existence  of  ulcers  in  simple  chronic  laryngitis  will  also 
aid  in  differentiating  between  the  two  affections.  The  contour  of  the 
syphilitic  ulcer  and  its  bright  red  areola  and  irregular  margin  are  not  easily 
mistaken  for  the  pale  and  peculiar  thickened  mucous  membrane  of  laryngeal 
phtihisis,  and  its  irregular  ashy-gray  ulcers.  The  syphilitic  ulcer,  more- 
over, advances  rapidly,  but  usually  painlessly;  the  phthisical  ulcer  pro- 
gresses slowly,  and  is  accompanied  with  much  pain. 

Prognosis. — Healing  of  the  ulcers  is  usually  considered  the  cure  of  a 
laryngeal  phthisis.  This,  however,  will  depend  upon  the  site  and  size  of 
the  lesions.  When  superficial  ulcers  upon  the  ventricular  bands,  vocal 
cords,  or  arytenoid  prominences  are  seen  early,  they  are  sometimes  curable. 
Ulcerations  of  the  epiglottis  are  incurable,  and  often  the  indirect  cause  of 
death.  Erosions  of  the  cartilages  are  always  exceedingly  troublesome,  and 
generally  lead  to  a  fatal  issue  ;  the  extent  of  the  pulmonary  disease  and  the 
general  cachexia  modify  the  prognosis  in  laryngeal  phthisis.  Extensive 
hypertrophy  of  the  laryngeal  mucous  membrane  does  not  seriously  influ- 
ence the  prognosis.  Judicious  local  and  general  treatment  will  afford 
relief  in  every  case,  and  frequently  postpone  the  fatal  issue. 

Treatment. — Treatment  should  be  both  constitutional  and  local.  The 
general  treatment  is  determined  by  the  laryngeal  symptoms,  the  condition 
of  the  patient,  and  the  co-existing  pulmonary  disease.  Cough  may  be 
quieted  by  the  internal  administration  of  bromide  of  sodium  or  solution  of 
morphia  (U.  S.  P.).     Its  relief  removes  a  source  of  irritation  which  is  con- 


(EDEMA    GLOTTIDIS.  25 

etantly  acting  on  the  inflamed  or  ulcerated  larynx,  and  by  affording  rest 
favors  repair  or  retards  the  advance  of  the  local  disease.  It  also  soothes 
the  disturbed  nervous  system,  and  allows  the  patient  to  gain  strength  by 
undisturbed  sleep.  In  connection  with  the  constitutional  and  hygienic 
treatment  of  the  accompanying  pulmonary  disease,  great  relief  can  be 
afforded  and  life  prolonged  by  the  following  local  management  of  the 
laryngeal  ulcers.  The  surface  of  a  phthisical  ulcer  should  be  thoroughly 
cleansed  by  means  of  an  alkaline  spray; — a  one  per  cent,  solution  of  the 
phosphate,  or  carbonate  of  soda,  with  glycerine  and  carbolic  acid  or  thymol, 
is  most  serviceable.  Finely  pulverized  iodoform  should  then  be  blown 
upon  the  ulcerated  surfaces.  When  there  is  much  pain  Magendie's  solu- 
tion maybe  sprayed  upon  the  ulcerated  or  inflamed  tissues.  The  laryngeal 
sponge  or  brush  is  always  contra-indicated.  Tracheotomy  to  rest  the  larynx 
and  lessen  the  suffering  is  sometimes  Justifiable.  It  is  of  doubtful  curative 
value,  and  may  hasten  the  impending  crisis  by  accelerating  the  progress  of 
the  pulmonary  lesions. 

CHEOISTIC    CATAERHAL    LAEYISTGITIS    OF    SYPHILIS. 

The  course,  symptoms,  and  appearance  of  chronic  catarrhal  laryngitis 
may  be  modified  by  constitutional  syphilis.  Constitutional  infection  may 
cause  a  syphilitic  non-ulcerative  laryngitis,  as  a  secondary  or  tertiary  mani- 
festation. In  its  advanced  stage  it  is  often  complicated  by  ulceration.  The 
vascularity  of  the  mucous  surface  does  not  show  the  rapid  variations  seen 
in  ordinary  catarrhal  laryngitis  ;  it  is  far  more  persistent.  The  arterial 
red  of  catarrhal  laryngitis  is  replaced  by  a  deep  red  or  even  a  livid  hue. 
The  discomfort  which  it  causes  does  not,  as  in  simple  laryngitis,  correspond 
in  severity  with  the  intensity  of  the  congestion.  A  syphilitic  history  and 
the  disappearance  of  local  manifestations  under  appropriate  internal  medi- 
cation aid  in  determining  its  character.  The  treatment  consists  in  the 
application  of  tincture  of  iodine  by  means  of  sprays,  brushes,  or  vaporizers, 
with  or  without  the  insufflation  of  iodoform  ;  simple  applications  of  iodo- 
form by  means  of  Ely's  laryngeal  powder-blower  are  often  markedly  bene- 
ficial. The  parts  should  be  thoroughly  cleaned  with  alkaline  sprays  before 
each  application.  In  all  cases  local  and  constitutional  treatment  should  be 
combined.  A  rapid  increase  in  the  size  of  the  dose  of  iodide  of  potassium 
is  often  required  to  effect  the  desired  changes. 

(EDEMA    GLOTTIDIS. 

(Edema  Glottidis  is  a  term  which  has  been  used  to  indicate  the 
occurrence  of  a  dropsical  effusion  or  inflammatory  exudation  into  the  areolar 
tissue  beneath  the  laryngeal  membrane  above  the  vocal  bands.  Strictly 
speaking,  it  is  not  oedema  of  the  glottis,  but  of  the  upper  .portion  of  the 
larynx.  Its  gravity,  and  the  necessity  of  its  prompt  relief,  make  the  early 
recognition  of  its  existence,  and  of  the  pathological  conditions  which  lead 
to  its  occurrence  and  attend  its  development,  very  important. 


26  DISEASES    OF    THE    EESPIRATOEY    ORGANS. 

Morbid  Anatomy.— The  effusion,  which  is  almost  always  serous,  takes 
place  in  the  loose  cellular  tissue  beneath  the  mucous  membrane  of  the  up- 
per part  of  the  larynx,  principally  in  the  ary-epiglottic  folds,  and  at  the 
base  of  the  epiglottis  ;  as  a  consequence,  these  parts  become  prominent  and 
the  epiglottis  swollen.  On  either  side  there  may  be  a  tumor  an  inch  or 
?jQore  in  diameter,  projecting  into  the  cavity  of  the  larynx  and  pharynx  ; 
in  some  cases  these  tumors  touch  each  other,  completely  occluding  the  la- 
ryngeal cavity.  The  mucous  membrane  may  be  either  red  or  pale.  On 
pricking  the  tumors,  a  clear,  or  turbid,  or  even  a  purulent  fluid  may  es- 
cape ;  after  which  the  parts  previously  distended  collapse,  and  the  mucous 
membrane  is  left  wrinkled  and  folded.  The  effusion  may  occur  wholly  or 
principally  on  one  side.  Not  infrequently  after  death,  owing  to  the  dis- 
appearance of  the  effusion,  the  wrinkled  condition  of  the  mucous  mem- 
brane is  all  that  is  found,  or,  at  least,  there  is  much  less  effusion  than 
might  have  been  expected  from  the  appearance  of  the  parts  during  life. 

Etiology.— (Edema  of  the  glottis  rarely  if  ever  occurs  as  a  primary  affec- 
tion, but  is  secondary  to,  or  is  a  complication  of,  some  local  laryngeal  dis- 
ease or  constitutional  disorder.  Any  inflammatory  affection  of  the  larynx 
or  of  the  adjacent  tissues  may  give  rise  to  it,  such  as  acute  laryngitis  (espe- 
cially that  due  to  local  irritation),  erysipelas  of  the  neck,  deep-seated  cer- 
vical abscesses,  and  acute  tonsillitis.  It  occasionally  occurs  as  a  complica- 
tion of  the  laryngeal  ulceration  of  typhus  and  typhoid  fever,  small-pox  and 
scarlatina.  Sometimes  it  is  the  immediate  cause  of  death  in  the  general 
dropsy  of  Bright's  disease,  and  in  the  venous  obstniction  which  attends 
some  forms  of  cardiac  disease  and  thoracic  aneurism. 

Symptoms. — The  prominent  symptom  of  this  affection  is  dyspnoea,  and 
the  difficulty  in  breathing  is  mainly  confined  to  inspiration.  ISTo  difficulty 
in  swallowing  is  experienced,  nor  is  there  tenderness  on  pressure  over  the 
larynx.  Fever  and  the  other  constitutional  symptoms  which  attend  acute 
laryngitis  are  absent.  It  is  accompanied  by  paroxysms  of  extreme  dyspnoea 
— suffocative  breathing  being  usually  the  first  indication  of  its  occurrence  ; 
there  is  also  an  uneasy  sensation  in  the  region  of  the  larynx,  and  a  constant 
inclination  on  the  part  of  the  patient  to  rid  the  upper  part  of  the  throat  of 
some  supposed  secretion.  If  the  index  finger  be  carried  below  the  epiglot- 
tis, oedematous  tumors  may  be  distinctly  felt.  Hoarseness  or  huskiness  of 
voice  may  not  be  present,  unless  laryngitis  coexist.  The  laryngoscope  re- 
veals two  tense,  smooth,  rounded  swellings  immediately  behind  the  epi- 
glottis ;  these  swellings,  after  meeting  in  the  centre,  with  a  sulcus  between 
them,  appear  oval.  The  oedema  is  usually  most  marked  at  the  ventricular 
folds,  which  explains  the  nature  of  the  urgent  dyspnoea.  Whenever,  dur- 
ing the  progress  of  any  disease  in  which  oedema  glottidis  is  liable  to  occur, 
there  is  the  slightest  difficulty  in  respiration,  the  difficulty  being  limited 
to  inspiration,  the  possible  occurrence  of  this  complication  should  be  re- 
membered. 

Differential  Diagnosis. — The  circumstances  under  which  oedema  glottidis 
is  developed,  the  suddenness  of  its  occurrence,  the  peculiar  character  of  the 
respiration,  indicating  obstruction  at  the  upper  portion  of  the  larynx,  and 


ACUTE   CEOTJPOUS   LARNYGITI8.  27 

the  absence  of  febrile  excitement,  constitute  a  group  of  symptoms  almost 
pathognomonic.  When  to  these  is  added  the  presence  of  cedematous  tu- 
mors at  the  upper  portion  of  the  larynx,  the  differential  diagnosis  between 
it  and  other  laryngeal  affections  is  easily  made. 

Prognosis. — The  tendency  of  this  affection  is  to  speedily  destroy  life,  but 
in  most  instances  death  may  be  averted  by  prompt  and  efficient  surgical 
interference. 

Treatment. — There  is  no  time  to  be  lost  in  fruitless  medication.  In  ex- 
treme cases,  laryngotomy  or  tracheotomy  must  be  performed  early.  It  is 
recommended,  by  some,  to  scarify  the  edges  of  the  cedematous  epiglottis  or 
ventricular  bands  and  ary-epiglottic  folds,  so  as  to  give  free  exit  to  the 
effused  fluid  before  resorting  to  these  operations.  This  scarification  can 
rarely  be  accomplished,  except  by  an  experienced  hand,  and,  in  extreme 
cases,  the  delay  and  danger  which  attend  such  an  attempt  are  hardly  justi- 
fiable. 

ACUTE    CROUPOUS    LARYNGITIS. 

{Membranous  Croup.) 

Croupous  inflammation  of  the  larynx  differs  from  catarrhal  in  the  nat- 
ure of  its  inflammatory  products.  The  inflammatory  process  may  be 
limited  to  the  larynx,  or  it  may  extend  into  the  trachea  ;  and  broncho-tra- 
cheitis  so  frequently  accompanies  it  that  the  disease  has  received  the  name 
of  cynanche  tracJiealis,  but  in  all  instances  the  tracheal  inflammation  is 
secondary  to  the  laryngeal.    Croupous  laryngitis  is  a  local  inflammation. 

Morbid  Anatomy. — -When  fully  developed,  there  exists  over  a  varying  ex- 
tent of  the  mucous  membrane  a  whitish,  or  yellowish-white,  fibrinous 
layer,  often  spotted  here  and  there  with  dots  and  lines.  This  membranous 
exudation  may  be  limited  to  a  few  patches,  or  form  a  cylinder  which  may 
extend  into  the  trachea  and  bronchi.  At  one  time  it  is  firm  in  its  consist- 
ence, and  tenaciously  adheres  to  the  subjacent  membrane,  while  at  another 
it  is  soft  and  easily  separated  from  it.  Its  thickness  varies ;  sometimes  it  is 
scarcely  perceptible,  at  others  it  may  be  a  line  or  more  in  thickness.  Its 
surface  is  smooth,  it  adheres  firmly  to  the  vocal  cords  and  the  upper  part 
of  the  epiglottis.  After  the  membrane  is  once  formed,  it  may  be  cast  off 
in  the  form  of  a  cylinder,  in  bands,  or  shreds.  Its  separation  is  effected  by 
the  secretion  of  the  follicles  which  have  been  obstructed,  as  well  as  by  a 
serous  exudation  from  the  previously  inflamed  membrane.  It  may  break 
up  into  threads,  and  be  expectorated  as  such,  or  it  may  undergo  a  gran- 
ular, fatty,  or,  more  rarely,  a  mucous  degeneration,  and  so  become  a  fluid 
resembling  mucus. 

In  its  earlier  stages,  the  mucous  membrane  of  the  larynx  presents  the 
same  appearance  as  in  catarrhal  inflammation.  When  the  false  membrane 
has  formed,  it  takes  the  place  of  the  epithelium,  and  is  situated  on  the  ho- 
mogeneous boundary  layer  of  the  mucous  membrane  which  exists  in  the 
greater  part  of  the  larynx.  The  tissue  is  pale,  except  when  it  is  dotted 
with  ecchymoses,  which  correspond  to  similar  spots  in  the  membranous 


28 


DISEASES   OF   THE   EESPIRATORY   ORGAIfrS. 


Fig.  6. 

Vertical  section  of  mucoug  membrane  of 
Larynx  in  membranous  lariiygitis.  A. 
Membranous  exudation.  B.  Surface  epi- 
thelium infiltrated  with  pus.  C.  An  enlarged 
blood-vessel  in  the  sub-mucosa.     x  500. 


exudation.  The  laryngeal  membrane  is  somewhat  swollen,  and  moister  than 
normal.  Generally,  the  submucous  tissue  is  only  slightly  involved.  A 
microscopic  examination  of  this  membranous  exudation  shows  it  to  consist 
of  a  homogeneous,  shining  net-work,  in  the  meshes  of  which  are  inclosed 
pus-cells,  rarely  epithelium  ;  it  may  be  made  up  of  alternate  layers  of  fibrin 
and  cells.  As  the  membranous  exudation  is  cast  off,  the  epithelium  is 
quickly  replaced,  and  the  laryngeal  membrane  returns  to  its  normal  condi- 
tion. Sometimes,  after  the  membrane 
is  thrown  off,  it  is  reproduced.  The 
submucous  tissue  is  more  liable  to  be 
involved  in  adults  than  in  children. 
Very  frequently  membranous  pharyn- 
gitis precedes  and  is  associated  with 
croupous  laryngitis.  Pulmonary  con- 
gestion, oedema,  atelectasis,  emphy- 
sema, and  lobular  pneumonia  not  in- 
frequently occur  as  complications  in  the 
course  of  this  disease. 

Etiology. — Age  is  the  most  prominent 
predisposing  cause.  It  is  rare  in  adults 
(except  from  traumatic  causes),  or  in 
very  young  infants.  The  time  of  its 
greatest  liability  is  between  the  period  of  dentition  and  puberty.  There 
is  no  evidence  that  its  development  is  due  to  any  specific  atmospheric 
poison.  Exposure  to  cold  and  moisture,  with  sudden  alterations  of  tem- 
perature, are  among  its  most  frequent  exciting  causes.  It  occurs  more  fre- 
quently during  the  winter  and  spring  months.  Delicate,  weakly  and 
ill-nourished  children,  rather  than  the  strong  and  healthy,  are  liable  to  it. 
It  not  infrequently  follows  the  sudden  disappearance  of  eczematous  erup- 
tions on  the  head  and  face ;  occasionally  it  follows  measles,  scarlatina  and 
variola,  and  sometimes  complicates  diphtheria,  and  when  diphtheria  is  pre- 
yailing  it  is  often  difficult  to  draw  the  line  between  them. 

Symptoms. — Acute  croupous  laryngitis  usually  begins  with  the  ordinary 
symptoms  of  a  simple  cold  ;  at  its  commencement  there  is  nothing  to  dis- 
tinguish it  from  an  ordinary  catarrh.  If  the  throat  is  examined  the  whole 
visible  mucous  membrane  will  be  found  red  and  tumefied.  Usually  the 
first  symptom  that  attracts  attention  is  a  slight  hoarseness ;  a  little  later  the 
respiration  becomes  difficult,  the  expiration  noisy,  and  it  is  accompanied 
by  a  high-pitched  stridulous  cough.  The  inspiration  that  immediately 
follows  the  cough  is  accompanied  by  a  lond  crowing  noise.  Although  there 
is  no  pain  or  tenderness  in  handling  the  larnyx,  there  is  some  difficulty  in 
swallowing,  and  the  child  frequently  puts  its  hand  to  its  throat  as  if  to  re- 
move some  obstruction.  With  the  first  croupy  paroxysm,  however  slight, 
the  pulse  is  accelerated  and  becomes  full  and  hard ;  there  is  increased  heat 
and  redness  of  the  surface,  especially  of  the  face,  with  injection  of  the 
conjunctival  vessels;  the  axillary  temperature  may  range  from  102°  F.  to 
104°  F.     These  febrile  symptoms  somewhat  subside  as  the  paroxysm  passes 


ACUTE   CEOUPOUS   LARYNGITIS.  .  29 

off,  to  return,  however,  with  greater  intensity  on  the  return  of  the  next 
paroxysm.  At  the  commencement  of  the  attack  the  paroxysms  of  dyspnoea 
are  more  frequent  and  severe  at  night  than  during  the  day. 

As  the  disease  advances  the  voice  is  entirely  lost ;  the  patient  sjoeaks  and 
OTes  in  a  whisper ;  the  cough  becomes  more  and  more  stridulous  in  charac- 
ter, without  expectoration  ;  the  head  is  thrown  back  ;  the  respiration  grows 
more  and  more  difficult,  and  with  each  inspiration  there  is  contraction  of 
the  lower  part  of  the  chest  and  sinking  in  of  the  soft  parts  above  the  clav- 
icles. The  vesicular  murmur  over  both  lungs  is  feeble  or  inaudible  ;  with 
9very  inspiration  the  epigastrium,  instead  of  projecting,  is  strongly  de- 
pressed, and  the  outward  movement  of  the  lower  ribs  is  arrested.  Every 
muscle  that  can  aid  in  expanding  the  chest  is  brought  into  violent  action. 
During  these  laborious  efforts  at  inspiration  the  nostrils  are  dilated.  As  the 
laryngeal  obstruction  increases,  the  paroxysms  of  dyspnoea  become  more 
urgent  and  without  remission  ;  there  is  a  restless  tossing  of  the  limbs,  and 
the  greatest  terror  is  depicted  on  the  face,  which,  at  one  time,  is  pale,  at 
another  livid ;  the  pulse  becomes  rapid  and  feeble ;  the  temperature  falls 
sometimes  below  the  normal  and  the  extremities  become  cold.  Gradually, 
as  the  blood  becomes  imperfectly  aerated,  the  patient  becomes  drowsy,  at 
times  rousing  up  and  gasping  for  air,  and  springing  from  one  place  to  an- 
other to  find  relief ;  the  lips  and  nails  become  blue,  the  respiration  shorter 
and  shorter,  until  at  last,  after  a  violent  paroxysm  of  dyspnoea,  the  patient 
becomes  unconscious  and  quietly  ceases  to  breathe.  The  disease  always  at- 
tains its  height  by  the  end  of  the  third  day;  death  may  occur  within  forty- 
eight  hours  after  its  commencement;  its  whole  duration  rarely  exceeds  five 
days. 

In  accordance  with  its  symptomatology,  croupous  laryngitis  may  be  di- 
vided into  three  stages  :  a  precursory  or  catarrlial  stage,  a  stage  of  develop- 
ment, and  a  suffocative  stage,  or  stage  of  collapse.  The  most  important 
fact  connected  with  its  clinical  history  is,  that  in  a  large  proportion  of 
cases  before  the  urgent  symptoms  come  on,  the  membranous  exudation  can 
be  seen  on  the  tonsils.  In  most  cases  the  membrane  is  first  formed  on  the 
tonsils  or  in  their  immediate  vicinity.  As  the  membrane  extends  into  the 
larynx  there  is  loss  of  voice,  a  stridulous  cough,  difficult  breathing,  and  the 
face  is  alternately  flushed  and  pale.  For  a  day  or  two,  while  the  mem- 
brane is  extending  and  becoming  thicker,  the  patient  remains  in  about  the 
same  condition,  gradually  growing  weaker,  the  capillary  circulation  on  the 
surface  becoming  more  and  more  imperfect,  the  respiration  more  and  more 
labored,  the  paroxysms  of  dyspnoea  more  and  more  frequent  and  severe, 
until  there  is  little  hope  of  recovery.  Sometimes  all  the  urgent  symptoms 
are  suddenly  relieved,  the  patient  coughs,  and  a  stringy  matter  is  expecto- 
rated, he  struggles  for  a  moment  in  a  violent  paroxysm  of  dyspnoea,  and 
a  perfect  membranous  cast  of  the  larynx,  and  perhaps  of  the  trachea,  and 
larger  bronchi  is  expectorated.  Now  he  passes  into  a  quiet  sleep,  and  re- 
covery seems  certain  ;  but  still  there  is  great  danger — from  the  formation  of 
a  new  membrane  ;  from  the  extension  of  the  inflammation  into  the  minute 
bronchial  tubes,  giving  rise  to  capillary  bronchitis  and  pneumonia  ;  and 


30  DISEASES   OF  THE  KESPIEATOEY   ORGANS. 

from  the  exhaustion  that  has  occurred  before  the  membrane  was  thrown 
off.  A  laryngoscopic  examination  is  rarely  possible  in  this  class  of 
patients. 

Differential  Diagnosis.— The  two  affections  of  the  larynx  which  are  most 
liable  to  be  confounded  with  this  form  of  laryngitis,  are  simple  catarrh  of 
the  larynx,  called  spasmodic  or  pseudo-croup,  occurring  in  nervous  subjects, 
and  purely  spasmodic  affections  of  the  larynx.  In  both,  the  laryngeal 
spasms  give  rise  to  croupy  symptoms.  In  spasmodic  croup  or  simple 
catarrh  of  the  larynx,  the  croupous  phenomena  come  on  suddenly,  the 
attack  usually  occurs  at  night,  it  is  not  preceded  or  accompanied  by  active 
febrile  symptoms,  there  is  no  complete  loss  of  voice,  and  there  is  absence  of 
membranous  exudation  on  the  tonsils  and  epiglottis.  All  of  these  condi- 
tions are  important  diagnostic  features  of  croupous  laryngitis.  Within 
twenty-four  hours  after  the  commencement  of  an  attack  of  catarrhal  croup, 
auscultation  of  the  chest  furnishes  signs  of  incipient  bronchial  catarrh. 
Spasm  of  the  glottis,  which  may  give  rise  to  croupy  symptoms,  is  excited 
in  infancy  by  a  variety  of  causes.  Among  these  are  dental  irritation,  gas- 
tric irritation,  enlargement  of  the  thymus  gland,  giving  rise  to  what  is 
called  thymic  asthma,  and  undue  excitability  of  the  nervous  system,  the  re- 
sult of  hereditary  predisposition.  These  laryngeal  spasms  may  be  recog- 
nized by  the  suddenness  and  violence  of  the  attack,  by  the  absence  of  the 
catarrhal  and  febrile  symptoms,  by  the  absence  of  alteration  of  the  voice, 
and  by  the  speedy  and  complete  relief  which  immediately  follows  the  spasm. 
Diphtheria  involving  the  larynx,  sometimes  mistaken  for  croup,  may  be 
distinguished  from  it  by  the  following  characteristics  :  first,  either  diph- 
theria is  epidemic,  or  there  is  a  history  of  contagion  ;  second,  the  develop- 
ment of  the  throat  symptoms  is  generally  preceded  for  some  days  by 
constitutional  disturbances ;  third,  the  glands  at  the  angle  of  the  jaws  are 
usually  enlarged,  and  the  laryngeal  symptoms  are  at  first  not  urgent ;  fourth, 
the  pharynx  presents  the  characteristic  diphtheritic  appearance  before  any 
laryngeal  symptoms  are  present. 

Prognosis. — There  are  no  data  from  which  to  estimate  the  ratio  of  mortality 
in  this  disease ;  unquestionably  it  is  one  of  the  most  fatal  diseases  of  child- 
hood. When  the  diagnosis  is  based  upon  the  presence  of  the  membranous 
exudation  on  the  tonsils  and  epiglottis,  recovery  seldom  occurs.  The  signs 
of  a  favorable  termination  are,  diminution  in  the  frequency  and  severity  of 
the  paroxysms  of  dyspnoea,  with  less  distress  in  breathing  during  intervals, 
a  gradual  return  of  the  voice,  and  a  moist  sound  with  the  cough.  If,  on 
the  other  hand,  the  paroxysms  of  dyspnoea  become  more  frequent  and  vio- 
lent, the  restlessness  and  dyspnoea  increase  during  the  intervals,  and  the 
cough  is  less  powerful  and  more  stridulous,  the  blueness  of  the  lips  and 
nose  more  marked,  and  the  patient  becomes  more  and  more  drowsy,  re- 
covery is  scarcely  possible.  The  younger  the  patient,  the  greater  the  danger. 
In  fatal  cases,  the  duration  of  the  disease  is  from  three  to  seven  days.  If 
recovery  takes  place,  it  is  slow,  weeks  often  elapsing  before  the  voice  re- 
turns, during  all  of  which  time  the  patient  is  subject  to  violent  paroxysms 
of  dyspnoea. 


ACUTE    CROUPOUS   LARYNGITIS.  31 

Treatment. — I  do  not  purpose  to  discuss  the  merits  of  the  various  plans  of 
treatment  which  have  been  proposed  for  the  management  of  membranous 
croup,  for  under  every  plan  the  disease  has  proved  fatal  in  the  majority  of 
cases.  Simple  catarrh  of  the  larynx  is  so  liable  to  be  mistaken  for 
croupous,  that  it  is  difficult  to  estimate  the  real  value  of  the  different 
remedial  agents  which  have  been  claimed  to  have  a  controlling  power  over 
it.  Statements  that  certain  plans  followed,  or  agents  employed,  have  been 
successful  in  the  majority  of  cases  arouse. distrust  of  the  diagnosis;  the  ex- 
istence of  croup  should  be  asserted  only  upon  positive  evidence  of  the 
presence  of  the  membranous  exudation.  With  the  written  history  of  mem- 
branous croup  before  us  there  is  no  evidence  that  calomel,  blood-letting,  or 
antimony  has  any  power  either  to  arrest  the  progress  of  the  inflammatory 
action  or  to  prevent  the  membranous  exudation.  In  the  treatment  of  this 
affection  it  is  of  the  first  importance  that  the  patient  should  be  placed  in  a 
large,  well-ventilated  apartment,  the  temperature  of  which  should  be  kept 
uniformly  at  75°  F.  to  80°  F.,  and  the  air  rendered  moist  by  steam.  In 
the  case  of  children,  a  tent  maybe  made  over  the  bed  by  means  of  blankets, 
into  which  is  made  to  pass  a  constant  current  of  steam  from  a  kettle  con- 
taining boiling  water.  As  soon  as  evidence  of  imperfect  oxygenation  appears, 
a  continuous  stream  of  oxygen  gas  should  be  carried  into  the  tent,  or  ar- 
rangements should  be  made  so  that  it  will  be  constantly  inhaled  by  the 
patient ;  sometimes,  in  addition  to  these  means,  lime  vapor,  produced  by 
slacking  large  quantities  of  quicklime  in  the  room,  will  be  found  of  service. 
During  the  whole  course  of  treatment,  sponges  dipped  in  boiling  water  and 
then  squeezed  as  dry  as  possible  should  be  applied  over  the  larynx.  When- 
ever there  are  indications  that  loosened  portions  of  membrane  act  as 
causes  of  dyspnoea,  an  emetic  may  be  administered  —  the  sulphate  of 
zinc  acts  most  promptly  and  efficaciously.  The  frequent  administration 
of  emetics  should  be  avoided,  on  account  of  their  depressing  influence. 
Topical  applications  are  not  to  be  resorted  to  in  its  treatment,  as  they  in- 
tensify rather  than  relieve  the  laryngeal  spasm,  which  plays  so  important  a 
part  in  producing  the  paroxysms  of  dyspnoea,  and  there  is  no  evidence  that 
they  have  any  control  over  the  inflammatory  process.  It  is  all  important 
that  this  class  of  patients,  from  the  onset  of  the  disease,  should  receive  a 
most  nutritious  diet ;  and  as  failure  of  the  vital  powers  becomes  apparent, 
stimulants  may  be  freely  administered.  As  regards  internal  medication,  I 
have  little  confidence  in  any  of  the  so-called  specifics.  At  the  commence- 
ment, before  the  occurrence  of  the  membranous  exudation,  thirty  grains  of 
the  sulphate  of  quinine,  in  five-grain  doses,  may  be  beneficially  adminis- 
tered to  a  child  three  years  of  age,  with  the  intent  of  aborting  the  disease, 
and  I  believe  I  have  evidence  that  quinine  thus  administered  has  prevented 
catarrhal  laryngitis  from  becoming  croupous.  After  the  formation  of  the 
membranous  exudation,  the  vapor  inhalation  and  the  oxygen  gas  are  the 
only  means  which  afford  any  hope  that  the  patient  can  be  safely  carried 
through  the  disease.  In  regard  to  the  propriety  of  tracheotomy  the  opinion 
of  the  profession  is  divided.  The  statistics  of  this  operation  in  this  disease 
are  not  to  be  relied  upon.     The  only  question  to  settle  is  :  has  one  life 


32  DISEASES   OF   THE   KESPIRATORY    ORGANS. 

been  saved  by  it  ?  If  this  can  be  answered  affirmatively  the  operation  is 
justifiable.  It  never  should  be  resorted  to  with  a  promise  even  of  relief ; 
if  there  are  evidences  that  the  membranous  formation  has  reached  the 
bronchi,  and  even  when  the  membrane  has  formed  in  the  trachea,  tempo- 
rary relief  from  the  dyspnoea  is  all  that  can  be  promised.  The  operation,  to 
be  successful,  must  be  performed  early,  and  not  be  delayed,  as  it  usually  is, 
until  the  patient  is  beyond  hope  of  recovery.  Its  success  also  undoubtedly 
depends  much  upon  the  manner  of  its  performance,  and  the  subsequent 
management  of  the  case. 


ULOEES  OF  THE  LAEYNX. 

The  remaining  laryngeal  affections  come  more  directly  within  the  prov- 
ince of  the  specialist,  and  only  the  most  prominent  points  in  their  history 
will  be  considered.  The  different  forms  of  laryngeal  ulcerations  are  in- 
cluded under  the  following  heads  :  the  catarrhal,  the  follicular,  variolous, 
typhous,  phthisical,  and  syphilitic.  The  most  common  forms  are  those 
occurring  in  phthisis  and  syphilis. 

Morbid  Anatomy. — Catarrhal  ulcers  are  usually  superficial,  and  at  first 
may  be  either  rounded  or  oval ;  afterwards,  as  the  loss  of  substance  be- 
comes more  extensive,  they  coalesce  and  have  an  irregular  outline.  The 
follicular  ulcer,  as  a  rule,  is  superficial,  with  a  limited  area  of  extension. 
It  sometimes  constitutes  a  serious  complication  of  laryngeal  phthisis. 
Though  of  common  occurrence  in  the  pharyngeal  and  faucial  cavities,  it  is 
seldom  seen  in  the  larynx.  These  ulcers  may  be  situated  upon  any  portion 
of  the  laryngeal  membrane  ;  when  they  are  located  upon  the  anterior  or 
posterior  ends  of  the  vocal  .bands,  they  have  a  tendency  to  spread  length- 
wise. 

Variolous  Ulcers  are  the  result  of  small-pox  pustules  on  the  laryngeal 
membrane.  They  commence  by  the  formation  of  soft,  non-umbilicated 
pustules,  which  after  a  little  rupture  and  form  a  rounded  ulcer,  which 
readily  heals. 

Typhous  Ulcers  are  generally  of  large  size,  and  deep,  penetrating  through 
the  mucous  membrane,  and  sometimes  involving  the  cartilages.  The 
edges  of  these  ulcers  are  everted,  and  of  a  dark  purple  color ;  their  com-' 
mouest  seat  is  the  posterior  wall  of  the  larynx,  and  the  edges  of  the  epi- 
glottis. 

Phthisical  Ulcers  may  be  superficial  or  deep  ;  the  most  frequent  seat  is 
the  inter-arytenoid  commissure.  They  are  complications  of  laryngeal 
phthisis.  The  deficient  vascularity  of  the  pale  and  thickened  arytenoids 
favors  the  occurrence  of  these  ulcers.  They  may  have  their  inception  in 
an  inflammation  of  the  follicles  of  the  epiglottis  or  neighboring  tissue,  and 
spread  by  coalescence  ;  sometimes  they  produce  deep  destruction  of  tissue. 
The  epiglottis  is  often  eroded  at  its  margin,  and  the  cartilage  may  be  ex- 
posed or  perforated.  Calcification,  as  well  as  necrosis  of  the  laryngeal 
cartilages,  occasionally  follows  phthisical  ulceration.     The  necessary  move- 


ULCERS    OF   THE   LARYNX.  33 

ment  of  the  arytenoid,  and  the  irritant  action  of  the  pulmonary  discharges, 
may  induce  ulceration  of  the  vocal  cords. 

Syphilitic  Ulcers  of  the  larynx  are  usually  met  with  among  the  tertiary 
manifestations  of  syphilis,  and  rarely  if  ever  occur  as  secondary  lesions  of 
the  disease.  These  tertiary  ulcers  frequently  begin  on  the  epiglottis  and 
spread  rapidly  ;  they  often  involve  the  mucous  membrane  of  the  entire 
larynx,  and  cause  great  destruction  of  tissue.  They  have  an  irregular  out- 
line, with  everted  edges  and  yellow  hue,  excavated  base,  and  at  times  pre- 
sent a  more  or  less  gangrenous  appearance.  In  some  cases  they  extend  to 
the  pharynx.  They  may  originate  in  the  breaking  down  of  syphilitic 
tubercle  or  gummata.  They  often  heal  at  the  point  attacked,  while  the 
ulceration  advances  in  other  places.  The  scars  which  result  from  the 
healing  of  the  ulcers  have  a  tendency  to  contract  and  narrow  the  calibre 
of  the  larynx.  The  papillary  growths  which  surround  these  ulcers  are 
especially  characteristic  of  their  syphilitic  origin. 

Etiology. — Catarrhal  laryngeal  ulcers  are  rarely  the  result  of  acute  la- 
ryngeal catarrh,  but,  as  has  been  mentioned,  are  of  not  infrequent  occur- 
rence in  chronic  catarrhal  laryngitis,  especially  that  which  accompanies 
pulmonary  phthisis.  The  follicular  variety  generally  results  from  the  ex- 
tension of  a  follicular  faucitis  from  the  pharynx  to  the  larynx,  or  at  least 
the  two  are  frequently  associated. 

Variolous  ulcers  have  their  origin  in  the  propagation  of  the  exanthem 
from  the  mouth  and  pharynx. 

Typhous  ulcers  have  their  origin  either  in  diphtheritic  infiltration  or  im- 
perfect nutrition  of  the  mucous  membrane  of  the  larynx. 

Syphilitic  ulcers  depend  upon  a  specific  constitutional  poison  acting  in 
conjunction  with  a  catarrhal  inflammation  of  the  mucous  membrane  of  the 
larynx. 

Phthisical  ulcers  are  always  secondary  to  pulmonary  phthisis,  and  are 
usually  the  result  of  degenerative  processes,  which  are  preceded  and  accom- 
panied by  a  chronic  catarrh  of  the  larynx  ;  if  tubercular  tissue  exists,  it  is 
in  the  form  of  gray  nodules,  which  may  develop  about  the  base  of  any 
chronic  ulcerative  process. 

Symptoms. — All  forms  of  laryngeal  ulcers  are  attended  by  the  general 
symptoms  of  chronic  laryngeal  catarrh.  When  a  patient  with  a  harsh, 
stridulous  cough  of  long  standing  (the  expectoration  containing  pure  blood 
and  laryngeal  tissue),  with  hoarseness  at  times  amounting  to  aphonia, 
complains  of  a  burning,  smarting,  pricking  sensation  in  the  larynx,  with 
tenderness  on  pressure,  which  is  increased  by  speaking,  and  of  dijfficult 
and  painful  deglutition,  attended  by  a  wavy  laryngeal  respiration,  there  is 
reason  to  suspect  the  existence  of  a  laryngeal  ulcer  ;  but  a  positive  diagnosis 
cannot  be  made  from  these  symptoms  alone,  as  extensive  ulceration  may 
exist  and  all  of  these  symptoms  he  wanting,  and  they  may  be  present  where 
there  is  only  laryngeal  catarrh  without  ulceration.  The  appearance  of  the 
posterior  wall  of  the  pharynx  is  always  of  great  diagnostic  importance. 
The  use  of  the  laryngoscope  clears  up  all  doubt  as  to  the  existence  or  non- 
existence of  laryngeal  ulcers.  By  a  careful  laryngoscopic  examination,  the 
3 


34  DISEASES   OF   THE   KESPIEATORT   ORGANS. 

existence,  as  well  as  the  seat  and  extent  of  these  ulcers  may  be  determined. 
Having  determined  their  existence,  the  history  of  the  patient  and  a  careful 
auscultatory  examination  of  the  chest  will  enable  one  to  decide  their  char- 
acter. 

Prognosis. — The  prognosis  depends  entirely  upon  their  character.  The 
catarrhal,  follicular,  typhous,  and  variolous  are  usually  readily  recovered 
from  ;  while  the  phthisical  and  syphilitic  rarely,  the  former  perhaps  never, 
entirely  heal  ;  or,  if  healed,  the  destruction  of  the  parts  is  so  great  that 
the  remaining  cicatrix  permanently  interferes  with  the  functions  of  the 
larynx. 

Treatment. — The  treatment  of  laryngeal  ulcers  has  been  considered  un- 
der the  heads  of  chronic  laryngeal  catarrh,  phthisical  and  syphilitic  lar- 
yngitis. Ulcers  which  arise  independently  of  these  conditions  require  no 
special  treatment. 

ISTEIIROSES    OF   THE    LARYNX. 

The  true  neuroses  which  are  met  with  in  the  larynx  are  due  to  defective 
innervation  of  the  recurrent  laryngeal  nerve.  They  will  be  considered 
under  the  following  heads  : — 

I.  Recurrent  Laryngeal  Paralysis.  II.  Paralysis  of  the  Abductors  of 
the  Vocal  Cords.  III.  Paralysis  of  the  Adductors  of  the  Vocal  Cords. 
IV.  Paralysis  of  the  Tensors  of  the  Vocal  Cords. 

Each  form  of  paralysis  may  be  limited  to  one  side,  or  may  affect  botl 
sides  of  the  larynx. 

Morbid  Anatomy. — Recurrent  laryngeal  paralysis  may  be  unilateral  or  bi- 
lateral. All  the  muscles  supplied  by  the  recurrent  laryngeal  nerves  are 
usually  affected  in  this  form  of  paralysis.  There  is  no  constant  morbid 
change  in  the  tissues  which  compose  the  larynx  ;  frequently,  however,  there 
is  thickening  of  the  laryngeal  mucous  membrane,  and  the  vocal  cords  lose 
their  pearly  lustre  ;  such  conditions  are  most  likely  to  be  met  with  in  pul- 
monary phthisis.  In  the  absence  of  appreciable  morbid  appearances,  this 
paralysis  is  produced  by  insufficient  or  unequal  supply  of  nerve  force.  In 
unilateral  paralysis  of  the  adductors,  only  one  of  the  recurrent  nerves  is 
diseased,  either  primarily  or  secondarily,  or  an  inflammatory  degenerative 
process  may  have  been  established  in  the  muscle  involved.  Bilateral  paral- 
ysis of  the  adductors  is  caused  by  compression  of  both  recurrent  nerves  by 
tumors,  aneurisms  of  the  aorta,  innominata,  or  subclavian  arteries,  and  by 
degenerative  processes  in  the  nerves.  Pathological  changes  at  the  apices  of 
the  lungs,  or  in  the  lymph  glands  in  contact  with  the  nerves,  may  also  give 
rise  to  it.  In  bilateral  paralysis  of  the  abductors  of  the  vocal  cords,  or 
openers  of  the  rima  glottidis,  there  is  generally  advanced  atrophy  of  the 
laryngeal  muscles,  which  is  evidently  dependent  upon  interruption  of  nerve 
force,  either  from  cerebral  disease  or  local  pressure  on  the  vagi,  or  on  both 
recurrent  nerves.  It  is  frequently  associated  with  constitutional  syphilis. 
Unilateral  paralysis  of  the  abductors  is  usufilly  of  central  origin,  and  is  rare. 
Unilateral  paralysis  of  the  vocal  cords,  of  a  functional  nature,  is  a  rare 


NEUROSES   OF  THE   LARYISTX.  35 

affection.  It  is  sometimes  observed  in  cases  of  chronic  lead  or  arsenical  poi- 
soning. Bilateral  functional  paralysis  is  of  common  occurrence — it  is  met 
with  most  frequently  in  liysterical  females.  In  unilateral  paralysis  of  the 
abductors,  local  pressure  by  different  kinds  of  tumors  is  most  frequently 
met  with,  and  the  wasting  of  muscular  tissue,  which  attends  such  pressure, 
is  usually  limited  to  one  side.  It  is  stated  that  paralysis  of  the  tensor  mus- 
cles of  the  Yocal  cords  indicates  changes  in  the  spinal  nerve.  This  condi- 
tion is  not,  as  is  frequently  stated,  that  of  functional  disturbance.  There 
may  be  organic  lesions  present,  such  as  follow  contusion  or  laceration  of 
nerve  tissue.  Atrophy  of  the  spinal  accessory  nerves,  consecutive  to  com- 
pression in  their  passage  through  the  foramen  lacerum  posterius,  has  occa- 
sionally been  met  with. 

Etiology. — The  etiology  and  morbid  anatomy  of  laryngeal  paralysis  cannot 
be  separated.  A  common  general  cause  of  laryngeal  paralysis  is  some  local 
change  in  the  mucous  tissues  of  the  larynx.  Women  rather  than  men  are 
subject  to  it.  Pressure  on,  or  traction  of,  the  pneumogastric  or  recurrent 
laryngeal  nerves,  by  tumors,  enlarged  glands,  and  thoracic  aneurisms,  is  a 
frequent  cause  of  laryngeal  paralysis.  Diphtheria,  typhus  and  malarial 
fevers  and  other  acute  blood  diseases  are  occasionally  followed  by  laryngeal 
paralysis  ;  under  these  circumstances  the  paralysis  is  undoubtedly  due  to 
the  direct  effects  of  the  special  poison  of  the  disease  upon  the  nerve  centres. 
The  action  of  certain  metallic  poisons,  such  as  lead,  arsenic,  mercury,  etc., 
upon  the  larynx,  after  months  or  years  of  exposure  to  their  poisonous  in- 
fluence, may  cause  it.  Central  diseases  in  the  brain  or  upper  portion  of  the 
spinal  cord  are  sometimes  its  cause.  Whenever  there  is  bilateral  paralysis 
of  the  abductors  its  cause  may  be  found  in  some  more  or  less  defined  lesion 
of  the  brain.  Paralysis  of  the  laryngeal  muscles  may  occur  as  a  late  mani- 
festation of  constitutional  syphilis.  In  rare  instances  laryngeal  paralysis 
may  be  due  to  atrophy  and  degeneration  of  the  laryngeal  muscles,  and  comes 
on  without  any  assignable  cause.  Temporary  laryngeal  paralysis,  occurring 
in  connection  with  hysterical  manifestations,  has  no  cause  save  the  erratic 
one  of  hysteria,  appearing  and  disappearing  without  any  apparent  cause. 
Mechanical  violence  not  infrequently  causes  paralysis  of  the  tensors  of  the 
larynx,  as  when  a  blow  is  struck,  or  there  is  a  fall  on  some  projection  ;  it 
also  may  occur  as  a  sequela  of  too  loud,  too  frequent,  and  too  prolonged 
exercise  of  the  voice  in  public  speaking. 

Symptoms. — The  phenomena  which  attend  the  different  forms  of  laryn- 
geal paralysis  are  for  the  most  part  local  in  character.  In  paralysis  of  the 
muscles  supplied  by  the  recurrent  laryngeal  nerve,  the  patient  is  voiceless 
and  unable  to  cough.  When  this  form  of  paralysis  is  of  hysterical  origin, 
the  voice  comes  and  goes  most  capriciously — now  it  is  normal,  and  in  a 
short  time  the  patient  may  become  comj^letely  aphonic  without  any  ap- 
parent cause.  A  laryngoscopic  examination  of  the  larynx  will  show  that  dur- 
ing attempted  phonation  the  vocal  cords  remain  apart,  midway  between  ex- 
treme abduction  and  adduction  :  they  may  be  perfectly  motionless.  In 
unilateral  recurrent  laryngeal  paralysis,  the  voice  may  be  but  slightly  im- 
paired.    In  rare  instances,  it  will  be  unchanged  during  ordinary  conversa- 


36 


DISEASES   OF   THE   KBSPIRATOKY    OEGANS. 


tion,  and  will  only  be  impaired  when  an  endeavor  is  made  to  sound  the 
higher  notes  in  singing,  or  after  some  extraordinary,  continued  effort  of  the 
vocal  organs.  The  sound  produced  during  coughing,  sneezing,  and  laugh- 
ing is  usually  much  changed  and  weakened.  The  laryngoscope  shows 
that  one  vocal  band  does  not  act  when  the  patient  attempts  to  speak  or 
cough.  As  has  already  been  stated,  this  form  of  paralysis  is  due  to  some 
cause  acting  directly  on  the  nerve  of  the  affected  side. 

Bilateral  paralysis  of  the  abductors  is  often  accompanied  by  decided 
hoarseness  and  huskiness  of  the  voice,  rarely  by  entire  loss  of  the  voice  ; 
articulate  speech  is  often  almost  normal,  and  then  suddenly,  as  though  the 
current  of  air  were  interrupted,  the  patient  is  unable  to  make  himself 
understood,  so  feeble,  so  utterly  lost,  has  his  phonetic  power  become.  The 
prominent  symptom  of  this  form  of  paralysis  is  dyspnoea,  with  noisy,  strid- 
ulous  inspiration,  which  is  always  more  or  less  marked,  but  becomes  greatly 
aggravated  after  violent  exertion,  or  on  deep  inspiration.  A  laryngoscopic 
examination  shows  both  vocal  bands  in  juxtaposition,  near  the  median  line, 
and  they  do  not  separate  when  a  full  inspiration  is  made  ;  on  the  con- 
trary, a  forced  inspiration  makes  them  approach  even  to  touching,  while  a 

forced  expiration  separates  them  a 
little.  In  unilateral  abductor  par- 
alysis, the  voice  is  shrill  and  dis- 
cordant, and  dyspnoea  is  present 
only  after  physical  exertion.  Dur- 
ing inspiration  the  paralyzed  band 
does  not  move,  but  its  edge  is  con- 
cave. It  frequently  remains  station- 
ary, near  the  median  line,  but  usual- 
ly it  remains  in  the   median  line 

Diagram  showing  position  of  the  vocal  bands  in  ab-    OU    aCCOUUt    of    the    UUOppOSed  COU- 

fa^yngosXe        "'^^'''^^''''^''""'''^"^        tractiou    of    the  abductors.      The 
Thedottediin^^aanda- indicate  the pontion  of  band   secms  shorter  than   normal, 

the  bands  inbilateralparalyiiis  of  the  abductors.    qnH  n«;nnllv  is   pnTiD-psjtprl     p^nppianv 
b  and  b' indicate  the  position  in  bilateral  par aly-    "^^^^  Ubudiiy  Jb   COllgebieu,  ebpeoiaiiy 

sis  of  the  adductors.  j^fl^gj.    attacks  of    dyspnoea.      Gen- 

erally there  is  no  difficulty  in  deglutition  in  any  form  of  laryngeal  paraly- 
sis. In  those  where  the  bands  do  not  approximate  sufficiently  to  guard 
the  entrance  to  the  larynx,  there  may  be  slight  dyspnoea. 

Differential  Diagnosis. — Laryngeal  paralysis  is  easily  recognized  when  a 
careful  laryngoscopical  examination  of  the  larynx  is  made.  The  character 
of  the  respiration  in  paralysis  of  the  abductors,  and  of  that  in  paralysis  of 
adductors,  is  usually  sufficiently  marked  to  distinguish  the  one  from  the 
other.  In  adductor  paralysis  the  respiration  is  always  performed  with  ease  ; 
while,  in  paralysis  of  the  abductors,  dyspnoea  and  stridulous  breathing  are 
always  present  in  a  greater  or  less  degree.  In  other  forms  of  laryngeal  par- 
alysis, the  respiration  is  normal. 

Prognosis. — In  those  cases  where  paralysis  of  the  vocal  bands  depends 
upon  a  morbid  condition  of  the  nerve  centres,  or  is  due  to  compression  of 
the  nerves  by  aneurisms  or  new  formations,  the  prognosis  is  always  grave. 


SPASMODIC   AFFECTIONS   OF  THE   LAKYNX.  37 

On  the  other  hand,  it  is  favorable  when  it  is  due  to  functional  causes,  or 
originates  in  catarrhal  inflammation  of  the  mucous  lining  of  the  vocal  or- 
gans. When  there  is  paralysis  of  the  adductors,  usually  the  prognosis  is 
favorable ;  while  with  paralysis  of  the  abductors  the  patient  is  always  in 
great  danger. 

Treatment. — In  recurrent  laryngeal  paralysis,  where  any  method  of  treat- 
ment can  be  of  service,  the  surest  and  best  is  the  application  of  the  electric 
current,  galvanic  or  Faradic,  one  pole  being  placed  over  the  thyroid  or 
cricoid  cartilage,  and  the  other  in  contact  with  the  vocal  cords.  These 
applications  must  be  employed  at  regular  intervals,  and  only  for  a  short 
period  at  any  time.  As  adjuvants,  stimulating  inhalations  may  be  employed, 
such  as  ammonia,  creosote,  etc.,  and  local  applications  of  iron,  nitrate  of 
silver,  etc.  Whenever  the  abductor  muscles  have  lost  power,  it  becomes 
a  question  whether  tracheotomy  shall  or  shall  not  be  performed  ;  if  the 
dyspnoea  becomes  so  intense  as  to  be  a  source  of  immediate  danger  to  the 
patient,  tracheotomy  should  be  performed  without  delay,  for  it  affords 
the  only  chance  of  prolonging  life.  Rest  of  the  voice  is  an  all-important 
element  of  treatment,  where  there  is  deficient  action  of  the  muscles  ;  and, 
in  obstinate  cases,  electricity,  with  the  induced  or  galvanic  current,  may 
be  used  with  advantage  to  the  patient.  In  all  forms  of  laryngeal  paralysis, 
general  treatment  is  indicated. 

SPASMODIC    AFFECTIONS    OF   THE    LAEYI^X. 

The  only  spasmodic  affection  of  the  larynx  which  I  shall  consider,  is  the 
common  form  known  as  spasm  of  the  glottis,  or  laryngismus  stridulus, 
which  is  occasioned  by  temporary  spasm  of  the  adductors  of  the  larynx ; 
this  gives  rise  to  temporary  paroxysms  of  dyspnoea  and  stridulous  breath- 
ing. 

Morbid  Anatomy. — There  are  various  opinions  in  regard  to  the  patholog- 
ical nature  of  spasms  of  the  glottis.  According  to  some,  there  exists  an 
altered  or  abnormal  condition  of  the  nerve  centres — especially  is  this  the 
case  in  children  ;  while  other  authorities  recognize  an  excessive  suscep^ 
tibility  of  the  glottic  nerves  to  receive  reflex  impressions.  When  an 
adult  is  affected,  there  is  frequently  some  catarrhal  or  other  inflammatory 
condition  of  the  mucous  membrane  of  the  larynx,  which  acts  as  an  effi- 
cient cause  of  the  spasm  ;  in  children,  the  mucous  lining  of  the  larynx 
is  usually  perfectly  healthy.  In  adults,  the  brain  is  normal  in  appearance ; 
in  children,  serous  effusion  is  frequently  found  in  the  ventricles  and  on  the 
surface  of  the  brain.  Evidences  of  rickets  are  frequently  apparent  in  the 
osseous  system  of  children  subject  to  laryngismus.  The  condition  of  the 
pneumogastric  nerve  has  been  variously  reported  by  those  who  have  writ- 
ten on  this  subject.  Unquestionably,  reflex  irritation  in  the  larynx  may 
arise  from  a  great  variety  of  causes. 

Etiology. — There  can  be  little  doubt  but  that  spasm  of  the  glottis  is 
usually  due  to  a  nerve  impulse  originating  in  some  form  of  irritation  and 
conveyed  by  the  laryngeal  nerves.    The  seat  of  the  irritation  may  be  in  the 


38  DISEASES   OF   THE   RESPIEATOKY    ORGAifS. 

brain,  or  at  a  point  in  the  course  of  the  nerves,  or  peripheral  and  reflex. 
Laryngeal  spasm  is  most  frequently  met  with  in  children,  when  indigestion, 
teething,  and  impressions  of  external  cold  are  usually  assigned  as  causes ; 
yet,  in  most  cases  of  this  class,  cerebral  irritation,  due  to  some  other  cause, 
already  exists.  Scrofulous  and  cachectic  children  are  said  to  be  especially 
subject  to  spasm  of  the  glottis.  In  adults,  it  is  observed  in  connection  with, 
hysterical  manifestations,  and  is  sometimes  the  result  of  pressure  on  the 
nerves  ;  it  also  occurs  in  connection  with  irritation  from  foreign  bodies. 
It  has  been  met  with  as  a  sequela  of  whooping-cough. 

Symptoms. — In  children,  the  laryngeal  spasm  usually  comes  on  at  night, 
during  sleep.  The  dyspnoea  attending  it  is  often  intense,  the  respirations 
are  stridulous  and  crowing  in  character,  and  the  child  presents  the  appear- 
ance of  deficient  oxygenation  of  the  blood.  It  is  sometimes  attended  by 
general  convulsions,  in  which  there  is  extreme  contraction  of  the  flexor 
muscles  of  the  extremities  ;  strabismus  and  involuntary  discharge  of  faeces 
and  urine  are  sometimes  present.  The  spasm  usually  subsides  suddenly,  the 
recovery  is  complete,  and  is  never  accompanied  or  followed  by  fever.  One  of 
the  characteristics  of  this  affection  is  the  tendency  to  recurrence  of  the  at- 
tacks. Death  from  suffocation  during  the  paroxysm  may  occur,  but  it  is  ex- 
ceedingly rare.  In  adults  a  spasmodic  affection  of  the  larynx  is  either  hys- 
terical in  its  nature  or  it  depends  upon  interrupted  pressure  along  the  course 
of  the  recurrent  nerves.  It  gives  rise  to  symptoms  similar  to  those  already 
described,  except  that  the  paroxysms  are  less  severe  and  are  more  persistent. 

Differential  Diagnosis. — The  only  disease  liable  to  be  mistaken  for  the 
one  under  consideration  is  croup,  and  its  diagnosis  has  already  been  con- 
sidered under  that  head. 

Prognosis. — Those  cases  which  depend  upon  reflex  causes  generally  re- 
cover. The  prognosis  in  every  case  will  depend,  however,  upon  the  vio- 
lence and  frequency  of  the  spasm,  the  age  of  the  patient,  and,  above  all, 
upon  the  cause  of  the  spasm  ;  a  spasm  of  the  glottis  depending  upon  un- 
interrupted pressure  of  an  aneurism  on  the  recurrent  nerve,  is  not  infre- 
quently the  immediate  cause  of  death. 

Treatment. — If  spasm  of  the  glottis  is  due  to  reflex  irritation,  the  cause 
of  the  irritation  should  be  immediately  removed.  In  children,  dentition 
or  an  overloaded  stomach  is  most  frequently  the  source  of  the  irritation. 
In  prolonged  attacks,  inhalation  of  ether  or  chloroform  maybe  tried,  or  a 
hot  bath,  or  an  emetic  may  be  promptly  administered.  During  the  inter- 
val between  the  paroxysms  careful  attention  must  be  paid  to  the  diet  and 
general  hygiene  of  the  patient.  If  the  spasms  are  severe  and  prolonged, 
and  the  patient  seems  to  be  sinking,  the  trachea  must  be  opened  and  arti- 
ficial respiration  resorted  to.  When  laryngismus  occurs  in  the  adult,  those 
means  which  have  been  proved  beneficial  for  children  may  be  employed  for 
its  relief.  When  laryngeal  spasm  occurs  as  an  hysterical  phenomenon,  it 
must  be  treated  in  the  same  manner  as  any  other  hysterical  symptom.  If 
it  occurs  in  connection  with  pressure  upon  any  portion  of  the  pneumogas- 
tric  nerve,  one  must  be  prepared  at  any  moment  to  perform  tracheotomy 
for  temporary  relief. 


TUMORS   OF  THE   LARYKX. 


39 


TUMORS    OF   THE    LARYNX. 

Laryngeal  growths  may  be  divided  into  two  classes,  benign  and  malig- 
nant. 

Morbid  Anatomy. — I  shall  only  briefly  consider  the  morbid  anatomy  of 
those  laryngeal  growths  with  which  one  should  become  familiar  on  account  of 
their  frequency  ;  otlier  forms  are  more  especially  interesting  on  account  of 
their  rarity.  Morbid  growths,  as  they  occur  in  the  larynx,  may  have  a  broad 
base  which  attaches  itself  to  the  interior  lining  membrane  of  the  larynx, 
or  they  may  hang,  as  it  were,  into  the  interior  of  the  larynx,  from  a  narrow 
neck  or  pedicle.  They  may  vary  in  size,  shape,  consistency,  and  number. 
They  may  fill  up  the  cavity  of  the  larynx  so  as  to  impair  respiration,  or 
they  may  be  of  such  small  size  as  to  pass  unnoticed.  Three-fifths  of  all 
the  benign  growths  which  occur  in  the  larynx  are  papillomata ;  where 
these  growths  are  congenital,  the  proportion  is  even  greater.     These  tumors 


Fig.  8. 


Fig.  9. 


Multiple  Papilloma  of  the  right  Vocal  Chord  as  seen  with 
the  Laryngoscope. 


The  Trachea  laid  open,  showing  the  same 
Tumor  as  seen  in  Fig.  8. 


grow  rapidly  ;  sometimes  they  attain  a  considerable  size  in  the  space  of  a 
few  months.  For  the  most  part,  their  structure  is  similar  to  that  of  the 
normal  papillae.  Their  basic  substance  is  formed  of  connective- tissue, 
which  receives  into  its  interior,  vessels  and  nerves,  while  the  surface  is 
covered  with  a  layer  of  epithelium.  They  have  decidedly  a  villous  appear- 
ance ;  some  of  these  growths  contain  spaces  filled  with  colloid  matter ; 
after  removal,  they  are  quite  likely  to  recur.  Relations  have  been  traced 
between  benign  papillary  growths  and  warty  cancers.  Some  cases  are 
related  where  papillomata  have  become  softened,  fatty  and  cheesy,  and 
have  been  removed  by  coughing. 


40  DISEASES    OF    THE    RESPIRATOKY    ORGANS. 

Fibromata  are  of  less  frequent  occurrence  than  papillomata  ;  they  grow 
less  rapidly,  and  are  never  congenital.  These  growths  are  composed  of 
white  fibres,  diverging  from,  and  interlacing  one  another  in  different  direc- 
tions ;  after  removal  they  do  not  return.  They  are  generally  smooth, 
rounded,  pedunculated  and  vascular. 

Fihro-cellular  growths  are  composed  of  fibro-cellular  tissue.  They  usually 
contain  a  serons  fluid,  are  of  slow  growth,  single,  and  after  removal  show 
no  disposition  to  return. 

Cystic  tumors  are  due  to  enlargement  of  the  glands  in  the  mucous  mem- 
brane. They  contain  a  white,  sebaceous-like  material,  and  have  thick 
walls.  This  variety  of  tumor  is  less  frequently  met  with  than  any  of  the 
other  varieties. 

Glandular  groioths  take  their  origin  in  the  larynx,  where  the  glands  and 
follicles  are  most  abundant.     They  sometimes  attain  considerable  size. 

Carcinomatous  growths  in  the  larynx  are  of  two  varieties,  epithelial  and 
medullary.  The  epithelial  is  the  more  frequent.  The  medullary  is  not  so 
liable  to  ulcerate  as  is  the  epithelial,  but  produces  more  displacement. 
Sometimes  profuse  hemorrhage  occurs  in  connection  with  epithelial  cancer 
of  the  larynx. 

Etiology  of  Laryngeal  Growths. — The  most  frequent  cause  of  laryngeal 
growths  is  unquestionably  chronic  or  frequently  recurring  laryngitis.  In 
some  cases  a  more  or  less  constant  irritation  of  the  vocal  organs  seems  to 
give  rise  to  their  development,  such  as  is  met  with  among  teachers,  singers 
and  public  speakers.  Around  the  ulcerations  of  syphilis  and  of  laryngeal 
phthisis  these  growths  are  found.  Those  whose  calling  subjects  them  con- 
stantly to  the  inhalation  of  irritating  vapors  or  dust,  are  especially  liable 
to  them.  Isron-malignant  tumors  of  the  larynx  are  always  associated  in 
their  origin  with  local  hypersemia.  In  malignant  growths,  in  addition  to 
the  local  changes,  there  are  constitutional  influences  in  operation  which 
impart  to  them  a  specific  character.     They  are  sometimes  congenital. 

Symptoms. — The -symptoms  which  attend  laryngeal  growths  are  for  the 
most  part  local  in  character,  and  these  local  symptoms  will  necessarily  vary 
with  the  size,  situation,  and  nature  of  these  morbid  growths,  as  well  as  with 
the  size  of  the  larynx.  The  development  of  these  tumors  is  rarely  accom- 
panied by  pain,  but  sometimes  there  is  a  sense  of  uneasiness  as  though  a 
foreign  mass  were  in  the  larynx.  Eespiration  may  be  more  or  less  interfered 
with,  and  there  may  be  severe  dyspnoea  ;  but  usually  it  is  present  only  after 
violent  physical  exertion,  running,  jumping,  going  up  a  long  flight  of 
stairs,  etc.  The  breathing  is  sometimes  stridulous  in  character,  and  fre- 
quent suffocative  attacks  due  to  spasm  may  come  on.  When  the  growth  is 
above  the  glottis,  all  the  difficulty  in  breathing  is  on  inspiration ;  the  ex- 
piration is  quite  free.  The  voice  is  always  more  or  less  changed;  it  is  not 
only  altered  in  quality  and  liable  to  sudden  changes  in  intensity,  but  some- 
times it  is  completely  lost.  Cough  is  present  in  many  cases ;  it  is  usually 
due  to  accompanying  laryngitis  ;  not  infrequently  it  is  voluntarily  excited 
by  the  desire  on  the  part  of  the  patient  to  get  rid  of  the  laryngeal  obstruc- 
tion.    In  the  expectoration,  which  is  usually  increased  by  coughing,  frag- 


BRONCHITIS.  41 

ments  of  the  growth  are  sometimes  found;  as  a  rule  there  is  nothing  which 
can  be  considered  as  distinctive  about  it.  Dysphagia  is  present  in  the  ad- 
vanced stages  of  many  laryngeal  growths,  especially  when  they  are  malig- 
nant. The  most  positive  evidences  of  laryngeal  growths  are  furnished  by 
the  laryngoscopic  examinations.  By  moderately  expert  laryngoscopic  exam- 
inations the  seat,  size,  and,  in  some  cases,  the  nature  of  the  laryngeal 
growths  will  be  readily  determined. 

DifFerential  Diagnosis. — The  interference  with  the  functions  of  the  larynx 
will  direct  attention  to  this  organ,  and  if  the  laryngoscope  is  used  the  ex- 
istence of  these  growths  will  rarely  be  overlooked;  when  seen  it  will  hardly 
be  possible  to  confound  them  with  any  other  disease.  The  study  of  the 
histories  of  such  cases  as  are  recorded  in  laryngoscopic  manuals  will  be  of 
great  assistance  in  making  a  differential  diagnosis. 

Prognosis. — If  the  growth  be  pedunculated,  of  moderate  size,  and  single, 
with  ordinary  condition  of  tolerance,  the  voice  can,  in  many  instances,  be 
entirely  restored.  If  the  contrary  condition  exists,  relief  may  be  looked 
for,  but  never  complete  restoration  of  the  voice.  As  to  length  of  life, 
other  things  being  equal,  the  prognosis  is  more  favorable  in  adults  than  in 
children,  for  the  reason  that  evulsion  of  the  growth  by  the  intra-laryngeal 
methods  is  more  readily  and  certainly  accomplished  in  the  former  than 
in  the  latter.  Whenever  these  growths  are  cancerous  in  nature  they  ter- 
minate fatally. 

Treatment. — If  a  laryngeal  growth  is  small,  and  does  not  interfere  with 
the  voice  or  respiration,  the  rule  is  to  let  it  alone  ;  if,  on  the  other  hand,  it 
is  of  considerable  size,  and  is  increasing  rapidly,  endangering  life,  operative 
measures,  either  intra-  or  extra-laryngeal,  must  be  resorted  to.  These  more 
properly  fall  within  the  province  of  the  specialist  than  of  the  general  prac- 
titioner. Whenever  there  is  great  obstruction  to  respiration,  and  suffoca- 
tion seems  imminent,  tracheotomy  should  be  immediately  performed,  after 
which  the  intra-laryngeal  methods  of  procedure  may  be  resorted  to.  In 
malignant  laryngeal  growths,  all  remedial  measures  are  only  palliative. 

Ossification  and  calcareous  infiltration  of  the  cartilages  of  the  larynx 
are  met  with  in  those  cases  where  there  has  been  chronic  and  frequently 
recurring  laryngitis  ;  not  infrequently  the  calcareous  condition  of  the  carti- 
lage, which  is  sometimes  present  in  connection  with  chondritis  or  perichon- 
dritis, is  preceded  by  its  ossification. 

BKONCHITIS. 

Bronchitis  is  essentially  an  inflammation  of  the  mucous  membrane  of  the 
larynx,  trachea,  and  bronchial  tubes,  which  may  vary  in  extent,  intensity, 
duration,  and  in  the  nature  of  its  pathological  products.  Thus  it  may  be 
limited  to  the  larynx,  trachea,  and  larger  bronchi,  or  it  may  extend  into 
the  capillary  tubes;  it  may  be  mild  or  severe  in  character,  ran  a  rapid 
course,  or  be  indefinitely  protracted.  It  may  also  be  produced  by  a  variety 
of  causes,  some  external,  some  internal,  some  accidental,  and  others  consti- 
tutional.    It  may  be  primary  or  secondary, — jjrimary,  when  the  result  of 


42 


DISEASES    OF    THE    KESPIEATOEY    ORGANS. 


exposure,  or  produced  by  the  inhalation  of  irritating  gases ;  secondary* 
when  it  arises  from  constitutional  vice,  or  from  previously  existing  disease 
Again,  it  may  occur  as  a  complication  during  the  course  of  other  diseases, 
such  as  acute  blood  disease,  pulmonary  phthisis,  pulmonary  emphysema, 
and  cardiac  disease.  It  affects  all  ages  and  either  sex.  One  attack  predis- 
poses to  a  second.  Bronchitis,  clinically  and  pathologically,  may  be  di- 
vided into  the  following  varieties  : — (1)  Acute  Catarrhal  Bronchitis  of  the 
large  tubes ;  (2)  Acute  Capillary  Bronchitis ;  (3)  Chronic  Catarrhal 
Bronchitis;  (4)  Croupous  or  Plastic  Bronchitis  ;  and  (5)  Bronchiectasis. 


ACUTE  CATAEEHAL  BEONCHITIS. 

This  form  of  bronchial  inflammation  occurs  at  all  ages.     In  childhood 
and  old  age  it  most  frequently  involves  the   smaller  bronchi  ;  in  adult 
life  it  involves  the  larger  bronchi.     It  may  be  mild  or  severe  in  type. 

Morbid  Anatomy. — The  morbid  anatomy  of  this  variety  of  bronchitis  does 


Fig.  10. 
Transverse  section  of  a  portion  of  a  medium-sized  Bronchial  Tube  in  Acute  Catarrhal  Bronchitis. 

a.  Epithelial  layer,  in  part  raised,  covered  and  inMtrated  with  pus. 

b.  Transversely  divided  ends  of  the  internal  Jibroiis  layer, 
c  The  rnuscular  layer,  thickened. 

d.  Portion  of  an  hypertrophied  cartilaqe  plate.  The  mucoiis  glands,  in  the  external  layer,  are  seen  enlarged 
and  m  great  numbers  ;  and  one  of  the  ducts  increased  in  size  is  seen  opening  into  the  lumen  of  the  tube. 
X  250. 

not  differ  essentially,  whether  it  has  its  seat  in  the  large  or  small  bronchial 
tubes.  In  either  case  it  rarely  originates  in  the  tubes  themselves,  but  is  the 
continuation  of  a  similar  process  affecting  the  nasal,  pharyngeal  and  laryngeal 


ACUTE    CATARRHAL    BRONCHITIS.  43 

mucous  membrane,  or  is  the  extension  to  the  smaller  tubes  of  an  inflammation 
commencing  in  the  alveoli.  As  a  rule,  the  simple  variety  does  not  advance 
beyond  the  larger  bronchi  ;  when  the  smaller  tubes  are  involved  it  is  de- 
nominated cainllary .  In  some  cases  the  mucous  membrane  is  swollen  and 
reddened,  either  uniformly  or  in  points  or  patches.  Its  surface  may  be 
roughened  by  the  presence  of  enlarged  papillae  or  granulations.  It  is  usu- 
ally softer  and  moister  than  natural — occasionally  ecchymoses  are  observed 
in  it.  The  natural  longitudinal  rug^e  of  the  membrane  are  effaced,  giving 
a  smooth  appearance  to  the  reddened  surface.  The  bronchi  at  first  contain 
a  clear  transparent  mucus,  which,  as  the  disease  advances,  becomes  opaque, 
whitish,  yellowish,  or  greenish.  The  change  in  the  color  of  the  secretion  is 
owing  to  pus-cells  contained  in  the  fluid ;  at  the  onset  there  are  but  few 
present.  The  presence  of  desquamated  epithelium  in  the  tubes  after  death 
is  for  the  most  part  owing  to  the  separation  of  the  cells  from  the  membrane 
between  the  time  of  death  and  the  making  of  the  autopsy.  In  a  small  pro- 
portion of  cases,  the  only  evidence  of  bronchitis  which  is  found  at  the  post- 
mortem is  the  presence  of  mucus  or  muco-pus  in  the  tubes.  Sometimes 
the  tubes  are  more  rigid  than  normal.  These  changes  exist  whether  the 
larger  or  smaller  tubes  are  involved.  Generally,  the  tubes  on  both  sides  are 
equally  affected.  In  the  weak,  the  very  young  and  the  very  old,  or  when 
there  is  some  condition  which  prevents  or  enfeebles  the  cough,  the  mucus 
or  muco-pus  sometimes  gravitates  from  the  larger  into  the  smaller  tubes, 
and  gives  rise  to  yellow  spots  near  the  surface  of  the  lung  ;  this  is  especially 
liable  to  occur  in  young,  feeble  children. 

There  may  be  complications  with  acute  bronchitis.  The  swollen  mu- 
cous membrane,  or  the  accumulation  of  mucus  or  muco-pus  may  produce 
a  temporary  air  distention  of  the  alveoli^a  condition  frequently  met  with 
at  autopsies,  and  sometimes  mistaken  for  vesicular  emphysema.  Fully 
developed  emphysema,  as  well  as  atelectasis,  may  occur  as  the  result  of 
these  bronchial  obstructions.  Atelectasis  is  specially  liable  io  occur  in 
young  children.  In  these  patches  of  collapsed  lung,  or  as  the  result  of 
the  extension  of  inflammation  from  the  bronchi  to  the  alveoli,  lobular 
pneumonia  is  not  infrequently  developed  as  a  complication.  This  is  rare 
in  the  acute  bronchitis  of  the  adult,  but  frequent  in  children.  Pulmonary 
congestion  and  oedema  are  not  infrequent  complications  of  general  capil- 
lary bronchitis.  Temporary  bronchial  dilatation  often  occurs  in  children, 
when  the  disease  affects  the  smaller  tubes,  and  lasts  more  than  a  week. 

Etiology. — The  most  marked  predisposing  causes  of  acute  bronchial  ca- 
tarrh are  infancy  and  old  age,  indulgence  in  enervating  habits,  or  debility 
from  any  cause,  constitutional  diseases,  chronic  pulmonary  affections,  the 
breathing  of  impure  air  in  badly  ventilated  apartments,  and  sudden  changes 
in  temperature.  It  is  comparatively  rare  in  continuously  hot  or  cold  cli- 
mates. In  our  climate  it  prevails  most  in  the  spring  and  fall.  The  disease, 
when  primary,  is  either  due  to  some  sudden  atmospheric  change,  to  some 
morbific  agent  in  the  atmosphere,  or  to  the  action  of  cold  on  the  surface  of 
the  body  when  imperfectly  protected,  causing  a  chilling  of  the  surface.  It 
occurs  secondarily  in  connection  with  blood-poisoning,  as  in  measles,  ty- 


44 


DISEASES   OF   THE   KESPIRATORY   ORGANS. 


phoid  and  typhus  fevers,  gout,  rheumatism,  etc.  In  the  course  of  other 
pulmonary  affections,  and  in  chronic  cardiac  diseases,  it  is  of  quite  frequent 
occurrence.  It  may  be  produced  traumatically  by  the  inhalation  of  irritat- 
ing gases,  particles  of  dust,  etc.,  which  act  directly  upon  the  mucous 
membrane.  Those  who  live  in  the  open  air  are  less  liable  to  it  than  those 
living  in-doors.  At  times  bronchitis  prevails  epidemically,  associated  with 
influenza  and  due  to  the  action  of  some  unknown  atmospheric  influence. 

Symptoms. — A  common  "cold"  may  be  regarded  as  a  bronchitis  of  the 
larger  tubes.  This  simple  form  of  bronchial  catarrh  does  not  extend  below 
the  second  division  of  the  bronchi,  but  expends  itself  on  the  larynx,  trachea, 
and  large  bronchi.  Its  invasion  is  commonly  marked  by  coryza,  lachryma- 
tion,  sore  throat  and  slight  hoarseness,  with  chilliness  scarcely  amounting 
to  rigor.  The  occarrence  of  the  coryza,  with  an  uneasy  sensation  in  the 
frontal  sinuses,  gradually  passing  from  the  nasal  passages  to  the  larynx  and 
trachea,  is  diagnostic  of  its  primary  character.  The  pulse  is  slightly  in- 
creased in  force  and  frequency,  there  is  aching  in  the  back  and  limbs,  but  the 
general  febrile  symptoms  are  usually  mild  ;  in  very  young  and  weakly  chil- 
dren convulsions  may  occur.  As  the  bronchial  inflammation  becomes  fully 
established,  more  or  less  pain  and  discomfort  are  felt  behind  the  sternum  ; 
there  is  a  sense  of  tickling,  rawness  and  soreness  at  the  upper  portion  of  tVie 
chest,  which  amounts  to  actual  pain  on  coughing ;  the  respirations  ar/>* 
somewhat  increased  in  frequency,  and  there  is  a  sensation  of  constriction 
with  oppressed  breathing  which  may  be  somewhat  laborious,  but  there  if 
no  evident  dyspnoea.  The  cough,  an  essential  feature  of  the  disease,  a* 
first  is  dry  and  hacking,  sometimes  incessant,  especially  on  lying  down,  and 
on  waking  after  a  long  sleep  ;  it  may  be  paroxysmal  in  character.  After 
one  or  two  days  the  cough  becomes  loose,  and  is  attended  with  an  expec- 
toration of  frothy  mucus,  of  a  yel- 
lowish color  and  a  saline  taste ; 
gradually  this  becomes  muco-puru- 
lent  and  even  purulent.  As  soon  as 
^^  the  expectoration  becomes  free  the 
'_Jj'  patient  is  relieved.  The  disease 
lasts  from  four  or  five  days  to  two 
or  three  weeks,  and  ends  in  complete 
recovery  or  in  chronic  bronchitis. 

Physical  Signs. — In  slight  attacks 
of  acute  bronchial  catarrh  of  the 
larger  tubes,  there  may  be  no  physi- 
cal signs  to  indicate  its  existence. 
The  severer  forms  are  attended  by 
easily  recognized  physical  signs. 
As  a  rule,  inspection  and  palpation 
give  negative  results.  ^\\q  percus- 
sion sounds  are  normal,  unless  there  is  a  very  considerable  accumulation  of 
mucus  in  the  bronchial  tubes  ;  in  such  cases,  the  normal  resonance  is  dimin- 
ished posteriorly  in  the  infra-scapular  region.     On  auscultation  over  the 


Sibilant  rales 


Subcrepitant  rales 


Fib.  11. 
Diagram  illustrating  the  Physical  Sign?  of  Bronchitis. 


ACUTE    CATAERHAL    BRONCHITIS,  45 

affected  tubes,  the  respiratory  murmur  is  feeble,  temporarily  suppressed,  or 
sonorous  in  character.  In  the  dry  stage,  sibilant  and  sonorous  rales  may 
be  heard  on  both  sides  over  the  whole  chest,  more  distinctly  posteriorly.  In 
the  stage  of  secretion  with  the  sibilant  and  sonorous  rdles,  moist  rales,  large 
and  small  in  size,  are  heard  on  both  sides  of  the  chest.  These  rales  are  in- 
constant, coming  and  going,  and  changing  their  situation  ;  after  a  violent 
fit  of  coughing,  they  may  entirely  disappear  for  a  time.  When  they  are 
abundant  and  very  loud,  they  often  altogether  mask  the  respiratory  mur- 
mur. When  the  secretion  is  watery,  they  have  a  "  rattling  "  sound.  In 
some  cases,  secretion  takes  place  so  rapidly  that  moist  rales  are  heard  from 
the  first.     Vocal  resonance  in  bronchitis  is  normal. 

DifiFerential  Diagnosis. — It  is  hardly  possible  to  confound  bronchitis  of  the 
large  tubes  with  any  other  pulmonary  affection.  The  absence  of  lancina- 
ting pains  in  either  side,  the  bronchial  character  of  the  cough  and  expec- 
toration, the  coryza  and  hoarseness  which  precede  the  attack,  are  usually 
suflBcient  to  distinguish  it  from  pneumonia  and  pleurisy ;  besides,  its 
physical  signs,  if  properly  appreciated,  render  the  diagnosis  easy  and 
positive  in  all  cases.  The  early  stage  of  whooping-cough  may  be  con- 
founded with  it,  until  the  characteristic  cough  is  heard. 

Prognosis. — This  form  of  bronchitis,  unless  it  occurs  in  the  very  young, 
or  very  old  and  feeble,"  never  directly  destroys  life.  It  usually  terminates 
by  resolution  in  from  three  to  four  days  to  two  or  three  weeks ;  some- 
times it  becomes  chronic  :  in  such  cases  the  inflammation  is  likely  to 
extend  into  some  of  the  smaller  tubes,  giving  rise  to  circumscribed  capillary 
bronchitis. 

Treatment. — In  the  majority  of  cases,  this  form  of  bronchitis  is  easily 
managed.  In  mild  attacks  the  patient  is  not  sufficiently  ill  to  consult  a 
physician  ;  it  is  simply  regarded  as  a  severe  cold.  At  the  onset,  while  the 
coryza  is  present,  it  may  generally  be  arrested  by  a  Dover's  or  Tully's  pow- 
der and  a  warm  bath  at  night,  followed  in  the  morning  by  a  brisk  saline 
purge — in  the  case  of  children  by  a  full  dose  of  castor  oil.  The  patient 
should  remain  in  a  warm,  moist,  equable  temperature  for  a  day  or  two. 
gr.  XX.  of  quinine  or  of  salicylic  acid  acts  oftentimes  as  an  abortive  in 
adults.  If  this  plan  has  not  been  resorted  to,  or  has  not  proved  successful, 
then  moderate  but  continued  action  of  the  skin  and  kidneys  should  be  in- 
duced by  the  administration  of  mild  diaphoretics  and  diuretics,  the  patient 
remaining  in  a  warm,  even  temperature.  In  the  early  stage  of  the  disease, 
especially  in  the  case  of  children,  great  benefit  is  often  derived  from  steam 
inhalations.  Counter-irritation,  by  means  of  cups  and  mustard  sinapisms, 
to  the  upper  part  of  the  chest,  is  of  great  service  in  its  late  as  well  as  in  its 
early  stages.  If  the  disease  shows  a  tendency  to  pass  into  the  chronic 
stage,  or  to  extend  into  the  smaller  tubes,  from  eight  to  ten  grains  of 
the  sulphate  of  quinine  should  be  daily  administered  ;  in  children,  cod- 
liver  oil  with  lime-water  should  be  given.  A  succession  of  small  blisters 
applied  to  the  posterior  portion  of  the  chest  will  be  of  service  after  the 
acute  stage  is  past.  When  simple  bronchitis  occurs  in  those  of  a  gouty 
or  rheumatic  diathesis,  colchicum  must  be  given  in  connection  with  alkalies. 


46  DISEASES    OF    THE    KESPIEATOKT    OKGANS. 


ACUTE    CAPILLAET    BRONCHITIS. 

When  acute  catarrhal  inflammation  invades  the  small-sized  bronchia! 
tubes,  it  is  termed  capillary  bronchitis.  It  is  also  known  as  "  catarrhus 
senilis,"  bastard  pleurisy,  and  suffocative  catarrh.  In  most  instances,  this 
form  is  an  extension  of  simple  bronchitis,  whose  characteristic  symptoms 
have  preceded  ;  but  sometimes  the  smaller  as  well  as  the  larger  bronchial 
tubes  are  affected,  or  the  smaller  bronchi  may  be  the  primary  seat  of  the 
inflam^matory  process.  General  capillary  bronchitis  is  much  more  fre- 
quently met  with  in  infancy  and  old  age  than  during  any  other  periods  of 
life.  If  the  inflammation  is  limited,  and  only  a  few  of  the  smaller  tubes 
are  involved,  it  is  called  localized  capillary  bronchitis  ;  but  when  the  bron- 
chial inflammation  is  intense,  and  diffused  over  the  lining  membrane  of 
all  the  bronchial  tubes,  it  is  termed  general  capillary  bronchitis.  In  the 
symptoms  which  attend  its  development,  and  in  its  tendency  to  destroy 
life,  it  differs  very  much  from  bronchitis  of  the  larger  tubes.  The  morbid 
anatomy  of  this  form  of  bronchitis  has  been  already  sufficiently  described; 
but  its  symptomatology,  prognosis,  and  treatment  require  separate  consid- 
eration. The  causes  which  give  rise  to  capillary  bronchitis  are  similar  to 
those  which  have  been  named  in  connection  with  the  etiology  of  simple 
bronchitis,  except  in  those  instances  where  it  occurs  as  a  secondary  affection. 
The  danger  from  acute  catarrhal  inflammation  of  the  smaller  tubes  in  pa- 
tients with  Bright's  disease,  typhus  fever,  measles,  and  the  chronic  bron- 
chitis of  old  age,  should  never  be  lost  sight  of.  Some  of  the  worst  cases 
are  met  with  in  connection  with  emphysema  of  the  lungs. 

Symptoms. — The  milder  types  of  this  form  of  bronchitis  are  usually  pre- 
ceded by  inflammation  of  the  larger  tubes,  and  the  symptoms  of  invasion 
are  not  marked.  In  fact,  the  capillary  element  of  the  disease  might  not  be 
recognized,  were  it  not  for  its  physical  signs,  and  difficult  or  labored  respi- 
ration. On  the  other  hand,  the  severe  forms  may  be  ushered  in  by  distinct 
chills,  high  febrile  excitement,  and  great  dyspnoea.  The  patient  is  unable 
to  lie  down  on  account  of  the  difficulty  of  breathing,  and  the  countenance 
is  anxious  and  flushed.  Paroxysmal  orthopncea  is  not  uncommon.  The 
respirations  are  accelerated,  reaching  60  and  70  in  a  minute,  attended  by 
great  muscular  effort.  The  pulse  is  feeble,  beating  from  100  to  130  in  a 
minute.  The  axillary  temperature  is  raised  to  103°  F.,  but  as  the  disease 
advances  it  may  fall  to  100°  F.,  although  the  pulse  and  respiration  remain 
frequent.  The  patient,  at  the  commencement  of  the  attack,  has  an  inces- 
sant hacking  cough,  which  is  often  so  violent  as  to  compel  him  to  sit  up, 
bend  forward,  and  hold  his  sides.  At  first,  there  is  little  if  any  expectora- 
tion ;  if  expectoration  is  present,  it  is  a  thick,  tenacious  mucus ;  later,  it 
becomes  more  abundant  and  less  tenacious.  So  viscid  and  tough  is  the  ex- 
pectorated material,  that  cast-like  masses  of  the  bronchioles  may  be  formed. 
When  some  of  the  sputa  is  put  in  water,  the  froth  floats  and  is  connected 
by  filaments  with  the  heavier  masses  underneath  the  surface.  The  cough 
may  be  accompanied  by  a  rattling  sound  in  the  trachea.     There  is  great 


ACUTE    CAPILLARY   BEONCHITIS.  47 

exhaustion.  If  the  disease  progresses,  all  the  phenomena  of  deficient  oxy- 
genation are  developed.  The  face  betokens  great  distress  and  has  a  livid 
aspect,  the  lips  become  blue,  and  there  is  blueness  of  the  finger-ends,  with 
fulness  of  the  jugular  veins.  The  respiratory  acts  become  more  and  more 
labored  and  imperfect,  the  expectoration  becomes  more  and  more  abun- 
dant, and  the  matter  expectorated  thin,  frothy,  and  less  tenacious.  There 
is  great  restlessness,  with  signs  of  impending  suffocation,  and  the  surface 
of  the  body  is  covered  with  a  cold,  clammy  sweat.  As  death  approaches, 
the  pulse  becomes  small  and  thready,  the  respiratory  efforts  are  less  violent 
and.  less  frequent,  muttering  delirium  comes  on,  or  the  patient  lies  in  a 
state  of  partial  coma,  both  cough  and  expectoration  cease,  and  he  dies 
asphyxiated.  These  symptoms  vary  somewhat  with  the  age  and  peculiari- 
ties of  the  individual  affected,  and  with  the  diseases  which  it  may  com- 
plicate. In  aged  persons,  or  in  those  who  are  constitutionally  weak  from 
any  cause,  the  fever  is  very  apt  to  take  on  an  adynamic  type.  When  it 
occurs  in  connection  with  acute  blood  diseases,  it  is  likely  to  come  on  very 
insidiously,  without  any  of  its  usual  symptoms  being  prominent.   ■ 

Physical  Signs. — In  addition  to  the  signs  belonging  to  simple  bronchitis, 
the  percussion  sound  in  the  early  part  of  the  disease  may  be  somewhat 
exaggerated  in  the  infraclavicular  regions,  the  percussion  resonance  may 
be  diminished  on  account  of  the  attendant  pulmonary  oedema,  and  the 
accumulation  of  morbid  products  in  the  small  bronchi.  While  resonance 
is  diminished  in  the  lower  portions,  the  superior  portions  of  the  lung  may 
give  an  emphysematoas  percussion  note. 

Auscultation. — If  the  bronchitis  is  extensive,  the  vesicular  murmur  over 
both  lungs  is  feeble  or  suppressed,  and  the  inspiration  may  be  masked  by 
high-pitched,  hissing,  sibilant  rales  ;  as  the  disease  advances  the  subcrepi- 
tant  distinctive  rale  of  capillary  bronchitis  is  heard  all  over  the  chest,  but  es- 
pecially in  the  infra-scapular  region.  {See  Fig.  11. )  If  the  subcrepitant  rales 
are  abundant  and  are  heard  over  the  whole  chest,  they  indicate  very  positively 
the  existence  of  a  general  capillary  bronchitis.  These  rales  may  be  present 
over  circumscribed  spaces  posteriorly,  as  the  result  of  the  gravitation  of  the 
fluid  secretion  from  the  larger  into  the  smaller  tubes.  If  they  are  confined 
to  the  apex  or  base  of  one  lung,  with  resonance  on  jDercussion,  they  indicate 
the  existence  of  a  localized  capillary  bronchitis. 

Differential  Diagnosis. — Capillary  bronchitis  may  be  confounded  with  'pneu- 
monia, pulmonary  oedema,  and  phthisis.  It  differs  from  simple  bronchi- 
tis in  the  higher  temperature,  greater  frequency  of  the  respiration,  the  ex- 
treme dyspnoea,  the  interference  with  the  general  capillary  circulation,  and  the 
presence  of  the  hissing,  sibilant,  and  subcrepitant  rales.  It  is  distinguished 
from  'pneumonia  by  the  absence  of  pain  in  the  side,  prolonged  initial  chill, 
and  the  characteristic  pneumonic  sputa,  by  the  greater  frequency  and  labor 
of  respiration,  and  the  more  intense  dyspnoea,  by  its  lower  temperature,  by 
the  normal  or  exaggerated  resonance  on  percussion,  by  the  presence  of  the 
subcrepitant  rales  on  loth  sides  of  the  chest,  and  by  the  absence  of  bronchial 
breathing  and  of  increase  in  the  vocal  fremitus.  The  points  of  differential 
diagnosis  between  capillary  bronchitis   and  phthisis   will  be   considered 


48  DISEASES   OF   THE   EESPIRATORY    ORGANS. 

under  the  latter  head.  The  existence  of  the  physical  signs  of  capillary 
bronchitis  at  the  apex  of  one  lung,  accompanied  by  evidence  of  pulmon- 
ary consolidation  at  that  point,  always  leads  to  the  suspicion  of  incipient 
phthisis.  The  physical  signs,  pyrexia,  and  history  of  the  patient  will  suf- 
fice to  distinguish  it  from  asthma. 

Prognosis. — General  capillary  bronchitis  is  a  disease  attended  with  great 
danger,  especially  when  it  occurs  in  infancy  or  old  age,  or  when  it  super- 
venes upon  some  grave  organic  disease,  as  phthisis,  Bright's,  heart  disease, 
and  acute  blood  diseases.  When  it  occurs  in  persons  suffering  from  pul- 
monary emphysema,  although  for  a  time  the  symptoms  are  urgent,  it  rarely 
proves  fatal.  It  usually  lasts  from  three  to  five  days  ;  but  when  very  exten- 
sive may  prove  fatal  in  twelve  hours.  Among  the  unfavorable  symptoms 
may  be  named  great  difficulty  of  expectoration,  shallow  breathing,  cessa- 
tion of  cough,  urgent  dyspnoea  with  evidences  of  incipient  asphyxia,  and 
the  presence  of  adynamic  symptoms.  In  this  disease,  death  results  from 
asphyxia  caused  by  imperfect  oxygenation  of  the  blood. 

Treatment. — All  the  so-called  antiphlogistic  remedies  lessen,  if  they  do 
not  destroy,  the  chances  of  recovery.  From  the  commencement  of  the 
attack,  the  treatment  must  be  supporting.  In  general  capillary  bronchitis, 
the  patient  must  be  kept  in  bed,  the  surface  of  the  body  covered  with  flan- 
nel, the  temperature  of  the  apartment  must  range  from  75°  to  80°  F.  and  the 
air  must  be  moistened  with  steam.  Children  should  be  placed  in  the  steam 
tent,  as  advised  in  the  treatment  of  membranous  croup.  Dry  cups  should 
be  applied  over  the  whole  surface  of  the  chest,  after  which  it  should  be 
covered  with  an  oil-silk  jacket.  The  inhalation  of  steam  usually  increases 
the  bronchial  secretion,  facilitates  expectoration,  and  for  a  time,  at  least, 
relieves  the  difficult  breathing.  If  symptoms  of  imperfect  oxygenation 
are  developed,  the  inhalation  of  oxygen  gas  in  connection  with  the  steam 
will  often  afford  the  most  marked  relief.  The  internal  administration  of 
muriate  of  ammonia,  or  chlorate  of  potash  in  five  or  ten  grain  doses  every 
two  hours  to  the  adult  (two  grains  may  be  given  to  a  child  two  years  of 
age),  often  seems  to  have  a  controlling  influence  over  the  inflammatory 
processes.  Iodide  of  potassium  is  of  benefit  in  children  threatened  with 
atelectasis  and  lobular  pneumonia.  The  so-called  expectorants  are  of  little 
service.  Sometimes,  when  suffocation  is  imminent  and  the  power  of  ex- 
pectoration is  entirely  lost,  stimulating  emetics  will  be  found  of  service, 
especially  in  very  young  children  ;  the  action  of  the  emetic  seems  to  sup- 
ply the  want  of  voluntary  power  to  expectorate,  and  it  dislodges  the  accu- 
mulated secretion  in  the  bronchial  tubes  ;  care  must  be  taken  not  to  repeat 
emesis  so  often  as  to  produce  exhaustion. 

In  the  advanced  stage  of  the  disease,  when  the  pulse  becomes  small  and 
thready,  quinine  and  stimulants  must  be  freely  administered.  The  chief 
object  of  treatment  in  this  disease  is  to  sustain  the  life  of  the  patient  until 
the  inflammatory  process  has  passed  through  its  different  stages.  As  re- 
gards the  use  of  stimulants,  there  is  no  disease  (especially  of  childhood)  in 
which  their  judicious  use  is  so  markedly  beneficial.  They  should  be 
commenced  early,  and  given  in  sufficiently  large  quantities  to  overcome  the 


CHRONIC   CATARRHAL  BRONCHITIS.  49 

Bigns  of  exhaustion,  which  are  present  very  early.  To  allay  spasm  of  the 
bronchial  tubes,  which  is  occasionally  present  in  this  form  of  bronchitis, 
and  gives  rise  to  the  most  distressing  paroxysms  of  dyspnoea,  full  doses  of 
hydrocyanic  acid  may  be  given,  and  this  is  often  followed  by  most  marked 
relief.  Opium  should  never  be  given,  for  by  its  action  the  power  of  expec- 
toration is  often  diminished,  and  it  favors  the  dangerous  accumulation  of 
inflammatory  products  in  the  bronchial  tubes.  Each  case  should  be  stud- 
ied by  itself,  with  attention  to  the  constitutional  conditions  under  which 
it  occurs,  and  the  treatment  should  be  so  modified  as  to  meet  the  indica- 
tions. The  general  management  of  capillary  bronchitis  associated  with 
Bright's  disease  is  very  different  from  that  of  capillary  bronchitis  occur- 
ring in  a  person  previously  healthy.  During  the  whole  course  of  the  dis- 
ease when  this  complication  is  present  the  patient  should  receive  the  largest 
possible  amount  of  concentrated  nutrition — the  yolk  of  eggs  and  milk  are 
generally  well  borne  by  this  class  of  patients.  Precaution  must  be  taken 
against  the  slightest  exposure  to  changes  in  temperature  during  convales- 
cence. 

There  are  certain  peculiarities  which  attend  the  capillary  bronchitis  of 
young  children.  It  differs  from  the  bronchitis  of  adults  in  the  greater 
liability  to  extension  of  the  bronchial  inflammation  to  the  alveoli,  with 
consequent  lobular  pneumonia;  also,  in  the  liability  to  the  occurrence  of 
atelectasis  or  collapse  of  the  lobules,  the  result  of  the  plugging  up  of  the 
small  bronchi  by  accumulation  of  secretion  in  them,  with  intense  swelling 
of  the  mucous  membrane.  The  occurrence  of  lobular  atelectasis  cannot 
be  determined  with  certainty  either  by  the  rational  or  physical  signs.  It 
may  be  suspected  in  young  children  whenever  physical  signs  indicative  of 
extensive  capillary  bronchitis  are  associated  with  extreme  dysj^noea  and  evi- 
dence of  defective  oxygenation  of  the  blood,  the  physical  signs  and  other 
symptoms  of  broncho-pneumonia  being  absent.  The  development  of  lobu- 
lar pneumonia  is  certain  to  follow  lobular  atelectasis,  if  the  life  of  the  pa- 
tient is  sufficiently  prolonged  after  the  occurrence  of  the  latter.  In  the 
treatment  of  bronchitis  of  young  children,  the  liability  to  these  complica- 
tions should  always  be  borne  in  mind. 

CHRONIC    CATAEEHAL    BEONCHITIS. 

This  is  a  very  common  disease,  and  results  from  any  cause  which  excites 
and  keeps  up  a  low  grade  of  inflammation  of  the  bronchial  mucous  mem- 
brane. It  is  usually  a  disease  of  adult  life.  One  of  its  chief  characteristics 
is  its  tendency  to  recurrence  ;  the  attacks  increase  in  severity  and  duration 
at  each  return,  until  the  individual  is  rarelyfree  from  it.  Chronic  bronchitis 
may  hQ  primary  ov  secondary.  Primary,  when  it  is  the  result  of  exposure 
to  wet  or  cold,  or  when  it  is  excited  by  the  daily  inhalation  of  dust,  vapors, 
or  other  irritating  substances.  Secondary,  when  due  to  some  constitutional 
vice,  as  gout,  rheumatism,  syphilis,  etc.;  or  some  local  affection,  as  cardiac 
or  renal  disease.  It  may  occur  as  a  complication  of  other  pulmonary  affec- 
tions, as  phthisis,  pulmonary  emphysema,  etc. 
4 


50 


DISEASES   OF   THE    KESPIRATOET   ORGANS. 


Morbid  Anatomy. — As  in  acute  broncliitis,  any  portion  of  the  bronchial 
and  tracheal  membrane  may  be  the  seat  of  the  inflammatory  action.  Thus 
it  may  be  limited  to  the  large  bronchi,  or  it  may  extend  into  the  capillary 
tubes.  Usually,  the  inflamed  membrane  has  a  slaty,  reddish  blue,  or  even 
a  violet  color.  In  the  more  chronic  cases,  its  tissue  is  frequently  hyper- 
trophied,  its  glands  are  enlarged  and  prominent,  and  their  ducts  so  in- 
creased in  size  that  their  mouths  are  readily  visible.  The  mucus  secreted 
may  be  in  transparent  gelatinous  masses  and  small  in  quantity,  it  may  be 
muco-purulent,  or  a  serous  fluid  may  be  exuded  in  great  abundance.     As  a 

rather  infrequent  occurrence,  the 
surface  of  the  membrane  |)resents  an 
uneven  appearance,  due  to  the  pres- 
ence of  little  villosities  covered  by 
normal  epithelium  ;  occasionally  fol- 
licular ulcerations  are  met  with. 
These  papillary  excrescences  and 
ulcerations  are  usually  arranged  lon- 
gitudinally. In  the  early  stage,  the 
other  coats  of  the  bronchial  tubes 
may  be  weak  or  yielding ;  later,  an 
increase  in  connective-tissue  takes 
place,  leading  to  thickening  and  in- 
duration. The  cartilages  are  some- 
times normal,  at  other  times  hyper- 
trophied,  and  at  times  calcified.  In 
the  posterior  wall  of  the  trachea  and 


e-.' 


Fig.  13. 


Transverse  Section  of  Bronchial  Wall  in  Chronic 
Catarrhal  Bronchitis. 


A.  Epithelium  covered  with  mucus  and  pus. 

B.  Internal  elastic  coat. 

C.  Muscular  layer-      On  the  right  an  erilarged  duct  is 

seen  piercing  the  last  two  coats. 

D.-Sufymucous  tissue  containing  hypertrophied  carti-    ,,       ,  ,  -,  .  ,.  »  , , 

lage,  increased  connective-tissue,    enlarged  glands    the  larger  bronchl,  Separation  01  the 

and  vessels,     x  250.  i        j^i  i         i         j.-  « 

muscular  nbres,  and  relaxation  oi 
the  bronchial  wall  occur,  with  a  protrusion  of  the  mucous  membrane 
through  fissures  in  its  middle  coat.  These  diverticuli  may  involve  a  large 
or  small  extent  of  the  posterior  bronchial  wall.  The  submucous  coat  shows 
increase  in  connective-tissue.  In  very  old  subjects  the  ultimate  bronchi 
may  be  changed  into  calcified  cylinders,  each  with  a  minute  canal  running 
ihrough  it. 

In  very  chronic  cases,  where  there  has  been  a  puriform  secretion  for  a 
long  time,  the  bronchial  mucous  membrane  not  infrequently  presents 
slight,  or  no  apparent  alteration.  The  results  of  chronic  bronchitis  are 
dilatation  and  stenosis  of  the  bronchial  tubes,  an  accumulation  of  secre- 
tion in  a  state  of  cheesy  degeneration  more  or  less  obstructing  their 
calibre,  pulmonary  emphysema,  and  induration  of  lung  tissue  adjacent 
to  the  inflamed  bronchi.  Ulcerations  of  the  bronchial  membrane  rarely 
occur ;  if  present  they  are  slight  and  superficial,  and  for  the  most  part 
are  found  in  the  bronchitis  which  accompanies  phthisis.  In  old  age 
deep  ulcers  may  be  formed,  and  fistulous  communications  may  be  estab- 
lished with  the  oesophagus,  aorta,  pleural  cavity,  large  blood-vessels,  pul- 
monary parenchyma,  or,  very  rarely,  externally.  In  tertiary  syphilis, 
(chronic  bronchitis  may  be  accompanied  by  gummy  tumors  of  the  mucous 


CHEONIC    CATARKHAL   BROJTCHITIS.  51 

membrane  of  the  trachea  and  primary  bronchi,  or  by  a  fibrous  induration 
which  leads  to  stenosis. 

Fetid  Bronchitis. — An  excessively  fetid  order  of  the  breath  and  of  the 
matter  expectorated  in  the  course  of  a  chronic  bronchitis,  may  find  no  ex- 
planation after  death,  except  decomposition  of  the  accumulated  bronchial 
secretion.  This  decomposition  usually  takes  place  in  bronchial  dilatations  ; 
it  may  arise  independently  of  any  bronchial  dilatation.  It  is  claimed  that 
germs,  usually  atmospheric,  enter,  and,  lodging  in  a  cavity,  cause  putres- 
cence. This  decomposition  of  the  secretion  may  exert  no  special  injurious 
influence,  or  it  may  give  rise  to  gangrene  of  the  bronchial  mucous  mem- 
brane, and  may  thus  involve  the  adjacent  lung  tissue,  causing  more  or  less 
extensive  gangrene  of  the  lungs.  About  the  tubes  the  characteristic 
changes  of  peribronchitis  are  nearly  always  found  ;  these  changes  are  best 
marked  at  the  periphery  of  the  lung.  The  changes  that  take  place  in  the 
small  bronchi,  in  that  form  of  bronchial  catarrh  which  accompanies 
phthisis,  will  be  considered  under  the  head  of  phthisis. 

Etiology. — The  most  interesting  part  of  the  history  of  chronic  catarrhal 
bronchitis  is  its  etiology.  When  primart/,  it  arises  almost  always  from  ex- 
ternal causes ;  such  as  exposure  to  cold  and  wet,  the  inhalation  of  dust  or 
unwholesome  air.  It  is  unquestionably  the  exception  for  chronic  bronchi- 
tis to  be  developed  from  exposure  to  what  are  termed  the  ordinary  causes 
of  ''taking  cold,"  without  some  special  predisposition,  such  as  long-contin- 
ued mechanical  irritation  of  the  bronchial  membrane,  constitutional  vice, 
or  some  previously  existing  organic  disease.  Acute  bronchitis  may  fre- 
quently be  the  result  of  some  temporary  exposure,  but  if  it  becomes  chronic, 
there  will  almost  invariably  be  found  to  exist  a  predisposing  cause.  Bron- 
chial irritation  may  exist,  perhaps  for  years,  as  the  result  of  some  mechan- 
ical irritation  (as  in  the  case  of  stone-cutters,  grain-heavers,  etc.),  and  not 
particularly  inconvenience  the  individual,  until  an  acute  catarrh  is  devel- 
oped from  exposure  ;  this  invariably  becomes  chronic,  and  sooner  or  later 
leads  to  the  develojament  of  broncho-pneumonia,  and  a  condition  called 
knife-grinders'  or  stone-cutters'  phthisis  follows. 

Secondary/  chronic  bronchitis,  or  that  which  arises  from  some  previously 
existing  acquired  or  congenital  dyscrasia,  is  of  more  frequent  occurrence. 
An  hereditary  tendency  to  gout  frequently  manifests  itself  in  a  form  of 
chronic  bronchitis.  Sometimes  in  the  same  individual  attacks  of  bronchitis 
and  gout  alternate.  In  some  instances  the  gouty  diathesis  only  produces  a 
strong  predisposition  to  bronchitis,  which  requires  for  its  development  some 
external  exciting  cause  much  slighter  than  would  produce  the  disease  in 
health  ;  in  other  instances,  there  is  for  a  long  time  a  slight  bronchial  ca- 
tarrh, which,  as  life  advances,  slowly  merges  into  chronic.  'Not  infre- 
quently chronic  bronchitis  occurs  in  connection  with  psoriasis  and  eczema, 
and  these  affections  alternate  one  with  the  other  ;  as  one  disappears  the  other 
manifests  itself  ;  under  such  circumstances  it  seems  evident  that  these  dif- 
ferent affections  are  manifestations  of  the  same  constitutional  vice.  Pul- 
monary emphysema  is  produced  in  many  instances  by  chronic  bronchitis  ; 
sometimes,  however,  it  occurs  independently  of  it,  and  then  it  is  a  strong 


53  DISEASES    OF    THE    EESPIEATORT    ORGANS. 

predisposing  cause  to  the  development  of  the  latter.  Disease  of  the  left 
side  of  the  heart  predisposes  to  bronchitis,  which  is  sub-acute  in  character 
and  chronic  in  duration.  Chronic  bronchitis  is  very  often  associated  with 
asthma.     Chronic  alcoholismus  is  one  of  its  frequent  causes. 

Symptoms. — The  symptoms  of  this  form  of  bronchitis  vary  with  the  con- 
stitutional and  local  causes  under  the  influence  of  which  it  is  developed. 
There  are,  however,  certain  prominent  characteristics  common  to  all  varie- 
ties, the  most  constant  of  which  are  cough  and  expectoration.  The  pecu- 
liarity of  the  cough,  and  the  quantity  and  quality  of  the  matter  expectorated, 
determine  to  a  great  extent  the  character  and  severity  of  the  bronchitis. 
In  some  cases  the  cough  is  slight,  the  expectoration  moderate  in  quantity, 
and  muco-purulent  in  character;  this  occurs  in  the  mildest  variety — a 
variety  which  comes  on  in  the  winter  and  disappears,  or  is  mitigated,  in 
summer.  After  a  time  it  becomes  permanent,  and  is  liable  to  exacerbations 
in  cold,  damp  weather.  It  is  the  simplest  form  of  chronic  bronchial 
catarrh.  In  another  class  of  cases  the  cough  is  violent  and  more  constant, 
severest  in  the  morning — the  expectoration  is  either  tenacious  and  scanty, 
or  thin,  semi-transparent  and  abundant ;  it  is  sometimes  streaked  with 
blood,  and  frequently  is  difScult  to  expectorate.  So  severe  is  the  cough  that 
vomiting  is  very  commonly  induced,  the  contents  of  the  stomach  and 
bronchi  being  simultaneously  expelled.  The  matter  expectorated  varies  in 
color  from  an  ashy-yellow  to  a  deep  green  ;  it  is  slightly  aerated,  and  not 
infrequently  sinks  in  water.  Its  odor  varies  :  sometimes  it  is  sweet  and 
nauseous  ;  at  other  times  it  has  a  fetor  similar  to  that  of  gangrene  of  the 
lungs.  The  microscope  shows  it  to  be  composed  of  granular  matter,  broken 
down  epithelial  and  pus-cells,  and  sometimes  blood-globules  and  small  fila- 
ments of  bronchial  tissue.  Some  cases  of  this  form  of  bronchitis  are  at- 
tended by  loss  of  flesh,  fever,  and  night  sweats.  It  occurs  most  frequently 
in  strumous,  broken-down  subjects,  especially  those  given  to  alcoholic 
excess.  More  or  less  extensive  bronchial  dilatations  are  usually  present  in 
this  variety  of  bronchitis. 

Again,  there  is  a  class  of  cases  in  which  the  cough  is  exceedingly 
troublesome  and  paroxysmal  in  character--the  expectoration  is  scanty, 
consisting  of  small,  rounded,  semi-transparent  masses  of  tough  mucus. 
This  variety  is  met  with  almost  exclusively  in  connection  with  pul- 
monary emphysema,  gout,  spasmodic  asthma  and  irritant  inhalations, 
and  has  received  the  name  of  "dry  catarrh."  There  is  also  a  variety 
of  chronic  bronchitis,  not  infrequently  met  with  in  old  people,  especially 
in  connection  with  heart  disease,  in  which  the  cough  is  paroxysmal,  and 
often  violent,  and  the  paroxysms  are  attended  by  a  peculiar  flux  from  the 
bronchi.  The  expectoration  often  amounts  to  four  or  five  pints  in  twenty- 
four  hours,  and  is  either  watery  and  transparent,  or  gelatinous  and  ropy, 
resembling  an  emulsion  of  white-of-egg  and  water.  The  patient  often  finds 
great  relief  after  a  paroxysm  of  coughing  and  expectoration.  In  some  cases 
this  variety  of  bronchitis  is  accompanied  by  loss  of  strength  and  flesh  ;  it 
has  received  the  name  bronchorrhoea.  In  some  cases  of  simple  chronic 
bronchitis  the  sputa  are  moulded  in  the  form  of  the  smaller  tubes.     Blood 


CHROKIC    CATARRHAL   BROKCHITIS.  53 

in  the  sputa  indicates  superficial  ulceration.  A  brownish  fluid  expectora- 
tion is  sometimes  present ;  and  in  this  are  fatty  granules  and  crystals  of 
cholesterin  and  margarin.  In  all  these  varieties  there  is  dyspncea  and 
labored  respiration  —  the  respiration  is  much  more  accelerated  in  other 
chronic  pulmonary  affections  than  in  bronchitis,  but  it  is  never  so  labored. 
The  pulse  in  a  purely  chronic  bronchitis  does  not  exceed  the  normal  fre- 
quency, and  on  this  account  it  may  readily  be  distinguished  from  pneu- 
monia and  phthisis  ;  besides,  in  chronic  bronchitis  the  temperature  is  rarely 
much  above  the  normal,  excepting  in  those  cases  which  are  accompanied  by 
a  fetid  expectoration.  A  little  uneasiness  or  soreness  is  often  felt  behind 
the  sternum,  which  is  increased  by  violent  coughing  ;  but  pain  in  the  side 
is  rarely  present.  Individuals  with  any  form  of  chronic  bronchitis  are  un- 
able to  sustain  prolonged  physical  exertion  without  great  exhaustion,  and 
they  are  markedly  affected  by  atmospheric  changes. 

Physical  Signs. — These  are  very  nearly  the  same  as  in  acute  bronchitis. 

Inspection  shows  labored  respiration  with  diminished  expansion  on  inspi- 
ration.    The  chest  may  appear  more  convex  than  normal. 

Palpation. — Vocal  fremitus  varies  :  if  the  bronchial  walls  of  the  larger 
tubes  are  thickened,  it  is  exaggerated  ;  if  the  tubes  are  obstructed,  or  much 
dilated,  it  is  diminished  or  absent.  In  the  simple  forms  of  chronic  bron- 
chitis the  vocal  fremitus  is  normal. 

The  percussion  sound  rarely  differs  from  that  in  health  :  if  the  accumu- 
lation of  a  thick  secretion  gives  rise  to  obstruction  in  some  of  the  bronchi, 
then  localized  temporary  dulness  on  percussion  is  the  result. 

On  auscultation,  the  vesicular  murmur  is  more  or  less  deficient  over  the 
whole  chest,  and  the  respiratory  sound  is  coarse,  loud,  and  harsh,  with 
prolonged  expiration.  After  free  expectoration,  it  will  often  be  audible  at 
points  where  it  had  been  inaudible  a  moment  before  ;  it  is  accompanied, 
and  sometimes  entirely  masked,  by  rdles  of  every  variety,  but  chiefly  sono- 
rous and  sibilant.  Large  and  small  mucous  rales  are  present  in  those  cases 
in  which  there  is  abundant  liquid  secretion.  These  rales  are  constantly 
varying  in  size  and  character — at  times  they  may  be  altogether  absent; 
they  are  altered  in  character  and  position  by  coughing  and  by  full  inspira- 
tion. Vocal  resonance  may  be  normal,  diminished,  or  slightly  exaggerated. 
Large  and  persistent  gurgles  in  the  lower  portion  of  the  lung  suggest  the 
existence  of  bronchiectasis. 

Differential  Diagnosis. — The  diagnosis  of  chronic  bronchitis  is  rarely  at- 
tended with  difficulty,  except  in  connection  with  pulmonary  phthisis.  It 
may  be  distinguished  from  pleuritic  effusions,  not  only  by  the  cough  and 
expectoration  which  attend  it,  but  by  the  continuance  of  vocal  fremitus, 
and  the  existence  of  resonance  on  percussion.  From  pneumonic  consolida- 
tion, by  the  absence  of  bronchial  breathing,  of  rusty  expectoration, 
accelerated  breathing,  and  high  pulse-rate  and  temperature.  In  those 
cases  of  chronic  bronchitis  in  which  the  general  health  suffers,  ema- 
ciation takes  place  and  bronchial  dilatation  occurs.  The  bronchitis 
sometimes  so  closely  simulates  phthisis  in  its  rational  and  physical  signs, 
that  the   differential   diagnosis  is  exceedingly   difficult ;    the  points  of 


54  DISEASES   OF   THE   EESPIRATOEY   ORGAN'S. 

difference  will  be  more  fully  considered  under  the  head  of  pulmonary 
phthisis. 

Prognosis. — This  disease  rarely,  if  ever,  directly  destroys  life  ;  but  when 
it  occurs  in  the  old  and  feeble,  it  is  always  attended  with  danger,  on  ac- 
count of  the  frequent  occurrence  of  acute  attacks  involving  the  small  bron- 
chi. Any  pulmonary  affection  associated  with  chronic  bronchitis  renders 
the  condition  of  the  patient  more  serious,  on  account  of  the  liability  to 
bronchial  obstruction  from  the  accumulation  of  the  secretion  in  the  bron- 
chial tubes.  It  is  very  apt  to  lead  to  the  development  of  pulmonary  em- 
physema, pulmonary  collapse,  dilated  bronchi,  and  fibrous  phthisis.  It  is 
rarely  recovered  from  when  it  occurs  in  those  past  middle  life.  Hepatic 
congestion,  abdominal  dropsy,  and  general  anasarca  are  frequent  attend- 
ants of  chronic  bronchitis.  Seventy-five  per  cent,  of  such  cases  are  compli- 
cated by  the  presence  of  small,  granular  kidney. 

Treatment. — The  one  important  fact  to  be  borne  in  mind  in  the  treat- 
ment of  this  affection  is,  that  it  rarely  occurs  as  a  primary  disease,  but  is 
due  to  some  constitutional  disorder.  The  patient  must  be  removed  from 
every  possible  source  of  bronchial  irritation,  and  be  protected  from  expos- 
ure to  sudden  changes  of  temperature ;  flannels  should  be  worn  next  the 
skin,  and  if  a  suitable  climate  cannot  be  obtained,  the  patient  must  keep 
in-doors  during  bad  weather,  in  well -ventilated  apartments,  the  tempera- 
ture of  which  should  range  from  65°  to  70°  F.  Night  air  and  cold 
winds  must  be  avoided.  The  region  best  adapted  to  patients  affected  with 
any  of  the  forms  of  bronchitis,  is  one  with  a  moderately  warm,  dry  atmos- 
phere, protected  from  cold  winds,  and  of  moderately  high  altitude.  In  cases 
that  are  attended  by  emaciation,  a  long  sea-voy  age  is  often  of  the  greatest 
benefit.  The  diet  at  all  times  should  be  most  nutritious.  As  regards  the 
use  of  stimulants,  no  definite  statement  can  be  made,  but,  as  a  rule,  mod- 
erate stimulation  is  of  service. 

In  no  disease  is  a  careful  study  of  each  individual  case  more  important. 
The  immediate  and  remote  cause  of  the  affection  must,  if  possible,  be 
determined.  If  the  bronchitis  is  the  result  of  an  irritant  inhalation, 
removal  from  exposure  to  this  is  of  the  greatest  importance.  If  cardiac 
disease  exist,  which  keeps  up  the  bronchial  affection  by  inducing  hyper- 
semia  of  the  mucous  membrane,  the  treatment  should  be  directed  to 
the  cardiac  affection,  and,  if  possible,  the  heart's  action  regulated.  If 
a  gouty  or  rheumatic  diathesis  exist,  the  use  of  colchicum  and  alkalies 
is  indicated.  Steam  inhalations  of  hyoscyamus,  conium,  or  stramonium 
are  often  of  great  service  in  gouty  bronchitis.  When  pulmonary  emphy- 
sema is  associated  with,  or  is  the  apparent  cause  of  the  bronchitis,  the 
internal  administration  of  iodide  of  potassium  will  be  followed  by  most 
marked  relief.  Dilute  nitric  acid,  and  the  ethereal  extract  of  the  acetate 
of  iron  are  beneficial.  In  general  anasmia  accompanying  bronchitis,  prepa- 
rations of  iron  are  indicated ;  in  fact,  in  the  majority  of  cases  of  chronic 
bronchitis,  a  general  tonic  plan  of  treatment  is  attended  by  the  most 
marked  benefit.  Quinine,  mineral  acids,  bitter  vegetable  infusions  com- 
bined with  iron,  often  prove  of  great  service.     Bronchial  catarrh,  alternat- 


BRONCHIECTASIS.  55 

Ing  with  chronic  skin  affections,  yields   most  readily  to  preparations  of 
arsenic  and  sulphate  of  zinc. 

The  treatment  of  the  immediate  symptoms  must  depend  upon  the  quan- 
tity of  the  expectoration,  the  degree  of  difficulty  which  attends  its  dis- 
charge, and  the  presence  or  absence  of  any  sj)asmodic  action  of  tlie 
bronchial  tubes.  When  the  bronchial  secretions  are  excessive  in  quantity, 
steam  inhalations  of  tar,  creosote,  copaiba,  and  naphtha  are  often  of 
great  service  in  limiting  their  formation ;  the  vapor  of  iodine,  muriate 
of  ammonia,  and  the  different  balsams  are  also  of  service  in  accomplish- 
ing the  same  purpose.  These  remedies  may  be  given  internally  at  the 
same  time.  When  the  power  of  expectoration  is  deficient,  owing  to  the 
adhesive  character  of  the  expectoration,  stimulating  expectorants  are 
indicated,  such  as  senega,  serpentaria,  camphor,  tincture  of  benzoin, 
combined  with  such  alkalies  as  carbonate  of  j)otash  and  soda.  In  those 
cases  where  the  bronchial  membrane  is  extremely  irritable,  the  secretions 
scanty,  and  the  cough  attended  by  violent  paroxysms,  narcotics  and  seda- 
tives should  be  administered  in  full  doses ;  opium,  hydrocyanic  acid,  hy- 
oscyamus,  belladonna,  and  conium  are  the  most  trustworthy  agents  of  this 
class.  Where  there  is  much  spasm  of  the  bronchi,  shown  by  the  breath- 
ing and  cough,  a  few  drops  of  ether  or  chloroform  may  be  inhaled  ;  when 
the  tendency  to  the  spasm  is  great,  the  narcotics  and  sedatives  already  re- 
ferred to  should  be  administered.  Tincture  of  cannabis  indica  acts  well 
in  some  of  those  cases.  In  all  varieties  of  chronic  bronchitis,  localized 
counter- irritation  over  the  seat  of  the  most  extensive  bronchial  changes 
may  sometimes  be  employed  with  benefit,  such  as  may  be  produced  by  dry 
cups,  sinapisms,  blisters,  croton-oil,  and  turpentine.  It  is  never  necessary 
or  desirable  to  abstract  blood,  either  locally  or  generally.  Occasionally, 
emetics  may  be  employed  with  benefit,  when  the  bronchial  secretion  accu- 
mulates in  the  larger  tubes  and  cannot  be  expectorated.  The  close  con- 
nection of  chronic  bronchitis  with  dilatation  of  the  bronchi  renders 
it  necessary  to  consider  briefly  some  of  the  prominent  features  of  the 
latter. 

BRONCHIECTASIS. 

Bronchiectasis,  or  dilatation  of  the  bronchial  tubes,  is  closely  connected 
with  chronic  troncliitis. ' 

Morbid  Anatomy. — It  may  be  general  or  partial.  When  partial,  it  is 
called  saccular  or  ampullar.  The  dilatation  may  be  cylindrical,  fusiform, 
or  sacculated.  When  dilatations  are  connected  together  by  tubes  of  norfual 
calibre,  the  condition  is  distinguished  as  the  "  monil if orm"  di\sita.tion, of 
Cruveilhier.  In  bronchiectatic  cavities,  the  result  of  chronic  bronchitis, 
the  walls  are  hypertrophied,  the  mucous  membrane  is  thickened,  and  may 
be  covered  over  with  small  papillary  outgrowths.  The  submucous  tissue 
is  hypertrophied  and  loses  to  a  great  extent  its  elastic  fibres,  and  the  mu- 

'  First  described  by  Laennec. 


DISEASES    OF    THE    RESPIRATORY    ORGANS. 


Fig.  13. 


Diagram  illustrating  forms  of  dilatation 
of  the  Bronchi. 

A.  " Moniliform"  dilatation— the  tube  ii     i      ,         ■,^ 

between  the  enlargements  being  of  may  result;  Dut  neither  gangrene   nor 

vwmal size.  ..i       i  i  •    i       ti    j    i- 

B.  •■' saccifwrn"  diiaiation-severai of  occurs    With    bronchial    dilatation    as 
c! FmmaampZc^^^y'^l^^^^        as    colkpse   and   fibroid    tliickening. 

IM  conneciiug  tube. 


cons  glands  are  atrophied.  The  muscular  fibres  are  often  dissociated.' 
Bronchiectasis  is  rarely  met  with  independent  of  some  stenosis ;  we  often 
find  alternate  stenosis  and  dilatation.  On  the  tracheal  side  these  bronchial 
dilatations  usually  communicate  with  a  slightly  enlarged  bronchial  tube; 

but,  on  the  peripheral  side,  the  continuity 
of  the  tube  is  almost  or  entirely  lost  by 
narrowing  or  actual  obliteration.  Cystic 
cavities  may  be  found ;  these  are  isolated 
bronchial  dilatations,  whose  supplying  bron- 
chus has  become  permanently  obstructed. 
Pus,  muco-pus,  crystals  of  margarin,  fibres 
of  lung-tissue,  and  even  chalky  debris 
have  been  found  in  these  cavities.  The 
lung  tissue  close  to  the  bronchiectases  is 
altered  in  various  ways  ;  there  may  be  fibroid 
induration,  emphysema,  lobular  pneumonia, 
and  atrophy.  The  contents  of  a  bronchiec- 
tatic  cavity  may  decompose  and,  ulceration 
occurring,  gangrene   or   abscess   of  the  lung 

abscess 
often 
and   fibroid    thickening.       The 
small  bronchi,  and  the  bronchi  in  the  lower 
lobes,  are  the  parts  most  often  involved  in  bronchiectasis. 

Etiology. — Chronic  bronchitis  is  the  most  frequent  cause.  Atelectasis, 
lobular  collapse,  fibroid  induration,  and  old  pleuritic  thickenings  also 
cause  it.  Phthisical  processes  are  nearly  always  accompanied  by  more  or 
less  bronchial  dilatation. 

Symptoms. — Many  of  the  symptoms  are  referred  to  under  the  head  of 
^^ fetid  bro7ic1iitis.'"  An  abundant,  fetid,  purulent,  and  often  nummular 
expectoration,  frequent  and  paroxysmal  cough,  a  very  fetid  breath,  some 
emaciation,  occasional  profuse  haemoptysis,  and  not  infrequently  night 
sweats,  associated  with  the  symptoms  of  chronic  bronchitis,  are  the  character- 
istics of  bronchiectasis.  The  pulse  is  accelerated,  and  there  is  hectic  fever 
during  its  advanced  stage. 

Physical  Signs. — Insijection  shows  retraction,  prolonged  expiratory  motion, 
with  diminished  expansion  on  the  afl'ected  side,  or  of  the  whole  of  the  chest 
if  both  sides  are  involved. 

Palpation, — There  is  increased  vocal  fremitus.  , 

Percussion  elicits  dulness  if  the  dilatation  is  filled,  or  if  it  is  sur- 
rounded by  consolidated  lung.  There  will  be  extra  resonance  if  the  dilata- 
tion is  empty  and  superficial,  and  there  may  be  a  cracked-pot  resonance  if 
the  dilatation  is  very  large,  surrounded  by  fibrous  tissue, and  near  the  surface. 
Auscultation. — The  respiratory  sounds  maybe  harsh,  blowing,  bronchial, 
cavernous,  or  amphoric,  according  to  the  seat,  size,  and  condition  of  the 
dilatation.     Large  and  small  gurgles  are  often  heard. 


'  In  children  these  bronchiectases  not  infrequently  disappear  when  the  bronchitis  which  caused  them 
disappears. 


CROUPOUS   BROKCHITIS.  57 

Its  differential  diagnosis  will  be  considered  in  connection  with  phthisis. 
This  condition  cannot  be  cured.  It  may  exist  for  many  years  without  ma- 
terially impairing  the  general  health.  Death  may  be  caused  by  gangrene, 
abscess,  exhaustion,  or  some  complication. 

Treatment. — Its  treatment  is  that  of  chronic  catarrhal  bronchitis  {q.  v). 
It  is  benefited  by  the  daily  use  of  antiseptic  sprays  of  creosote,  carbolic 
acid,  etc.;  by  a  residence  in  a  moderately  high,  warm  and  dry  locality;  by 
a  carefully  regulated,  nourishing  diet,  and  a  proper  hygiene  ;  and  in  most 
instances  by  tonics  in  addition  to  cod-liver  oil. 

CROUPOUS    BRONCHITIS. 

Under  this  head  will  be  considered  croupous,  pseudo-membranous,  or 
plastic  inflammation  of  the  bronchial  mucous  membrane,  as  it  occurs  inde- 
pendently of  laryngeal  croup  on  the  one  hand,  and  of  croupous  pneumonia 
on  the  other,  or  of  that  form  of  catarrhal  bronchitis  during  the  course  of 
which  a  few  membranous  flakes  are  expectorated.  This  disease  may  pursue 
either  an  acute  or  chronic  course.  Both  forms  are  rare  ;  the  acute  is  the 
more  infrequent. 

Morbid  Anatomy. — It  differs  from  catarrhal  bronchitis  in  the  character  of 
the  exudation,  as  plastic  material  is  poured  out  into  the  tubes  in  the  form 
of  casts,  which  are  either  solid  or  hollow,  according  as  the  small  or  large 
tubes  are  affected.  In  the  chronic  form,  the  membranous  exudation  occurs 
over  a  circumscribed  portion  of  the  bronchial  membrane  ;  in  the  acute,  it 
is  distributed  over  a  greater  portion  of  the  bronchi.  The  membrane  may 
be  firmly  adherent  or  loosely  attached  to  the  mucous  surface.  These  casts 
are  of  a  whitish  color,  sometimes  dotted  over  with  blood-spots.  Microscop- 
ically, they  consist  of  fibrillated  fibrin,  abundant  granular  matter,  oil- 
globules,  exudation  corpuscles,  and  fusiform  ovoid  cells.  They  always 
consist  of  concentric  laminse.  Acetic  acid  causes  them  to  swell.  In  some 
cases  no  membrane  exists  ;  the  bronchial  membrane  is  pale  and  congested. 

Etiology. — There  is  no  known  special  exciting  or  predisposing  cause  to  this 
disease — it  is  supposed  to  be  due  to  some  diathetic  state.  It  is  most  fre- 
quently met  with  in  young  adults,  and  occurs  more  frequently  in  females  than 
in  males,  and  in  those  of  feeble,  delicate  constitutions,  rather  than  in  those 
who  are  strong  and  healthy.  It  has  been  seen  associated  with  asthma  and 
emphysema.     The  strumous  and  phthisical  are  markedly  predisposed  to  it. 

Symptoms. — The  acute  form  is  usually  preceded  by  catarrhal  symptoms 
of  short  duration.  It  is  attended  by  fever,  by  dyspnoea  (often  severe),  by 
a  dry,  hoarse,  ringing  cough  (not  as  stridulous  as  in  croup),  and  by  a  sense 
of  constriction  and  oppression  across  the  chest.  After  severe  paroxysms  of 
coughing,  either  fragments  of  membrane,  or  membranous  casts  or  cylin- 
ders are  expectorated,  usually  in  small  masses.  The  membranous  expecto- 
ration, in  rare  instances,  is  wanting,  and  occasionally  not  even  cough  is 
present.  There  are  no  symptoms  of  laryngeal  obstruction.  When  the  dis- 
ease progresses  toward  a  fatal  termination,  the  dyspnoea  rapidly  increases 
in  severity,  and  is  finally  superseded  by  those  phenomena  which  precede 
death  by  asjihyxia. 


58 


DISEASES    OF    THE    EESPIKATORT    ORGAlSrS. 


TJie  cJirofiic  form  is  generally  preceded  by  catarrhal  bronchitis,  which 
sometimes  has  lasted  for  a  long  time;  severe  haemoptysis  may  have  preceded 
its  development.  Not  infrequently,  in  pulmonary  phthisis,  where  haemop- 
tysis has  occurred,  casts  of  bronchial  tubes  are  expectorated,  which  are 
nothing  more  than  decolorized  blood-clots.  The  history  of  the  chronic 
form  of  plastic  bronchitis  is  rarely  a  continuous  one,  but  is  made  up  of  in- 
tervals of  health  and  paroxysms  of  disease  ;  during  the  latter,  expectora- 
tion of  membrane  in  fragments  or  casts  occurs.  Their  removal  is  often  pre- 
ceded by  fits  of  severe  coughing,  and  by  paroxysms 
of  dyspnoea  of  variable  intensity,  lasting  usually  a 
few  hours,  sometimes  a  day  or  more ;  at  other 
times,  simple  sneezing  effects  their  removal.  Gen- 
erally, along  with  the  membrane,  there  is  catarrhal 
expectoration,  in  which  small  portions  of  mem- 
brane may  be  hidden.  In  about  one-third  of  the 
cases,  haemoptysis  (generally  slight)  has  either  pre- 
ceded or  accompanied  the  membranous  expectora- 
tion. The  membranous  exudation,  if  it  comes  from 
the  large  bronchi,  is  in  the  form  of  casts  ;  if  from 
the  small,  it  is  in  the  form  of  cylinders.  Occasion- 
ally, there  is  mucus  or  blood  in  the  interior  of  the 
casts,  while  streaks  of  blood  are  often  present  on 
the  exterior.  The  casts  are  of  variable  thickness 
and  length — usually  two  or  three  inches  long, 
laminated,  and  of  a  whitish  or  grayish  color. 
Microscopically,  they  are  composed  of  a  structureless  mass,  more  or 
less  fibrous  in  character,  in  which  cells  are  imbedded,  more  particularly 
pus  cells.  During  the  interval  between  the  paroxysms,  in  uncompli- 
cated plastic  bronchitis,  the  general  health  is  good  and  fever  is  not  present. 
Physical  Signs. — These  depend  upon  the  obstruction  produced  by  the 
membrane,  sometimes  upon  the  vibration  of  a  portion  of  it,  and  on  coinci- 
dent catarrh.  When  the  bronchial  tubes  are  obstructed,  there  is  feebleness 
or  absence  of  the  respiratory  murmur, — in  the  chronic  form,  over  a  limited 
portion  of  the  chest,  in  the  acute,  over  a  large  extent.  At  the  same  time, 
the  percussion  note  may  be  normal,  extra  resonant  or  dull  ;  the  latter  ex- 
isting when  collapse  of  the  lung  has  taken  place,  disappearing,  it  may  be, 
immediately  after  membranous  expectoration,  while  the  respiratory  mur- 
mur regains  its  normal  character,  thus  masking  the  exact  seat  of  the  dis- 
ease. Flapping  and  rubbing  sounds  have  been  described  as  a  result  of  vi- 
bration of  the  membrane.  Dry  and  moist  rales  are  also  usually  present,  due 
either  to  the  narrowing  of  the  tubes,  or  to  coincident  bronchial  catarrh. 

Diiferential  Diagnosis. — This  form  of  bronchitis  may  be  mistaken  for  acute- 
catarrhal  bronchitis,  pjieumonia,  or  pleurisy.  The  history  of  the  case,  the 
character  of  the  paroxysm,  the  membranous  expectoration,  and  the  accom- 
panying physical  signs,  will  generally  enable  one  to  make  the  diagnosis  of 
plastic  bronchitis  ;  without  the  membranous  expectoration,  howe\"er,  the  dif- 
erential  diagnosis  between  acute  croupous  and  acute  catarrhal  bronchitis 


Fig.  14. 

Mould  of  bronchial  twigs 
expectorated  in  a  case  of 
Plastic  Bronchitis.  One- 
half  the  original  size. 


BRONCHIAL    ASTHMA.  59 

cannot  be  made.  The  absence  of  the  symptoms  which  usually  attend  pneu- 
monia and  pleurisy  serves  to  exclude  them  from  the  question  of  diagnosis. 

Prognosis. — With  the  acute  form,  more  than  one-half  die  ;  with  the 
chronic  form,  if  death  occurs,  it  is  due  to  some  complication  ;  so  that,  in 
uncomplicated  cases  of  chronic  plastic  bronchitis  the  prognosis  as  re- 
gards life  is  good  ;  but  the  disease,  having  once  occurred,  it  is  very  apt  to 
return.  The  duration  of  the  disease  varies.  In  the  fatal  cases,  when  the 
disease  is  acute,  it  lasts  from  three  to  ten  days  ;  in  those  cases  that  recover, 
it  lasts  from  ten  to  fourteen  days.  In  the  chronic  form,  the  paroxysms 
usually  last  ten  or  twelve  days,  and  recur,  at  longer  or  shorter  intervals,  for 
months  or  years.  Complete  recovery  is  rare.  Croupous  bronchitis  is  very 
likely  to  lead  to  pneumonia  and  pulmonary  phthisis. 

Treatment. — The  acute  form  is  to  be  treated  the  same  as  croupous  laryn- 
gitis. In  the  chronic  form,  during  the  paroxysm,  alkaline  steam  inhala- 
tions should  be  resorted  to,  with  the  hope  of  removing  the  membrane  as 
quickly  as  possible.  The  patient  should  be  kept  in  a  warm,  equable 
temperature.  Durmg  the  interval,  the  general  system  should  be  invigorat- 
ed in  every  possible  way,  and  all  exposure  to  the  causes  of  bronchial  irri- 
tation should  be  avoided.  The  internal  administration  of  iodide  of  potas- 
sium has  been  highly  recommended  ;  quinine,  iron,  and  cod-liver  oil  are 
often  called  for.  If  the  paroxysms  continue  to  recur,  a  change  to  a  warm 
climate,  or  a  long  sea  voyage  must  be  tried.  There  is  no  known  remedy  o^ 
plan  of  treatment  which  promises  a  cure  in  this  disease. 

BEONCHIAL   ASTHMA. 

This  is  a  spasmodic  affection  of  the  bronchial  tubes,  which  gives  rise  to 
dyspnoea  of  a  paroxysmal  character.  The  spasmodic  contractions  may  be 
regarded  as  due  to  a  neurosis  loliicli  depends  upon  the  existence  of  a  peculiar 
diathesis.  Some  muscular  spasm  or  contraction  of  the  circular  muscular 
fibres  of  the  bronchial  tubes  is  the  essential  element  of  the  asthmatic  parox- 
ysm ;  and  the  consequent  narrowing  of  the  tubes  is  a  necessary  mechanical 
result.  Bronchial  catarrh,  when  present,  may  precede  the  paroxysm,  or  it 
may  not  come  on  until  its  close.  Although  bronchitis  plays  an  important 
part  in  the  development  of  asthma,  it  only  acts  as  an  exciting  cause,  as  there 
must  exist  a  special  neurotic  condition,  without  which  the  paroxysm  would 
not  occur. 

Etiology. — Unquestionably,  the  primary  cause  of  asthma  is  some  consti- 
tutional idiosyncrasy,  which  is  frequently  hereditary.  Heredity  is  traced 
in  about  forty  per  cent.  It  is  a  diathetic  disease,  and,  like  all  such  dis- 
eases, may  be  readily  transmitted  from  parent  to  offspring.  It  is  believed 
by  some  to  be  connected  with  a  gouty  or  rheumatic  diathesis.  No  period 
of  life  is  exempt  from  it ;  I  have  seen  a  well-marked  paroxysm  of  asthma 
in  an  infant  six  weeks  old,  born  of  an  asthmatic  mother. 

The  exciting  causes  of  the  asthmatic  paroxysms  may  be  grouped  into 
three  classes : 

First. — Those  cases  in  which  the  bronchial  spasm  is  produced  by  some 


60  DISEASES    OF   THE    RESPIRATORY    ORGAI^TS. 

material  respired  which  acts  directly  on  the  bronchial  mucous  membrane. 
In  this  class  are  included  all  those  cases  of  asthma  in  which  the  paroxysms 
are  excited  by  irritating  inhalations,  such  as  ipecacuanha  powder,  many 
chemical  vapors,  smoke,  dust,  fog,  emanations  from  newly  mown  hay, 
stables,  roses,  sulphur  matches,  burning  sealing-wax,  certain  atmos- 
pheric conditions,  and  the  emanations  from  certain  animals,  cats,  horses, 
etc.,  etc.  A  pure  mountain  air  excites  it  in  some,  and  relieves  it  in  others. 
Asthmatics  present  remarkable  peculiarities  as  to  the  conditions  of  atmos- 
phere which  suit  them  best.  Second. — Those  cases  which  are  of  more  dis- 
tinct reflex  origin.  In  this  class  are  included  those  in  which  the  asthmatic 
paroxysms  follow  errors  in  diet,  an  overloaded  rectum,  uterine  irritation, 
the  sudden  application  of  cold  to  the  surface,  the  irritation  of  an  enlarged 
prostate  gland,  or  of  hemorrhoidal  tumors.  Third. — Those  cases  which 
occur  as  complications,  or  in  connection  with  bronchitis,  heart  disease,  or 
emphysema,  and  are  most  likely  to  occur  after  fatigue  and  physical  exer- 
tion.    Bronchial  catarrh  is  one  of  its  most  frequent  causes. 

Each  individual  subject  to  asthma  is  susceptible  only  to  his  own  peculiar 
exciting  cause.  The  retrocession  of  gout  and  rheumatism,  syphilis,  renal 
diseases,  disappearance  of  chronic  skin  eruptions,  the  stoppage  of  an  habit- 
ual discharge,  or  the  healing  of  old  ulcers  may  be  followed  by  asthmatic 
paroxysms.  Certain  organic  diseases  of  the  brain  induce  it.  Angina,  neu- 
ralgia, gastralgia  and  asthma  often  alternate.  That  form  of  asthma  termed 
hay  asthma,  which  is  produced  by  emanations  from  newly  mown  hay,  oi 
other  vegetable  emanations,  is  always  preceded  or  accompanied  by  coryza 
and  bronchitis  ;  persons  may  have  the  coryza  and  bronchitis  for  years  with- 
out having  the  asthmatic  paroxysm,  yet  the  paroxysms  are  certain  to  come 
sooner  or  later,  and  differ  in  no  respect  from  other  asthmatic  paroxysms. 

Symptoms. — An  attack  of  asthma  may  or  may  not  be  preceded  by  precur- 
sory symptoms  ;  the  majority  of  those  suffering  from  asthma  know  when 
the  attack  is  coming  on,  by  some  peculiar  symptom  which  they  alone  rec- 
ognize. There  may  be  languor,  drowsiness,  depression  of  spirits,  or  tha 
opposite  condition,  abnormal  buoyancy  of  spirits.  Often  a  large  amount 
of  ''hysterical "  urine  is  passed  before  the  attack,  or  there  may  be  wakeful- 
ness, headache,  itching  of  the  chin,  etc.  Ordinarily,  the  individual  goes 
"to  bed  as  well  as  usual,  and  quietly  falls  asleep  ;  after  an  hour  or  two,  while 
he  is  still  asleep,  the  characteristic  wheezing  commences,  and  soon  he  is 
awakened  by  a  most  distressing  attack  of  dyspnoea.  He  feels  as  if  his  chest 
were  compressed,  and  he  were  about  to  be  suffocated ;  sits  up  in  bed  and  rests 
his  elbows  on  his  knees,  and  with  fixed  head,  elevated  shoulders  and  mouth 
open,  labors  for  breath.  There  may  be  immoderate  sneezing,  attended  by 
running  at  the  nose.  There  may  be  flatulent  distention  of  the  abdomen. 
His  face  becomes  red,  turgid  or  livid,  his  eyes  prominent,  his  surface  cov- 
ered with  perspiration  ;  he  springs  out  of  bed,  and  hastens  to  an  open  win- 
dow in  search  of  air ;  respiration  is  noisy  and  wheezing,  the  inspirations 
are  short  and  jerking,  while  the  expirations  are  prolonged,  and  terminate 
with  a  sudden  effort  at  expulsion.  The  number  of  respirations  varies  from 
sixteen  to  thirty  a  minute.     All  the  auxiliary  muscles  of  respiration  are 


BEONCHIAL   ASTHMA.  Ql 

brought  into  play  ;  yet  the  chest  remains  almost  motionless.  The  laboi 
may  be  so  great  that  the  patient  is  in  a  dripping  perspiration.  The  mouth 
is  wide  open,  the  nostrils  are  dilated,  the  cervical  and  facial  veins  are  tur- 
gid. If  the  bronchial  spasm  is  prolonged,  the  surface  temperature  falls  be- 
low the  normal,  the  extremities  become  cold,  blue  and  shrunken,  and  the 
patient  seems  to  be  dying.  The  pulse  during  the  paroxysm  is  small,  rapid, 
thready,  and  feeble  in  proportion  to  the  intensity  of  the  dysj^noea.  The 
duration  of  the  paroxysm  varies  ;  at  one  time  it  lasts  only  a  few  minutes, 
at  another  an  hour  or  two,  in  rare  instances  it  may  continue  two  or  three 
days  without  intermission. 

As  the  paroxysm  passes  off,  the  patient  begins  to  cough  and  expecto- 
rate ;  in  some  patients  the  expectoration  consists  of  a  few  small,  rounded 
masses  like  pearls  of  mucus,  and  contains  neither  pus  nor  watery  con- 
stituents ;  in  others  it  is  profuse  and  watery.  The  expectoration  occurs 
after  the  bronchial  spasm  has  ceased  ;  it  does  not  cause  its  cessation  ; 
and  even  when  the  attack  begins  "dry,"  there  is  some  expectoration  at 
the  end  of  the  paroxysm.  Occasionally  in  severe  attacks,  there  are 
blood-streaks  ]n  the  sputa,  and  sometimes  quite  profuse  hemorrhage  occurs. 
The  paroxysm  /ecurs  after  intervals  of  varying  length ;  some  experience 
an  attack  only  annually,  others  monthly,  and  others  only  when  sub- 
jected to  their  own  peculiar  exciting  cause.  Less  violent  attacks  may 
last  five  to  six  days.  During  the  interval,  if  the  asthma  is  not  due  to  any 
organic  disease,  the  condition  of  the  asthmatic  subject  varies ;  some  are 
perfectly  well ;  others  constantly  have  a  sense  of  thoracic  constriction, 
which  renders  the  breathing  somewhat  labored,  especially  during  active 
exercise.  Some  suffer  severely  from  a  bronchial  or  nasal  catarrh.  When 
the  catarrhal  element  predominates,  the  asthmatic  paroxysms  are  excited 
by  slight  exposure.  The  longer  the  attack,  the  less  abrupt  its  cessation 
and  more  profuse  the  sputa.  Immediately  after  a  paroxysm,  there  is  usu- 
ally a  feeling  of  exhaustion,  aching  and  ''soreness,"  which  passes  off  in  a 
few  hours,  and  the  individual  experiences  a  sense  of  relief,  and  has  for  a 
time  an  almost  certain  immunity  from  a  repetition  of  the  attack.  Some 
claim  that  the  urine  exhibits  a  remarkable  diminution  in  chloride  of  so- 
dium and  urea  just  after  an  attack,  while  later  both  return  to  the  normal.^ 
Analysis  of  expired  air  shows  oxygen  to  be  almost  wholly  replaced  by  car- 
bonic acid,  which  may  be  eleven  per  cent,  above  the  normal  quantity. 

Physical  Signs. — During  the  paroxysm  inspection  shows  labored  respira- 
tion, while  the  upper  part  of  the  chest  is  almost  motionless,  and  the 
muscles  of  the  neck  rigid;  the  inferior  costal  and  abdominal  respiration  is 
labored,  the  act  of  inspiration  is  slower  than  in  health,  and  expiration  is 
more  active  and  violent,  and  also  longer  than  normal.  Vocal  fremitus  and 
vocal  resonance  are  normal.  The  percussion  sound  is  slightly  exaggerated. 
On  auscultation  the  respiratory  murmur  is  jerking  and  irregular ;  some- 
times it  is  exaggerated,  at  other  times  it  is  suppressed.  Sibilant  and  sono- 
rous rales  of  a  high-pitched,  hissing  and  wheezing  character  are  diffused 

'  Sidney  Ringer. 


62  DISEASES    OP   THE    KESPIRATORT   ORGANS. 

over  the  whole  chest,  often  loud  enough  to  be  heard  at  a  distance  from  the 
patient.  These  are  best  marked  over  and  between  the  scapulge.  The 
respiratory  murmur  is  very  faint  or  absent,  especially  in  the  old  and  where 
expiration  is  prolonged  and  low  pitched.  All  sounds  are  loudest  during 
expiration.  The  rale  sounds  are  often  musical.  These  rales  are  constantly 
changing  their  character  and  site,  disappearing  at  one  point  and  making 
their  appearance  at  another.  At  the  close  of  the  paroxysm  some  moist 
rdles  may  be  heard  ;  or  if  bronchial  catarrh  exists  then  the  sounds  will  be 
moist  throughout. 

Differential  Diagnosis. — Spasmodic  asthma  will  rarely  be  confounded  with 
any  other  disease,  if  its  rational  and  physical  signs  are  properly  appreciated. 
The  phenomena  of  a  paroxysm  are  quite  distinctive,  while  the  physical 
signs  are  unmistakable.  The  afEections  with  which  there  is  a  possibility  of 
its  being  confounded  are  spasmodic  affections  of  the  larynx,  acute  capillary 
tronchitis,  angina  pectoris,  liydrotliorax,  pulmonary  oedema  and  congestion 
and  emphysema.  It  is  easily  distinguished  from  laryngeal  affections  by  the 
absence  of  the  change  in  the  voice  which  is  so  characteristic  of  laryngeal 
spasm,  and  by  the  presence  of  auscultatory  signs  never  heard  in  spasm  of  the 
glottis.  It  is  distinguished  from  ironchitis  by  the  slowness  of  respiration, 
by  the  absence  of  subcrepitant  rales  and  pyrexia,  and  by  the  suddenness  of 
its  advent.  In  angina  pectoris  there  are  no  sibilant  and  sonorous  rales. 
Angina  pectoris  is  accompanied  by  lancinating  pain — absent  in  asthma 
— and  there  are  no  attendant  physical  lung  symptoms.  In  hydrothorax 
there  is  no  resonance  on  percussion  over  the  entire  thorax,  no  succussion, 
and  no  change  in  the  line  of  dulness.  In  pulmonary  mdema  there  is 
dulness  ;  in  asthma  extra  resonance.  Liquid,  bubbling,  stationary  rdles 
are  heard  in  oedema  ;  in  asthma  the  rdles  are  dry  and  constantly  change 
position  and  character.  There  is  profuse  watery  expectoration  in  oedema, 
absent  in  asthma.  Asthmatic  dyspnoea  and  cardiac  dyspnoea  are  some- 
times confounded ;  in  some  respects  they  resemble  each  other — both  are 
paroxysmal,  both  are  intense,  and  both  generally  occur  at  night.  There 
is  little  wheezing  in  cardiac  dyspnoea.  In  both,  the  respiration  maybe  per- 
fectly normal  between  the  attacks,  but  a  careful  physical  examination  will 
enable  one  to  determine  whether  the  dyspnoea  is  asthmatic  or  cardiac. 

Emphysema  has  a  vesiculo-tympanitic  percussion  note,  not  present  in 
asthma.  Prolonged  low-pitched  expirations  exist  in  emphysema;  in  asthma 
the  expirations  are  never  loio  pitched.  The  barrel-shaped  chest  and  change 
in  the  position  of  the  heart  are  absent  in  asthma,  and  are  notable  signs  of 
emphysema.  The  two  conditions  are  often  found  together.  In  croup  the 
dyspnoea  is  inspiratory ;  in  asthma  it  is  expiratory.  The  condition  most 
likely  to  be  mistaken  for  asthma,  in  old  age,  is  latent  pericarditis  with 
effusion.  Spasmodic  dyspnoea  often  accompanies  it ;  but  it  is  marked  by 
a  feeble,  often  an  irregular  pulse,  diminished  cardiac  impulse,  obscure 
heart  sounds  and  increase  in  precordial  dalness,  and  there  are  no  rdles 
present. 

Prognosis, — Death  rarely,  if  ever,  occurs  from  uncomplicated  asthma. 
Asthmatic  patients  are  frequently  long-lived,  which  may  be  accounted  for  by 


BEONCHIAL   ASTHMA.  63 

the  fact  that  they  are  compelled  to  observe  the  most  rigid  hygiene  in  order 
to  avoid  their  asthmatic  attacks.  The  fact  that  a  person  has  had  one 
asthmatic  attack,  is  presumptive  evidence  that  he  will  have  another.  The 
prognosis,  as  to  recovery,  is  hopeful  in  proportion  to  the  youth  of  the 
patient.  If  the  attacks  only  come  on  at  long  intervals  and  are  not  severe 
and  prolonged  ;  if  during  the  intervals  the  patient  is  well  and  there  is  no 
organic  disease;  if  the  paroxysms  can  be  traced  to  some  obvious  cause  which 
may  be  avoided,  the  prognosis  as  to  the  complete  recovery  is  good.  At  first, 
the  attacks  are  violent  and  exhausting  ;  then  they  lose  their  periodical 
character  and  run  together,  as  it  were,  so  that  the  patient  is  never  wholly 
free  from  asthmatic  dyspnoea.  The  periodicity  varies  from  one  year  to  one 
month.  Emphysema,  chronic  passive  pulmonary  hypersemia,  right  car- 
diac hypertrophy  and  dilatation,  and  chronic  bronchitis  are  among  its 
complications. 

Treatment. — There  are  two  things  to  be  considered  in  the  treatment  of 
this  affection,  viz.,  the  relief  of  the  paroxysms  and  the  prevention  of  their 
recurrence.  The  first  thing  is  to  ascertain  the  exciting  cause  of  the 
paroxysm,  and,  if  it  is  still  in  operation,  to  remove  it  if  possible.  If  the 
paroxysm  is  dependent  on  an  overloaded  stomach,  an  emetic  should  be  ad- 
ministered; if  upon  a  loaded  rectum,  an  enema  should  be  given;  if  smoke, 
dust,  or  any  animal  or  vegetable  emanation  is  the  cause  of  the  attack,  it 
must  be  removed.  "  Eose  fever"  and  '' hay  fever  "  are  only  relieved  by 
removal  from  places  where  there  are  roses  or  hay.  If,  in  a  certain  locality, 
the  attacks  of  asthma  are  of  frequent  occurrence,  the  patient  should  re- 
move to  one  where  he  is  free  from  asthmatic  paroxysms.  Not  infrequently 
the  removal  of  the  exciting  cause  will  be  all  that  is  necessary  for  the  relief 
of  the  patient.  If  the  exciting  cause  cannot  be  removed,  or  if  its  removal 
is  not  followed  by  relief  of  the  paroxysm,  free  ventilation  should  be  secured, 
and  the  patient  should  be  placed  in  a  position  in  which  respiration  may  be 
carried  on  with  as  little  mechanical  impediment  as  possible.  Curtains  and 
obstructions  to  the  free  entrance  of  the  air  should  be  removed  from  the 
room.  Usually  the  best  position  during  an  attack  is  the  sitting  posture — 
in  a  chair  which  will  give  support  to  the  arms  and  so  elevate  the  shoulders. 
Some  old  people  are  relieved  by  sitting  before  a  hot  open  fire  in  a  close 
room. 

Having  placed  the  patient  under  the  most  favorable  circumstances  for  the 
relief  of  the  paroxysm,  the  next  thing  is  to  select  those  remedial  agents 
best  adapted  to  the  case.  This  selection  will  be  very  much  influenced  by 
the  patient's  own  experience  and  idiosyncrasy.  The  great  majority  of 
asthmatics  know  the  remedies  that  will  give  them  relief.  The  remedies 
that  give  relief  to  asthmatics  maybe  divided  into  three  classes:  6?ej5ress«w/s, 
sedatives,  and  stimulants.  Among  the  leading  depressants  are  antimony, 
ipecacuanha,  tobacco,  and  lobelia.  Ipecacuanha  is  to  be  given  in  quanti- 
ties/ws^  sufficient  to  produce  nausea,  and  tobacco  till  it  begins  to  sicken. 
If  a  patient  has  been  previously  relieved  by  the  use  of  depressants,  it  is  well 
to  inquire  which  one  of  this  class  he  made  use  of.  The  relief  obtained  by 
this  class  of  remedies  is  by  bringing  the  asthmatic  into  a  condition  of  com- 


64  DISEASES   OF   THE   KESPIRATORY    ORGANS. 

plete  relaxation.  Sometimes  this  may  be  accomplished  by  the  administra- 
tion of  one  full  dose  of  ipecacuanha. 

Sedatives  seem  to  act  in  two  ways  :  some  act  locally  on  the  nervous 
supply  of  the  lungs,  but  the  majority  give  relief  by  their  action  on  the 
general  nervous  system.  Those  which  experience  has  shown  to  be  most 
efficacious  in  arresting  the  asthmatic  spasm  are  stramonium,  chloroform, 
belladonna,  conium,  assafoetida,  the  bromides,  ether,  opium,  cannabis 
indica,  hyoscyamus,  and  the  fumes  of  burning  nitre  paper.  Smoking 
stramonium  often  relieves  when  the  internal  use  of  the  extract  is  inert. 
The  datura  tatula  is  by  many  regarded  as  more  efficacious  than  the  datura 
stramonium.  Smoking  tobacco  often  relieves  a  paroxysm.  Some  will  be 
promptly  relieved  by  the  inhalation  of  the  fumes  of  stramonium  leaves  ; 
others  by  the  inhalation  of  chloroform.  Perhaps  there  is  no  agent  in  this 
class  that  will  so  speedily  and  completely  relieve  the  spasm  as  chloro- 
form ;  but  the  relief  is  only  temporary  ;  so  soon  as  the  stupefying  effects 
have  passed  away  the  paroxysm  generally  returns  with  increased  violence. 

Ether  is  pleasanter  to  inhale  than  chloroform,  and  has  no  such  after 
effects.  A  combination  of  the  two  is  often  efficacious.  Trousseau  advo- 
cates inhalation  of  vapor  of  ammonia.  Quebracho  has  proved  efficacious 
in  a  few  instances.  Kecently  grindelia  robusta  has  been  strongly  advo- 
cated. In  this  class  of  remedial  agents  that  which  I  have  used  most  suc- 
cessfully is  opium  given  in  full  doses — small  doses  are  unavailing.  One- 
half  a  grain  of  the  sulphate  of  morphia  should  be  administered  at  once.  I 
prefer  its  hypodermic  use.  Atropine  may  be  combined  with  the  morphia  ; 
there  are  cases  which  are  quickly  relieved  by  this  combination,  which  are 
not  relieved  by  the  use  of  either  of  these  drugs  alone.  Conium,  hyoscya- 
mus and  belladonna  act  much  less  certainly.  They  should  be  tried,  how- 
ever. Nitrite  of  amyl  is  not  so  successful  as  its  physiological  action  Avould 
indicate.  Iodide  of  ethyl  is  advocated  by  some.^  Fumes  of  nitre  paper  is  one 
of  the  oldest  and  best  remedies.  The  paper  is  prepared  by  dipping  filter 
or  blotting  paper  in  a  solution  of  saltpetre.  How  it  acts  is  not  well  under- 
stood ;  certainly  not  by  relieving  the  bronchial  irritation,  for,  as  a  rule, 
the  patient  is  not  relieved  if  bronchitis  is  associated  with  the  asthma.  When 
this  remedy  is  employed  it  is  necessary  that  the  apartment  occupied  by  the 
patient  should  be  filled  with  its  fumes.  If  it  acts  favorably  it  will  do  so 
quickly,  and  its  administration  must  not  be  prolonged  if  relief  is  not 
promptly  obtained. 

Among  stimulants,  the  two  principal  remedies  are  coffee  and  alcohol. 
Coffee  is  the  more  efficacious.  It  should  be  taken  strong  without 
milk  or  sugar,  and  as  hot  as  it  can  be  swallowed  ;  it  should  always  be 
taken  on  an  empty  stomach.  Not  infrequently  a  paroxysm  of  asthma 
can  be  warded  off  by  taking  two  or  three  cups  of  strong  coffee  imme- 
diately upon  the  accession  of  the  first  asthmatic  symptom.  Alcohol 
is  another  stimulant  which  experience  has  led  me  to  regard  very  highly. 
It  is  of  little  importance  what  alcoholic  stimulant  is  employed,  but  it 
must  be  taken  hot  and  strong,  that  is  as  a  "hot  toddy,"  and   in  suffi- 

1  Gazette  Medical  de  Paris.  1878,  p.  69. 


BROKCHIAL   HEMORRHAGE.  65 

ciently  large  doses  for  the  patient  to  feel  its  intoxicating  effects.  As  a 
rule  asthmatic  patients  will  bear  large  quantities  of  alcoholic  stimulants 
without  becoming  intoxicated.  By  whichever  class  of  remedial  agents  the 
patient  is  relieved,  after  a  time  the  remedy  will  fail  or  cease  to  have  the 
desired  effect.  The  three  most  reliable  remedies  are  ipecacuanha  as  a  de- 
pressant, opium  as  a  sedative,  and  coffee  as  a  stimulant.  Compressed  air  I 
have  never  found  to  give  the  relief  promised  by  its  advocates  ;  nor  does 
inhalation  of  oxygen  allay  the  paroxysms  as  a  rule.  Certain  mineral  springs 
are  beneficial  for  asthmatics  ;  the  most  noted  are  Cmiterets,  Mont-Bore, 
and  Baux  Bonnes.  Faulkner  paints  the  track  of  the  pneumogastric  in 
the  neck  with  iodine  and  claims  remarkable  results.  Nitro-glycerine  and 
pilocarpin  have  both  been  used.^  In  the  intervals  the  treatment  is  hygi- 
enic ;  no  known  remedies  can  prevent  the  return  of  the  paroxysms,  whereas 
the  observance  of  certain  hygienic  rules  may  often  prevent  or  delay  their 
return.  When  skin  diseases  alternate  with  attacks  of  asthma,  arsenical 
preparations  are  beneficial.  "Where  the  cause  is  undiscoverable,  many  state 
that  iodide  of  potassium  not  only  prevents,  or  delays,  an  impending  attack, 
but  even  effects  a  permanent  cure.  Asthmatic  patients  are  usually  dysjoep- 
tic  ;  and  it  is  a  noticeable  fact  that,  in  such  cases,  as  long  as  they  exercise 
proper  care  as  to  diet  they  are  free  from  asthmatic  attacks.  This  is  not  to 
be  overlooked  in  the  management  of  asthmatics  betioeen  the  paroxysms.  A 
change  of  residence  is  all  important  in  cases  dependent  for  their  develop- 
ment upon  certain  atmospheric  causes.  There  is  no  definite  rule  for  this 
change  ;  each  one  must  decide  for  himself,  finding  by  experience  the  place 
in  which  he  is  free  from  his  attacks.  If  the  patient  is  anaemic  and  poorly 
nourished,  cod-liver  oil  and  iron  must  be  administered  during  the  interval. 
1  have  quite  a  number  of  asthmatics  under  observation  who,  by  taking 
daily  from  gr.  xv.  to  gr.  xx.  of  the  sulphate  of  quinine  can  prevent  parox- 
ysms of  asthma.  As  soon  as  the  daily  use  of  the  quinine  is  discontinued 
the  asthmatic  symptoms  begin  to  manifest  themselves,  and  soon  culminate 
in  a  paroxysm.  Helmholtz  found  relief  by  injecting  into  the  nostrils  a 
solution  of  quinia  when  he  suffered  from  "hay  fever."  The  diet,  espe- 
cially in  old  age,  should  be  strictly  regulated.  'No  fats,  no  water  within  one 
hour  before  dinner  or  supper,  or  till  three  hours  after — these  should  be 
laws  never  to  be  broken.  Flannel  must  be  worn  next  the  skin.  Exercise 
should  be  constant  but  moderate.  Should  the  frame,  however,  be  defect- 
ively developed,  active  gymnastic  exercise  is  then  to  be  advised. 

BRONCHIAL     HEMORRHAGE. 

In  the  majority  of  instances,  when  blood  is  expectorated  in  considerable 
quantities,  the  source  of  the  hemorrhage  is  the  bronchial  mucous  membrane. 
Spitting  of  blood  occurs  in  pulmonary  congestion,  pulmonary  apoplexy, 
and.  in  the  inflammatory  processes  affecting  the  lungs  and  bronchi  ;  but 
hemorrhage  from  the  bronchial  tubes  is  by  far  the  most  frequent  cause  of 

"  British  Medical  Journal,  Yol.  I.  1880,  p.  960. 


66  DISEASES   OF   THE  EESPIEATOEY  ORGANS. 

blood-spitting  or  hmnoptysis  ;  *  and  when  blood  comes  from  the  bronchial 
tubes  the  hemorrhage  is  properly  called  hronchorrliagia. 

Morbid  Anatomy. — If  the  bronchial  mucous  membrane  is  examined  soon 
after  or  during  a  bronchial  hemorrhage,  at  the  seat  of  the  hemorrhage  it 
will  be  found  swollen,  relaxed,  bleeding  on  slight  pressure,  and  of  a  uni- 
formly dark-red  color,  with  here  and  there  spots  of  ecchymosis.  The  lungs 
are  pale  but  are  marked  by  bright  pink  spots,  corresponding  to  the  air-cells 
into  which  blood  has  been  inhaled.  If  the  examination  is  made  some  time 
after  the  bleeding,  the  bronchial  membrane  will  either  present  a  pale  and 
bloodless  appearance,  or  no  traces  of  the  seat  of  the  hemorrhage  can  be 
found.  If  the  examination  is  made  during  or  soon  after  the  hemorrhage, 
the  bronchi  may  be  found  more  or  less  completely  filled  at  points  with 
blood-clots  ;  these  clots  are  usually  exsanguinated.  The  healthy  portions 
of  the  lungs  are  inflated.  In  haemoptysis  occurring  in  advanced  phthisis 
there  will  either  be  aneurism  of  a  pulmonary  vessel  in  a  cavity,  or  ulcera- 
tion of  an  exposed  vessel.  In  the  early  stage  of  phthisis  the  walls  of  the 
small  blood-vessels  suffer  nuclear  proliferation  and  stasis.  If  the  blood  has 
been  forced  from  the  bronchi  into  the  air-cells,  small,  red,  dense  nodules 
wiJl  be  found  scattered  through  the  lung-substance,  very  closely  resembling, 
in  their  gross  appearance,  pulmonary  infarction. 

Etiology. — Ulceration  of  the  bronchial  mucous  membrane  is  rarely  a 
source  of  bronchial  hemorrhage ;  and  seldom  does  an  aneurism  open  into  a 
bronchus.  The  two  prominent  causes  of  bronchial  hemorrhage  are  :  first, 
over-distention  of  the  capillaries  of  the  bronchial  mucous  membrane ; 
secondly,  weakness  of  the  capillary  walls  of  the  bronchial  membrane.  Such 
weakness  of  the  walls  of  the  capillaries  may  be  an  hereditary  or  an  acquired 
condition.  In  both  cases  there  is  probably  rupture,  which  may  escape 
detection  at  the  autopsy.  The  tendency  to  bronchial  hemorrhage  from 
weakened  capillaries  is  much  stronger  between  the  ages  of  fourteen  and 
thirty,  especially  in  young,  delicate  persons  born  of  phthisical  parents,  than 
at  any  other  time.  There  is  also  a  strong  disposition  to  this  form  of  hem- 
orrhage in  those  who  are  already  suffering  from  developed  phthisis,  or 
who  have  an  acquired  phthisical  diathesis.^  Usually  in  these  cases  the 
direct  cause  of  the  hemorrhage  is  a  sudden  distention  of  the  weakened 
bronchial  capillaries  from  violent  physical  exertion,  or  from  certain  peculiar 
■atmospheric  influences.  In  rare  instances  it  occurs  without  any  appreciable 
cause.  That  form  of  bronchial  catarrh  which  precedes  or  attends  the  devel- 
opment of  phthisis  is  very  frequently  preceded  or  attended  by  bronchial 
hemorrhage.  Here,  probably,  the  exciting  cause  of  the  hemorrhage  is  act- 
ive hyperasmia  of  the  bronchial  membrane.  Bronchial  hemorrhage  may 
be  induced  by  the  inhalation  of  irritating  gases  or  vapors  and  by  the  rare- 
fied air  of  high  elevations  ;  in  both  of  these  instances  the  hemorrhage  fol- 
lows over-distention  of  the  capillary  vessels  of  the  bronchial  membrane. 

1  Haemoptysis  means  spitting  of  pure  blood  only  :   i.  e.,  the  rusty  blood-stained  sputa  of  acute  pneu- 
monia do  not  constitute  an  haemoptysis. 

2  Rindfleisch  thinks  that  when  phthisis  follows  hcemoptysis  the  hemorrhage  is  due  to  "  vascular  tuber 
£ular  infiltration." 


BRONCHIAL  HEMOREHAGE.  67 

Any  form  of  obstructive  heart  disease  that  leads  to  passive  hyperaemia  of  the 
lungs  will  predispose  to  bronchial  hemorrhage.  Intense  active  hyper- 
semia  will  also  cause  it.  The  violent  coughing  of  bronchitis,  pertussis  and 
pneumonia  oftentimes  induces  it.  It  may  follow  suppression  of  any  habit- 
ual discharge,  and  is  then  called  **  vicarious  bronchorrhagia." 

Symptoms. — The  symptoms  which  attend  a  bronchial  hemorrhage  vary 
with  the  profuseness  of  the  hemorrhage.  If  the  quantity  of  blood  expec- 
torated is  very  small  no  symptoms  will  be  developed  except  the  spitting  of 
the  blood,  which  is  of  a  bright  red  color.  It  is  not  often,  however,  that 
the  symptoms  that  attend  a  bronchial  hemorrhage  are  so  trivial,  for  these 
hemorrhages  are  usually  profuse.  All  bronchial  hemorrhages  are  attended 
by  the  spitting  of  bright  red,  frothy,  arterial  blood.  A  very  profuse  bron- 
chial hemorrhage  may  come  on  suddenly  without  any  warning,  but  usually 
the  patient  has  had  some  previous  indication  of  its  occurrence,  such  as  a 
sense  of  constriction  at  the  upper  portion  of  the  chest,  or  a  sense  of  uneasi- 
ness during  inspiration,  which  he  cannot  account  for.  Those  who  have  had 
haemoptysis  may  suffer  prodromata,  such  as  headache,  dizziness,  palpitation, 
increased  pulse-tension  and  a  general  constriction  about  the  chest.  Cough 
may  or  may  not  precede  the  hemorrhage.  Usually  the  patient  feels  as  if 
some  fluid  had  suddenly  commenced  trickling  under  the  sternum,  and  he 
notices  an  unusual  sweetish  taste  in  the  mouth.  He  spits  and  finds  that 
the  fluid  is  blood,  although  there  may  have  been  no  cough  previous  to  the 
hemorrhage.  Now  he  feels  more  or  less  bronchial  irritation,  which  is  fol- 
lowed by  a  cough.  Loud  moist  rales  are  heard,  more  or  less  blood  is  expec- 
torated, short  intervals  occur  between  the  fits  of  coughing,  and  in  this  way 
blood  may  continue  to  be  expectorated  for  several  days,  or  the  expectoration 
may  continue  only  for  a  few  hours. 

The  amount  of  blood  expectorated  varies  ;  sometimes,  when  the  hem- 
orrhage is  profuse,  the  whole  quantity  may  reach  a  pound  or  more ;  at 
other  times  not  more  than  an  ounce  or  two  is  expectorated.  During  the 
occurrence  of  the  hemorrhage  the  countenance  of  the  patient  assumes  an 
anxious  expression  ;  he  becomes  tremulous  and  often  faints.  This,  how- 
ever, is  not  owing  wholly  to  the  loss  of  blood,  but  is  probably  due  to 
the  shock  to  the  nervous  system  from  the  sight  of  blood  and  knowledge 
of  the  fact  that  a  hemorrhage  from  the  lungs  has  taken  place.  The  pulse 
becomes  rapid  and  tense,  and,  unless  the  bleeding  is  profuse,  the  face 
is  red.  The  temperature  during  the  bleeding  is  usually  depressed,  but 
soon  returns  to  the  normal.  All  these  symptoms  may  be  present  when 
the  individual  has  not  lost  more  than  half  a  pound  of  blood.  Hemorrhage 
from  the  lungs  weakens  a  patient  more  than  an  equal  amount  of  hemor- 
rhage from  any  other  organ  of  the  body.  After  the  profuse  expectoration 
of  blood  has  ceased,  the  patient  goes  on  coughing  for  a  few  days, 
expectorating  small,  dark,  coagulated  masses  of  blood  or  blood-streaked 
sputa.  Sometimes  bronchial  hemorrhage  is  so  profuse  that  the  blood 
spouts  out  of  the  mouth  and  nose.  This  is  followed  by  nausea  and 
vomiting  of  blood,  but  it  is  worthy  of  notice  that  the  nausea  and  bloody 
vomiting  follow  and  do  not  precede  the  hemorrhage.     Death  may  occur 


(58  DISEASES   OF  THE   KESPIKATORY   ORGAKS. 

from  suffocation  in  these  cases.  Eapid  and  profuse  (but  wow-phthisical) 
haemoptysis  should  lead  to  the  suspicion  of  the  rupture  of  an  aneurism. 
Attacks  of  bronchial  hemorrhage  are  rarely  single  ;  usually  for  a  week  or 
two  they  recur  at  intervals.  At  length  the  patient  becomes  pale  and 
feeble,  then  recovery  gradually  takes  place,  so  that  in  a  few  weeks  he  may 
feel  better  than  before  the  hemorrhage.  This  is  the  most  favorable  termi- 
nation that  can  be  hoped  for,  except  in  those  cases  in  which  the  hemor- 
rhage is  comparatively  insignificant.  It  is  important  to  remember  that 
attacks  of  bronchial  hemorrhage,  however  profuse,  are  generally  recovered 
from  in  spite  of  extreme  prostration  and  tendency  to  syncope  which  some- 
times attend  their  occurrence.  When  the  recovery  from  a  bronchial 
hemorrhage  is  not  speedy  it  is  quite  likely  to  be  followed  by  more  or  less 
febrile  excitement,  the  temperature  rising,  perhaps,  to  101°  ¥.,  the  pulse 
becoming  accelerated  and  feeble.  The  patient  becomes  paler  and  weaker, 
has  almost  complete  loss  of  appetite,  and  is  troubled  with  a  hacking  cough, 
almost  constant,  which  is  accompanied  by  a  tenacious,  scanty,  muco-pur- 
ulent  expectoration.  The  respiration  is  hurried,  and  there  is  dyspnoea 
on  slight  exertion.  Under  these  circumstances  the  bronchial  hemorrhage 
is  followed  by  broncho-pneumonia,  Avhich,  in  the  majority  of  cases,  within 
a  few  weeks  goes  on  to  more  or  less  complete  resolution,  and  the  patient, 
by  means  of  change  of  air  and  proper  hygiene,  may  finally  recover.  There 
is  another  class  of  cases  in  which  the  hemorrhage  is  followed  by  still  more 
active  febrile  symptoms,  the  temperature  rises  higher,  the  pulse  is  more 
rapid  and  feeble,  emaciation  follows,  usually  accompanied  by  profuse  night 
sweats,  and  the  patient  dies  of  acute  phthisis  within  a  few  months  after  the 
fiirst  hemorrhage.  Previous  to  the  hemorrhage  he  has  good  health,  and 
there  were  no  physical  evidences  of  disease  of  the  lungs  or  bronchi.  (This 
subject  is  more  fully  considered  under  the  head  of  Acute  Phthisis.) 

A  physical  examination  of  the  chest  during  a  bronchial  hemorrhage  usu- 
ally gives  negative  results.  On  auscultation  nothing  abnormal  is  found, 
with  the  exception  of  a  few  large  and  small  moist  bronchial  rales.  It  is  not 
well  to  disturb  the  patient  by  frequent  examinations  of  the  chest. 

Differential  Diagnosis. — There  are  four  conditions  which  may  be  con- 
founded with  bronchial  hemorrhage,  namely,  epistaxis,  pulmonary  apO' 
plexy,  hcematemesis,  and  aneurisms  rupturing  into  the  air-passages. 

Epistaxis  is  very  easily  distinguished  from  bronchial  hemorrhage,  for 
the  nose-bleed  occurs  before  the  apparent  bronchial  hemorrhage,  and  the 
blood  is  always  coagulated  and  dark  colored.  It  is  not  attended  or  fol- 
lowed by  a  cough,  and  blood  can  always  be  detected  in  the  nostrils,  posterior 
nares,  or  pharynx.  The  characteristics  of  the  hsemoptysis  which  occurs  in 
connection  with  pulmonary  apoplexy  will  be  considered  under  that  head. 
The  diagnosis  between  these  two  forms  of  hsemopytsis  rests  upon  the  char- 
acter and  quantity  of  the  blood  expectorated,  and  the  existence  or  non- 
existence of  cardiac  disease  or  pyaemia ;  and  here  a  physical  examination 
is  of  great  importance. 

Hmmatemesis  is  to  be  distinguished  from  bronchial  hemorrhage  by  the 
fact  that  the  blood  in  haematemesis  is  always  coagulated  and  grumous,  of 


BKONCHIAL  HEMORKHAGE.  69 

a  dark  red  color,  and  vomiting  precedes  or  accompanies  the  hemorrhage. 
In  bronchial  hemorrliage  if  nausea  and  vomiting  are  i)resent  they  follow  the 
spitting  of  arterial  blood  ;  and  hamatemesis  is  not  accompanied  or  followed 
by  a  cough. '  The  gurgling  in  the  bronchi,  loose  cough,  and  bright  frothy 
appearance  of  the  blood  are  never  met  with  in  hsematemesis.  Blood  is 
alkaline  when  from  the  lungs,  and  acid  from  the  stomach.  "Spurious 
hcemoptysis  "  (bleeding  from  gums,  pharynx,  etc.,  as  from  bad  teeth)  may 
be  confounded  with  bronchorrhagia,  but  an  examination  of  the  mouth  soon 
reveals  the  true  state  of  affairs.  When  an  aneurism  ruptures  into  a  bron- 
chial tube,  the  hemorrhage  is  generally  profuse,  and  it  is  soon  followed  by 
death.  The  long  history  of  aneurism  which  precedes  the  rupture,  as  well 
as  the  physical  signs,  which  at*  least  will  have  led  to  the  suspicion  of 
aneurism,  are  in  most  instances  sufficient  to  enable  one  to  determine  the 
nature  of  the  hemorrhage. 

Prognosis. — Bronchial  hemorrhage  rarely  proves  immediately  fatal,  or 
directly  endangers  life.  The  prognosis  as  to  final  result  is  always  unfavor- 
able ;  it  is  in  a  large  proportion  of  cases  either  the  precursor  of  phthisis, 
or  a  sign  that  phthisis  already  exists.  It  certainly  always  demands  serious 
consideration.  The  prognosis  is  much  more  favorable  when  the  hemor- 
rhage is  due  to  the  excessive  action  of  the  heart,  or  bronchial  hypersemia 
induced  by  the  inhalation  of  irritating  substances  or  gases  than  when  it 
occurs  without  any  apparent  exciting  cause.  Should  haemoptysis  be  suffi- 
cient to  induce  angemia,  the  latter  condition  is  very  obstinate  and  persist- 
ent, more  so  than  when  it  follows  other  hemorrhages. 

Treatment. — Absolute  rest  in  a  cool  room  is  of  the  greatest  importance. 
The  patient  should  be  placed  in  bed  and  not  allowed  to  sit  up,  turn  over, 
or  even  speak  above  a  whisper.  If  the  cough  continues  and  is  constant,  or 
induces  the  hemorrhage,  it  must  be  quieted  by  full  doses  of  opium.  Ergot, 
tannin,  gallic  acid,  acetate  of  lead,  spirits  of  turpentine,  persulphate  of 
iron,  or  common  salt  may  be  administered  ;  the  balsams,  copaiba  or  sweet 
spirits  of  nitre,  maybe  given,  if  their  administration  wiJl  quiet  the  anxiety 
of  the  patient  or  friends.  It  has  never  seemed  to  me  that  styptics  or  astrin- 
gents have  any  control  over  bronchial  hemorrhages.  The  application  of  ice 
bags  to  the  surface  of  the  chest  may  be  resorted  to  in  extreme  cases,  but  it 
must  be  carefully  done,  for  the  reason  that  patients  to  whom  ice  bags  are  ap- 
plied are  exceedingly  liable  to  have  broncho-pneumonia  follow  their  attacks 
of  bronchial  hemorrhage.  Dry  cupping  over  the  surface  of  the  chest  is  of 
service  whenever  the  hemorrhage  is  preceded  or  attended  by  marked  pul- 
monary hyperaemia.  Patients  with  hasmoptysis  should  be  urged  to  eat  ice 
and  drink  freely  of  cold  drinks.  In  all  cases  it  is  important  to  keep  the 
patient  under  observation  until  all  bronchial  irritation  produced  by  the 
presence  of  blood  in  the  bronchial  tubes  has  subsided.  If  there  is  tendency 
to  a  return  of  the  hemorrhage,  everything  likely  to  bring  on  an  attack 
must  be  carefully  avoided,  and  the  nutrition  of  the  patient  must  be  im- 
proved by  the  administration  of  iron  combined  with  a  most  nutritious  but 
non-stimulating  diet.  Moderate  exercise  should  be  taken  daily  in  the  open 
air,  and  all  mental  and  physical  exertion  should  be  avoided. 


70 


DISEASES   OF   THE    RESPIRATORY   ORGANS. 


DISEASES  OF  THE  LUNGS  AND  PLEURA. 


I  shall  consider  the  diseases  of  the  lungs  and  pleura  under  the  following 
heads  : 

Pulmonary  Anmmia. 
Pulmonary  Collapse. 
Pulmonary  Emphysema. 
Morbid  growths   in   the    Lung 

and  Pleura. 
Parasitic  Diseases.  {Hydatids.) 
Pleurisy. 
Pulmonary  Phthisis. 


I. 

Acute  Lobar  Pneumonia. 

IX. 

II. 

Lobular  Pneumonia. 

X. 

III. 

Interstitial  Pneumonia. 

XL 

IV. 

Pulmonary  Hypercemia. 

XII. 

V. 

Pulmonary  (Edema. 

VI. 

Pulmonary  Infarction. 

XIII. 

VII. 

Pulmonary  Apoplexy. 

XIV. 

VIII. 

Pulmonary  Gangrene. 

XV. 

ACUTE   LOBAE    PlSTEUMOlSriA. 

Acute  Lobar  or  croupous  pneumonia  or  pneumonitis  is  an  acute  general 
disease  characterized  by  an  inflammation  of  the  vesicular  structure  of  the 
lungs,  with  an  exudation  into  the  alveoli  which  renders  them  impermeable 

to  air :  a  condition  called 
"  hepatization."  A  single 
lobe,  the  whole  of  a  lung  or 
both  lungs  may  be  simulta- 
neously involved. 

Morbid  Anatomy.  —  Ana- 
tomically as  well  as  clinical- 
ly, lobar  pneumonia  may  be 
divided  into  three  stages. 
First :  Sb  stage  of  congestion 
or  engorgement.  Second:  a 
stage  of  consolidation  or  red 
hepatization,  lliird :  a  stage 
of  gray  hepatization.  Arte- 
rial injection  preceding  en- 
gorgement cannot  be  demon- 
strated. Some  have  called 
this  injection  the  "dry  stage'' 
of  pneumonia. 

Stage  of  Congestion  or 
Engorgement. — In  this  stage 
the  portion  of  lung  involved 
in  the  pneumonic  process 
does  not  collapse  when  the 
thoracic  cavity  is  opened  ;  it  has  a  firmer  feel  than  normal,  and  is  more 
or  less  distended  ;  its  resiliency  is  lost ;  it  crepitates  less  than  normal ; 


Fig.  15. 

Section  of  Lung  showing  a  single  Alveolus  in  the  first  Stage  of 
Lobar  Pneumonia. 

A,  A.  Wall  of  alveolus. 

B,  B.  Distended,  varicose  and  tm-tuous  capillaries. 

C,  C.  Alveolar  epilhelial  cells. 

2>,  2).  Blood  globides  in  cavity  of  the  alveolus,     x  300. 


ACUTE   LOBAK   PNEUMONIA. 


71 


Fig.  16. 

Section  of  Lung  in  the  second  Stage  of  Lobar  Pnenmonia. 

The  pulmonary  alveoli  are  seen,  filled  ivith  Pus  corpuscles  {A,  A),  changed  Epithelial  cells  (B,  S), 
fibrillated  Fibrin  (C,  C),  and  red  Blood  globules  (Z>,  V).      x  250. 

and  often  pits  on  pressure.  It  is  not  wholly  airless,  for  air  can  be  pressed 
from  one  part  to  another.  It  is  somewhat  friable ;  its  color  is  a  dark 
brownish  red,  often  purple;  and  its  weight  and  specific  gravity  are 
increased. 


Pig.  17 
Vertical  Section  of  tlie  Lung  and  Pleura  in  tlie  second  Stage  of  PI  euro-Pneumonia. 

a.  Plastic  emidation  on  the  thickened  pleura. 

b.  Infiltration  pus. 

c.  Loose  epithelial  cells. 

d.  Enlarged  blood-vessels. 

The  alveoli  contain  red  blood-corimscles  ie),  pus  cells  (/),  changed  epithelial  cells  (g),  and  fibrillated 
fibrin  (i).     The  blood-vessels  (h)  in  the  alveolar  ivalls  are  seen  filled  with  red  corpuscles,     x  200. 


73  DISEASES   OF  THE   RESPIRATORY   ORGANS. 

On  section  a  thin,  frothy,  blood-stained  serum  exudes.  Sometimes 
it  flows  freely  on  pressure ;  it  may  be  tenacious.  When  alcohol  is 
added  to  the  fluid  it  coagulates  into  a  granular  and  amorphous  mass. 
Dark  blood  flows  from  the  distended  capillaries.  Occasionally,  just  under 
the  pleura  and  between  the  air  sacs,  there  are  small  spots  of  extrav- 
asation. , 

On  microscopical  examination  of  a  thin  section  of  the  affected  lung  tis- 
sue the  lumen  of  the  alveoli  will  be  found  diminished  by  the  distended, 
varicose  and  tortuous  capillaries.  Early  in  the  disease  some  of  the  air- 
sacs  may  be  collapsed  from  pressure.  The  alveolar  epithelium  is  swollen 
and  granular.  In  the  air-cells  are  exfoliated  epithelial  cells,  a  few  pus  cells, 
red  globules  and  serum.'  At  the  autopsy  it  is  sometimes  difficult  to  distin- 
guish the  stage  of  pneumonic  congestion  from  pulmonary  oedema  and  con- 
gestion. In  the  latter  the  fluid  in  the  alveoli  is  serum  and  contains  no 
cell  elements.  When  a  stream  of  water  flows  over  the  cut  surface  of  a 
pneumonic  lung  the  color  remains ;  in  oedema  and  congestion  it  dis- 
appears. 

Stage  of  Red  Hepatization. — This  stage  receives  its  name  from  the  color 
of  the  lung  and  its  resemblance,  when  cut,  to  liver-tissue.  The  aflected 
portion  has  a  dark  liver  or  mahogany  color,  and  is  mottled,  the  mottling 
becoming  more  marked  as  the  stage  advances.  The  volume  of  the  affected 
lung  is  increased;  so  much  so  that  it  often  bears  the  impress  of  the  ribs. 
It  is  solid,  firmer,  and  heavier  than  normal.  Pressure  does  not  indent,  but 
tears  it ;  it  is  friable,  easily  torn,  and  its  torn  surfaces  have  a  granular 
appearance.  Its  specific  gravity  is  increased.  It  is  airless,  and  there  is 
entire  absence  of  crepitation.     Artificial  inflation  is  impossible. 

On  section  the  cut  surface  has  a  granular  appearance ;  the  granules 
correspond  to  plugs  of  inflammatory  exudation,  which  fill  the  air-cells 
and  the  small  bronchi.  Torn  surfaces  show  the  granulations  better  than 
cut  surfaces.  The  granules  can  be  lifted  out  by  means  of  a  fine  needle. 
When  cut  a  dirty  red  viscid  fluid  slowly  oozes  from  the  surface,  or  it  may 
only  appear  after  twelve  or  twenty-four  hours'  exposure  to  the  air.  This 
may  be  scraped  from  the  cut  surface.  A  piece  of  the  inflamed  lung  quick- 
ly sinks  in  water.  Small  spots  of  extravasation  are  sometimes  seen.  When 
a  stream  of  water  is  poured  over  the  cut  surface  the  color  changes  from  a 
maroon  to  a  gray  or  a  yellow-gray. 

On  microscopical  examination  the  alveoli  are  found  filled  with  a  solid 
exudation  composed  of  a  net-work  of  fibrillated  fibrin,  in  whose  meshes  are 
pus-cells,  red  globules,  and  changed  epithelial  cells.  The  latter  are  in 
various  forms — round,  oval,  quadrangular,  triangular  or  irregular — and 
have  received  dift'ereht  names,  according  to  the  views  entertained  by  differ- 

1  It  is  still  a  disputed  question  whether  the  bronchial  or  pulmonary  vessels  are  the  chief  source  of  the 
pneumonic  exudation.  The  lung-tissue  is  nourished  by  tlie  bronchial  arteries,  while  the  pulmonary  ves- 
sels are  the  medium  for  the  interchange  of  gases.  Hence  it  is  claimed  that  only  the  bronchial  vessels  are 
implicated.  Virchow  has  shown  that  pneumonic  processes  can  be  established  when  large  branches  of  the 
pulmonary  artery  are  plugged;  yet  he  admits  that  the  pulmonary  capillaries  have,  secondarily,  much  to  do 
with  the  exudation.  Again,  it  is  claimed  that  early  in  the  disease  the  parts  supplied  ny  the  bronchial 
vessels  are  not  injected  as  they  would  be  were  they  alone  at  fault.  Probably  both  sets  of  vessels  are 
involved. 


ACUTE   LOBAR    PNEUMONTA. 


73 


ent  observers  in  regard  to  their  origin.  At  first  these  cells  contain  fibrinous 
material,  but  later  they  become  granular,  and  then  fat  globules  accumulate 
in  them.  They  may  become  discolored  from  imbibition  of  haematin.  The 
whole  contents  of  an  alveolus  now  present  a  more  or  less  round  form.  The 
interstitial  connective-tissue  between  the  lobules  may  be  infiltrated  with 
pus  and  fibrin  ;  the  pulmonary  pleura  is  always  coated  with  fibrin  if  the 
surface  of  the  lung  is  involved;  and  if  the  pleurisy  precedes  the  pneu- 
monia, or  if  it  is  extensive  and  an  abundant  plastic  exudation  covers  the 


Section  of  Lung  in  third  Stage  of  Lobar  Pneumonia,  showing  the  Alveoli  filled  with  Granular  Matter  and 

Crlls. 

A.  Granular  fibrin. 

B.  Ptis  cells. 

C.  Mono-micleated  cells. 

The  blood-vessels  (D)  of  the  alveolar  walls  are  much  less  distended  than  in  the  preceding  stages,    x  850. 


pleura  over  the  inflamed  portion  of  the  lung,  it  receives  the  name  oi pleuro- 
pneumonia. The  anatomical  changes  within  the  lung  are,  however, 
unmodified  by  the  more  extensive  pleurisy,  although  it  undoubtedly  delays 
the  processes  of  pneumonic  resolution  in  the  third  stage.  The  red  blood 
globules  give  the  color  to  the  lung.  This  stage  may  last  from  twenty-four 
hours  to  several  days. 

Gray  Hepatization. — In  the  early  part  of  this  stage  the  lung  remains  of 
the  same  consistency  as  in  the  second  stage.  There  is  no  sharp  transition 
from  red  to  gray  hepatization.     The   mottling  gradually  becomes  more 


74  DISEASES   OF  THE   RESPIEATORT   ORGANS. 

marked,  so  that  the  affected  portion  becomes  "  marbled,"  or  has  a  "  gran- 
ite" look.  The  surface  is  gray.  The  consistency  becomes  less  and  less 
until  the  tissue  is  a  mere  pulp,  readily  breaking  down  on  pressure.  The 
change  in  color  is  due  to  pressure  on  the  blood-vessels,  to  the  decoloration 
of  the  red  blood  globules,  and  to  the  fatty  and  granular  change  in  the 
inflammatory  products.  The  weight,  friability,  and  density  of  the  lung 
are  increased. 

On  section  the  surface  presents  a  uniformly  dirty  gray  appearance.  A  red- 
dish gray  or  dirty  white  puriform  fluid  flows  either  spontaneously  or  on  slight 
pressure  from  the  cut  surface.  The  "  granular  "  look  of  the  second  stage  has 
disappeared  or  is  indistinct.  The  amount  of  the  accompanying  oedema  va- 
ries ;  when  it  is  excessive  a  large  quantity  of  serum  exudes,  and  the  tissue 
does  not  break  down  so  readily  as  in  other  forms  of  gray  hepatization. 

On  microscopical  examination  the  alveoli  are  found  filled  with  numerous 
round,  mono-nucleated  cells ;  and  the  intercellular  fibres  that  bound  the 
elements  together  have  become  granular.  The  alveoli  are  filled  with  a  fluid 
or  semi-fluid  mass,  in  which  numbers  of  discrete  oil  globules  and  protein 
granules  are  freely  mingled.  The  contents  of  the  alveoli  are  shrunken,  and 
between  them  and  the  alveolar  wall  is  a  layer  of  fluid,  so  that,  in  a  thin 
section,  the  contents  of  an  air  sac  are  readily  lifted  out  by  a  camel's-hair 
brush.  The  pleura  over  the  affected  portion  is  covered  with  a  thin  plastic 
exudation. 

Lobar  pneumonia  may  terminate :  (1),  in  resolution  (recovery) ;  (2), 
suppuration  (purulent  infiltration) ;  (3),  abscess;  (4),  gangrene;  or  (5), 
cJironic  pneumonia. 

During  resolution  the  lung  is  moist,  lighter  than  during  hepatization, 
has  a  yellow  or  a  yellow-green  color,  and  shows  a  marked  loss  of  elasticity. 
On  section  it  is  now  granular,  of  a  yellow-gray  hue,  and  a  tenacious  puriform 
fluid  readily  escapes  when  the  section  is  pressed.  Some  oedema  may  still 
remain.  Microscopically  the  vessels  are  seen  to  have  returned  to  their  normal 
calibre  ;  the  alveolar  epithelium  is  restored,  the  cells  in  the  alveoli  are 
degenerated  and  broken  down  into  a  detritus.  The  coloring  matter  of  the 
blood  gives  origin  to  the  pigment  so  plentifully  scattered  throughout  the 
liquefied  mass.  The  contents  are  either  expectorated  or  absorbed  ;  and  the 
lung  returns  to  its  normal  condition. 

When  purulent  infiltration  or  suppuration  occurs,  the  surface  of  the  lung 
becomes  yellow,  its  substance  is  soft,  friable,  moist,  and  it  feels  "  miry,"  as 
if  an  abscess  were  being  pressed.  On  section  a  diffluent  purulent  fluid  ex- 
udes from  the  cut  surface.  The  yellow  color  is  due  to  the  cells  that  are 
undergoing  fatty  change  and  to  the  anaemia  resulting  from  over-distention 
of  aveoli  with  pus.  Microscopically  the  pus  cells  are  seen  to  crowd  the 
alveoli  and  to  infiltrate  the  inter-alveolar  tissue.  This  infiltration  may, 
by  its  presence,  interfere  with  the  nutrition  of  the  lung  tissue,  and  the 
alveolar  walls  may  become  thin,  indistinct  and  rupture. 

Abscess  may  follow  purulent  infiltration,  a  small  anfractuous  cavity  be- 
ing formed  by  the  rupture  of  several  alveolar  septa.  These  abscesses  vary 
in  size  from  that  of  a  pea  to  one  which  may  occupy  an  entire  lobe.     They 


ACUTE   LOBAE  PNEUMON'IA. 


75 


may  have  a  thick  well-defined  wall.  Their  interior  is  crossed  by  shreds 
of  broken-down  tissue.  They  increase  either  by  peripheral  growth  or  by 
fusion  of  several  small  abscesses.  Their  most  common  seat  is  in  the 
lower  lobes.  These  abscesses  may  be  obliterated  by  a  process  of  granula- 
tion and  cicatrization.  In  such  cases  the  abscesses  are  small,  and  com- 
municate with  a  bronchus  which  allows  a  free  discharge  of  their  contents ; 
or  they  may  be  encapsulated  in  firm  cicatricial  tissue,  their  contents  sub- 
sequently undergoing  cheesy  and  then  calcareous  changes.  They  may  open 
into  the  pleural  cavity  (causing  pyo-pneumothorax),  or  into  the  pericar- 
dium.   External  fistulous  openings  have  occurred. 

Gangrene  occurs  in  about  two  per  cent,  of  all  cases.  It  is  liable  to  occur 
when  there  is  great  constitutional  weakness,  and  in  chronic  alcoholismus  or 
in  septicaemia.  It  may  be  circumscribed  or  diffused.  The  gangrenous 
portion  consists  of  a  dirty  pulpy  debris, 
sometimes  without  the  "  gangrenous 
fetor."     When  the  part  becomes  dif- 


fluent a  cavity  is  formed  and  shreds 
of  gangrenous  lung  tissue  are  found 
in  a  fetid  fluid.  About  this  there  is 
a  zone  of  gray  hepatized  friable  tissue, 
which  in  turn  is  bounded  by  normal 
lung  tissue.  In  diffused  gangrene, 
the  cavities  are  large  and  shreds  of 
tissue  and  vascular  bands  cross  from 
side  to  side,  and  the  cavity  swarms 
with  bacteria.  Sloughing  of  the 
pleura  may  follow  such  a  process. 

Chronic  pneumonia  may  be  a  result 
of  lobar  pneumonia,  when  resolution 


Fig.  19. 
Purulent  Infiltration. 


Section  of  Lung  showing  a  single  alveolus. 
^   ^         ^  .  •   •    1    •     n  ^'  ^^'^^olar  ioall,  largely  inflUrated. 

IS  delayed   and  an  interstitial    mflam-    -B.  Transverse  section  of  a  small  artery  with  infil- 

.  .         ,    1  T  1      T     T       .  traf.ionofits  walls. 

matory   process   is  established    during    C.  Epithelial  cells  of  alveolar  wall. 
j_-i„„i  j;  r  .•!•  rm        D.  Capillaries  Of  Wall  of  the  air-vesicle. 

the  stage  ot  gray  hepatization.     The  e.  Pas  corpuscles. 

nponlinrlv    >iQvr1    anri  mrlorviaf/Mics  n^n  The  alveolar  cavify  IS  filled  With  pvscorpuscles^ 

peculiarly    nara   ana  oeaematOUS  con-    gramdar  fibrin,  ana  a  few  large  nucleated  cells. 

dition    that   sometimes  marks    gray   "*  ^^' 

hepatization  is,  by  some,  regarded  as  an  intermediate  stage  between  croupous 
and  interstitial  pneumonia.  Finally,  the  alveolar  contents  in  the  third  stage 
may  undergo  subsequent  cheesy  changes.  Whether  this  occurs  independent 
of  tubercle  is  doubtful.  This  is  sometimes  called  cheesy  infiltration  as 
opposed  to  tubercular  infiltration. 

In  childhood,  except  before  the  second  year,  croupous  pneumonia  is  rare. 
Double  pneumonia  is,  however,  more  frequent  than  m  adult  life.  The 
morbid  appearances  are  the  same  as  in  adults.  In  old  age  the  changes  are 
somewhat  different ;  the  process  usually  begins  in  the  upper  lobes.  In  the 
stage  of  engorgement  crepitation  is  absent;  and  in  the  second  stage  the  lung 
is  blue  or  nearly  black.  A  section  shows  granules  that  are  much  larger 
than  in  adult  life.  "Granulations"  are  very  often  absent  in  senile  pneu- 
monia.    Gangrene  is  far  more  frequently  a  termination  of  lobar  pneumonia 


76  DISEASES   OF   THE   EESPIRATOKY    ORGANS. 

in  old  age  than  at  any  other  period.  The  highly  rarefied  state  of  the  lungs 
at  this  time  of  life  seems  to  favor  the  development  of  the  small  abscesses  so 
common  in  the  aged. 

The  most  frequent  seat  of  lobar  pneumonia  is  the  lower  lobe  of  the  right 
lung  ;  the  next  most  frequent  seat  is  the  lower  lobe  of  the  left  lung ;  then 
the  upper  lobe  of  the  right,  the  middle  lobe  of  this  lung  being  least  fre- 
quently involved. 

Double  pneumonia  has  been  variously  estimated  as  occurring  in  from  5 
to  15  per  cent,  of  cases.  Even  in  ei)idemics  it  rarely  ranges  above  12  to  15 
per  cent.  Double  pneumonia  is  more  frequent  in  the  senile  than  in  the 
adult  period  of  life. 

The  stage  of  congestion  lasts  from  one  to  three  days ;  red  hepatiza- 
tion from  three  to  seven  days  ;  and  gray  hepatization  from  two  to  thirteen 
days.  In  old  age  the  stages  merge  rapidly  into  each  other ;  abscess 
of  the  lung  may  occur  within  36  or  48  hours  after  the  onset.  Ked  hepa- 
tization is  not  infrequently  reached  within  the  first  six  or  eight  hours 
in  the  aged.  The  changes  in  the  pulmonary  pleura  over  a  pneumonic 
lung  are  quite  characteristic.  An  uneven,  thin,  downy-looking  layer  of 
plastic  exudation  covers  its  surface.  This  plastic  layer  may  conceal  the 
liver-brown  color  of  the  pneumonic  lung.  As  the  third  stage  is  reached 
the  opposing  surfaces  of  the  pleura  may  become  agglutinated.  The  pleurit- 
ic changes  follow  very  closely  those  which  occur  within  the  lung.  The 
cells  in  the  pleuritic  exudation  are  mainly  pus.  The  pleuritic  membrane 
is  opaque,  congested  and  ecchymotic.  It  may  become  so  thick  as  to  give  a 
dull  note  on  percussion  after  resolution  is  reached.  The  right  heart  is 
dilated  ;  and  immediately  after  death  both  ventricles  may  contain  clots. 
The  pulmonary  vessels  going  to  the  involved  part  may  contain  thrombi. 

Pericarditis  is  so  frequent  that  it  must  be  regarded  as  more  than  a  coin- 
cidence or  complication.  The  liver  and  spleen  are  congested.  The  splenic 
changes  resemble  those  which  occur  in  fevers.  The  lymphatics  of  the 
lung  are  choked  with  fibrin  and  blood  corpuscles.  The  deeper  lymphatics 
contain  products  identical  with  those  in  the  pulmonary  alveoli.  In  the 
lymphatic  vessels  and  in  the  bronchial  glands  there  is  always  some  evidence 
of  inflammation. 

Gastro-intestinal  catarrh  is  sometimes  present ;  and  may  be  attended 
by  hemorrhage.  The  vessels  of  the  brain  are  more  or  less  engorged.  Men- 
ingitis is  a  not  infrequent  complication  of  pneumonia. 

Etiology. — The  specific  cause  of  pneumonia  is  as  yet  undetermined. 
The  very  existence  of  such  a  cause  is,  as  yet,  conjectural.  Among  the  pre- 
disposing causes  age  ranks  first.  There  are  three  periods  in  life  in  which 
the  liability  to  pneumonia  is  greatest :  early  childhood  ;  20  to  40  ;  and  after 
60.  Though  catarrhal  pneumonia  is  very  frequent  in  children,'  the  state- 
ment that  lobar  pneumonia  is  rare  at  that  period  is  not  correct.  From  reli- 
able data  it  appears  that  lobar  pneumonia  is  five  times  more  frequent  in  the 
first  two  years  of  life  than  in  the  whole  succeeding  eighteen.  Nine-tenths 
of  all  deaths  after  the  sixty-fiftli  year  are  caused  by  lobar  pneumonia. 

1  Yogel.  Kinderkr.  s.  222. 


ACUTE    LOBAE   PNEUMOKIA,  77 

Sex.  In  early  life  (before  the  third  year)  both  sexes  are  equally  at- 
tacked. Between  twenty  and  forty,  when  the  condition  of  the  sexes  is 
most  diverse,  the  proportion  of  males  to  females  attacked  is  3  or  2  to  1. 
After  sixty,  when  the  condition  of  the  sexes  again  is  similar,  there  is  little 
disproportion  ;  but  always  in  favor  of  males.  Whenever  women  work,  or  are 
exposed,  as  men,  the  disease  makes  no  discrimination  as  to  sex.  The  inier- 
peral  state  does  not  seem  to  increase  the  predisposition  to  pneumonia;  but 
it  is  more  apt  to  occur  at  the  time  of  the  catamenia. 

The  general  hodily  condition  oi  and  before  the  pneumonic  seizure  has  but 
little  predisposing  influence.  It  is  a  question  whether  the  strong  or  the  weak 
are  oftenest  attacked.  Convalescents  from  acute  and  severe  illness,  habitual 
alcohol  drinkers  and  those  who  are  "  malarious  "  are  far  more  liable  to  pneu- 
monia than  those  who  are  free  from  such  conditions.  Enervating  habits, 
poverty,  dyscrasia  (cancer  and  chronic  nervous  diseases  especially)  and  anti- 
hygienic  surroundings  are  predisposing  causes.  Diphtheria,  measles,  erysipe- 
las, small-pox  and  the  other  acute  infectious  diseases  must  be  regarded  as  pre- 
disposing causes.  Chronic  and  acute  uraemia  and  all  diseases  which  arise 
from  the  retention  of  excrementitious  products  are  powerful  predisposing 
causes.  Chronic  blood  diseases  act  in  like  manner.  Long-continued  passive 
pulmonary  hyperaemia — e.  g.,  from  heart  disease  or  from  hypostasis — leads  to 
pneumonia.  The  pneumonia  that  frequently  occurs  during  acute  articular 
rheumatism  has  been  regarded  by  some  as  "  metastatic  from  the  joints."  A 
more  rational  view  is  that  it  is  due  to  the  blood  changes  which  are  part  of  the 
rheumatic  fever.  One  attack  of  pneumonia  predisposes  to  others  ;  twenty- 
eight  attacks  have  been  noted  in  one  individual.  When  pneumonia  follows 
a  severe  blow  or  injury  to  the  chest  or  shock  from  any  traumatic  cause,  the 
injury  or  shock  must  be  looked  on  as  a  predisposing  cause.  In  the  aged 
lobar  pneumonia  has  developed  as  soon  as  four  hours  after  fracture  in  the 
hip  joint.  Cold  does  not  affect  the  pneumonia  rate  except  in  the  old. 
March  and  April  statistics  usually  exhibit  the  highest  pneumonia  rate.  A 
continuously  low  or  high  temperature  has  much  less  influence  than  a 
changeable  temperature.  Its  etiology  shows  that  it  is  a  disease  predisposed 
to  by  all  things  that  depress  the  vital  powers.  Children  and  the  aged  are 
greatly  depressed  by  the  intense  cold  of  winter  and  the  chilling  winds  of 
March  and  April.     In  Europe  it  is  often  called  the  "  May  epidemic." 

Pneumonia  is  unknown  in  the  Polar  regions ;  it  -is  common  along  the 
coast  of  the  Mediterranean  Sea.  Elevation  above  the  sea  seems  to  predis- 
pose to  it  both  in  hot  and  cold  climates.  North  and  east  winds  favor  its 
development.  Eainy  seasons  do  not  influence  the  pneumonia  rate  to  any 
appreciable  degree;  nor  do  damp  or  marshy  districts.  But  both  have  a 
marked  influence  over  bronchitis  and  other  local  pulmonary  diseases.  It  is 
a  well-established  fact  that  pneumonia  occurs  oftener  among  the  poor  than 
among  the  rich,  the  private  soldiers  than  their  officers,  the  sailor  on  shore 
oftener  than  on  ship,  the  soldier  oftener  than  the  civilian  at  the  same  mili- 
tary post.  All  this  is  explained  by  the  better  hygienic  surroundings  of  the 
one  class  as  compared  with  the  other.  The  less  the  resistance  capable  of 
being  opposed  to  some  (unknown)  pneumonic  influence,  the  more  strongly 


78  DISEASES   OF  THE   EESPIRATOEY   ORGAN'S. 

predisposed  is  the  individaal.  Every  increase  in  population  in  a  district 
increases  the  pneumonia  rate.  ^  In  New  York  City  from  1840  to  1858  the 
mortality  rate  of  pneumonia  was  5.85  per  cent.  From  1859  to  1877  it  was 
6.2  per  cent. 

The  question  now  meets  us  :  is  pneumonia  a  specific  constitutional  dis- 
ease, an  acute  infectious  disease,  or  a  local  inflammation  ? 

The  following  tend  to  prove  that  it  is  not  a  local  malady.  All  kinds  of 
solid  and  gaseous  inhalations  and  traumatism  have  failed  to  produce  lobar 
pneumonia.^  They  always  induced  lobular  and  not  lobar  pneumonia.  Sec- 
tion of  the  vagi  produces  hepatization,  but  not  croupous  pneumonic  con- 
solidation. Cold  does  not  influence  the  prevalence  of  pneumonia  as  it 
would  were  it  a  local  disease  {e.g.,  bronchitis).  Wet  and  cold  increase  a 
bronchitis  but  not  a  pneumonia  rate.  Lobar  pneumonia  is  more  prevalent 
in  our  Southern  than  in  our  Northern  States.  Epidemics  in  the  West 
Indies  were  more  devastating  than  those  in  Iceland.  On  our  continent 
the  prevalence  of  pneumonia  increases  from  pole  to  equator.  All  acute 
general  diseases  increase  with  the  population ;  pneumonia  does  this.  Sta- 
tistics show  pneumonia  to  be  more  frequent  in  New  York  City  now  than 
twenty  years  ago.^  While  cold  has  something  to  do  with  its  development, 
the  exciting  effect  of  cold  cannot  be  accepted.  Again,  there  is  no  relation 
between  the  amount  of  lung  involved  and  the  intensity  of  the  symptoms.* 
In  local  inflammations  the  reverse  of  this  is  true.  No  second  chill  occurs 
when  another  lobe,  part,  or  the  other  lung  is  attacked.^  Prodromata  some- 
times occur  in  pneumonia.  But  the  absence  of  regular  and  constant  pro- 
dromata, the  absence  of  a  (known)  period  of  incubation,  of  a  typical  tem- 
perature range,  and  of  characteristic  surface  phenomena,  the  fact  that  the 
disease  is  not  contagious — these  are  the  reasons  advanced  by  those  who  re- 
gard it  as  a  local,  not  a  general  disease.  The  resemblances  of  pneumonia 
to  acute  general  diseases  are  :  distinct  initiatory  chill,  an  orderly  pyrexia, 
a  rather  typical  course,  i.  e.,  a  day  of  abrupt  crisis,  a  definite  duration,  and 
the  symptoms  following  in  regular  sequence.  There  is  a  peculiar  facies  ; 
an  occasional  herpetic  eruption  ;  nephritis  is  not  rare  ;  the  cerebral  symp- 
toms resemble  those  of  the  exanthems  ;  there  are  sweats  and  sudamina  ; 
and  its  mode  of  commencement — coma  in  the  old  and  convulsions  in  the 
young — indicate  that  it  is  an  acute  general  disease.  Etiologically  it  is  often 
developed  under  conditions  similar  to  those  which  attend  the  development 
of  diphtheria  and  cerebro-spinal  meningitis ;  atmospheric  conditions 
are  acknowledged  factors  in  its  causation.  English  writers  describe  a 
*' sewer-gas  pneumonia."  There  have  been  epidemics  of  pneumonia  in 
garrisons  and  aboard  ship  where  there  was  overcrowding,  bad  hygiene, 

1  Hirscti  says:  "  The  amount  of  mean  fluctuation  in  the  mortality  from  pneumonia  is  in  inverse  ratio  to 
the  density  of  the  population." 

^Virchoiu's  A7-chiv,Bd.  LXXX.  Reidenhain, Sityl.  K.  K.  Akad  zaWien,867.  Beitz,  GendHn,  Hist.  Anat. 
des  Inflam 

^  N.  T.  Med.  Record :  Article  on  Causes  of  Death  in  Acute  Pneumonia. — Loomis. 

■*"The  local  inflammation  *  *  *  offers  no  sort  of  parallelism  to  the  accompanying  fever. "^ 
Slurges. 

^  "  Small  consolidations  with  high  fever  and  severe  constitutional  symptoms,  and  extensive  infiltrations 
with  a  comparatively  slight  fever— this  is  the  rule,  not  the  exception."— Ziemssen's  Cycl.  Vol.  5,  p.  146. 


ACUTE  LOBAR   PNEUMOKIA.  79 

etc.,  etc.^  There  is  a  ^'pythogenic"  pneumonia  arising  under  miasmatic 
influences  which  is  contagious."  The  epidemic  form  of  pneumonia  at  cer- 
tain times  bears  the  distinct  characteristics  of  a  specific  infectious  disease.* 
Miasmatic  and  zymotic  pneumonia  are  names  indicative  of  a  supposed 
origin.  We  have  abortive  cases  of  pneumonia,  just  as  we  have  abortive 
typhoid  and  cerebro-spinal  meningitis.  Again,  the  names  sthenic,  asthenic, 
malignant,  icteric,  etc.,  etc.,  indicate  varieties  similar  to  those  found  in 
fevers  and  acute  general  diseases.  Pneumonia  is  allied  to  acute  general 
diseases  by  the  fact  that  certain  complications  occur  with  more  or  less 
regularity — lesions  in  the  peri-  and  endocardium  and  albuminuria — and 
that  abortion  is  usually  induced  when  it  attacks  pregnant  women.  It  has 
visceral  and  blood  changes  very  like  those  of  fevers.  Pneumonia  is  some- 
times a  disease  of  intra-uterine  life.  No  local  disease  occurs  in  the  foetus, 
but  fevers  frequently  do. 

The  success  of  modern  methods  of  treatment  based  on  this  belief  bears 
evidence  to  its  being  a  general  (self-limiting)  acute  febrile  disease.  The 
nature  and  action  of  the  poison  that  may  be  supposed  to  cause  pneumonia 
are  indicated  by  the  following  facts  : — hyperinosis  does  not  seem  capable 
of  causing  pneumonia  :  fibrin  increases  as  hepatization  advances  and  does 
not  ante-date  it  or  the  pyrexia.^  Its  resemblance  to  the  acute  general  diseases 
is  mainly  in  its  nervous  phenomena,  and  the  complications  which  render 
pneumonia  dangerous  are  those  which  diminish  the  nerve  supply  or  weaken 
the  muscle-power  of  the  heart. 

Symptoms. — Subjective  or  rational  symptoms.  The  invasion  in  about 
one-fourth  of  the  cases  is  preceded  by  prodromata.^  In  old  age  they  are 
more  frequent  than  in  adult  life  (60  per  cent.).  They  rarely  occur  in  chil- 
dren. For  a  day  or  longer  there  may  be  malaise,  anorexia,  headache,  dull 
pains  in  the  limbs,  back  and  lumbar  region,  vertigo,  epistaxis,  and  slight 
diarrhoea,  or  there  may  be  slight  jaundice,  flashes  of  heat  and  rigors.  Fly- 
ing pains  in  the  limbs  and  chest  are  common  in  old  age.  Eise  in  tempera- 
ture is  sometimes  a  prodrome.  In  Bellevue  Hospital  in  1877  a  patient,  for 
two  or  three  days  preceding  the  initial  chill,  had  a  temperature  of  102° 
-103°  F.  In  epidemics  febrile  symptoms  and  diarrhoea  are  common.''  In 
most  cases  the  invasion  is  sudden  and  the  disease  is  ushered  in  by  a  distinct 
chill.' 

Generally  the  patient  is  seized  with  a  chill  in  the  night.     This  chill  is 


1  In  the  U.  S.  Sanitary  Conimission  Meynoirs  Dr.  Russel  reports  :  "  The  surgeons  on  duty  with  the  reg- 
iments in  the  barracks  (Benton,  Mo.)  report  that  men  occupying  the  same  bunks  with  those  afEected  were 
Tery  much  more  liable  to  be  attacked  than  those  more  remote.  Some  of  the  most  intelligent  surgeons 
believed  that  it  was  actually  contagious." 

2  Dublin  Med.  .lournfxl,  Vol.  I.  1874. 

3  Berliner  Klinische  Wochenschrift,  1879,  No.  'S^%.—Kuhn. 

■*  Pneumonia  resembles  quinsy  and  acute  articular  rheumatism.  Trousseau  finds  a  resemblance  between 
erysipelas  and  pneumonia.  Sturges  places  it  in  a  "middle  class  "  between  specific  diseases  and  local  in- 
flammations. Cohnheim  calls  it  a  miasmatic  contagious  disease.  The  idea  of  its  being  a  specific  general 
disease  dates  from  the  eighteenth  century.— A'tw.  Theo.  More/.  1786,  StracMns. 

^  Grisolle  found  them  in  about  25  per  cent,  of  his  cases.    Fox  found  them  in  28  per  cent. 

*  London  Lancet^  1878,  Vol.  II. 

'  77-80-92  per  cent,  are  the  figures  given  by  Pox,  Louis,  Hubs,  Grisolle  and  Lebert  as  representing  the 
frequency  of  the  initiatory  chill. 


80  DISEASES    OF   THE    RESPIRATORY  ORGAN'S.  " 

intense  and  prolonged,  more  so  than  in  any  other  disease  except  pyaemia 
and  malarial  fever.  It  lasts  from  one  half  an  hour  to  three  hours.  Its 
abruptness  and  violence  are  characteristic.  In  children,  headache,  nausea, 
vomiting,  delirium  and  convulsions  may  usher  in  the  disease,  its  onset 
resembling  that  of  an  exanthem  ;  when  these  do  not  occur  in  all  their  in- 
tensity, the  child  is  restless  or  stupid,  and  there  are  thirst  and  anorexia, 
increasing  towards  night.  Again,  a  child  may  awake  in  the  middle  of  the 
night  with  a  burning  skin,  bounding  pulse,  flushed  face  and  hacking  cough. 
When,  in  children,  the  pneumonia  is  ushered  in  by  convulsions  followed 
by  a  loss  of  consciousness,  the  consolidation  is  usually  at  the  apex, 

A  distinct  chill  is  less  frequent  in  the  pneumonia  of  old  age  ;  yet  when  an 
old  person  has  a  marked  chill  pneumonia  may  always  be  suspected  ;  although 
less  frequent  it  is  more  diagnostic  than  in  adults.  A  protracted  fit  of  shiv- 
ering and  pain  in  the  side  are  the  two  initial  symptoms  in  about  50  per 
cent,  of  the  cases  of  acute  sthenic  senile'  pneumonia.  In  the  other  half  of 
the  cases  the  onset  is  attended  by  slight  increase  in  the  frequency,  and 
irregularity  of  the  respirations,  slight  pyrexia,  short  hacking  cough,  and  a 
feeling  of  great  exhaustion.  Intense  weakness  may  be  the  only  symptom. 
Nausea,  vomiting,  diarrhoea  and  collapse,  or  a  semi -comatose  condition,  not 
infrequently  usher  in  a  senile  lobar  pneumonia.  In  a  very  few  cases,  stu- 
por, coma,  and  disturbance  of  intellect  may  be  the  only  early  noticeable 
symptoms,  and  they  may  persist  during  the  whole  course  of  the  disease. 
The  initial  cliill  (whenever  occurring)  is  rarely  repeated. 

With  the  initial  symptoms  there  is  a  rapid  rise  in  temperature  accom- 
panied by  pain  in  the  side,  which  is  aggravated  by  coughing  and  by  deep 
inspiration.  The  breathing  is  accelerated,  there  is  dyspnoea,  cough,  expecto- 
ration, the  countenance  is  flushed  and  anxious,  there  is  headache,  loss  of 
appetite,  and  intense  thirst.  The  urine  is  scanty  and  dark.  The  bowels  are 
constipated.  The  tongue  is  heavily  coated.  The  symptoms  increase  until 
the  day  of  crisis,  when  they  either  suddenly  remit  and  the  patient  breaks 
out  in  a  profuse  sweat,  or  they  subside  by  lysis.  The  defervescence  is  usually 
reached  between  the  fifth  and  ninth  day. 

The  following  is  an  analysis  of  the  prominent  objective  symptoms  of 
pneumonia : 

The  respiration  is  more  constantly  increased  in  frequency  in  pneu- 
monia than  in  any  other  acute  disease,  and  varies  from  30  to  80  per  min- 
ute. Usually,  in  acute  diseases,  the  respirations  increase  with  the  pulse 
rate  ;  in  lobar  pneumonia  the  ratio  between  pulse  and  respiration  is  early 
perverted.  The  respiration  may  be  80  per  minute  and  the  pulse  rate  not 
more  than  100.  The  acceleration  is  not  in  proportion  to  the  amount  of 
lung  involved,  and  it  does  not  depend  on  the  pain  in  the  chest  or  the  py- 
rexia. It  \^ panting,  not  "catching,"  in  character.  It  may  or  may  not  be 
accompanied  by  dyspnoea.  In  children  accelerated  breathing  is  more 
marked  than  in  adults.  The  discrepancy  between  the  pulse  and  respiration 
is  not  as  marked  as  in  adults  ;  in  the  former  the  pulse  may  range  between 
150  and  160,  and  in  the  latter  between  80  and  90.  Expansion  of  the  nos- 
trils is  an  early  symptom  in  the  pneumonia  of  children.     In  old  age  expi- 


ACUTE   LOBAR   PN"EUMONIA.  81 

ration  is  sudden,  the  whole  act  is  ''  panting."  The  average  number  of  respi- 
rations per  minute  is  22,  and  the  duration  of  inspiration  is  to  that  of  expi- 
ration as  6  to  9.  It  is  rarely  accompanied  by  dyspnoea.  An  exaggeration 
of  (normal)  senile  "  catching  breathing"  is  one  of  the  most  frequent  forms 
of  abnormal  respiration  in  senile  pneumonia. 

Dyspnma,  although  frequent,  is  by  no  means  constant.  It  does  not  de- 
pend upon  the  amount  of  lung  involved,  since  double  pneumonia  may 
be  accompanied  by  less  dyspnoea  than  when  only  a  single  lobe  is  involved. 
It  is  often  so  great  that  the  patient  is  unable  to  lie  down.  The  greatest 
dyspnoea  occurs  where  there  is  marked  nervous  prostration.  In  "  second- 
ary" and  complicated  pneumonia  the  dyspnoea  is  greater  than  in  primary 
uncomplicated  pneumonia  ;  it  is  panting,  not  labored.  In  cMUlren,  dysp- 
noea is  most  marked  when  the  apex  of  the  lung  is  involved.  In  old  age 
dyspnoea  is  so  infrequent  that  even  with  respiration  at  70  they  do  not 
complain  of  difficult  breathing.  When  a  patient  over  seventy  years  who  is 
asthmatic,  or  who  has  chronic  bronchitis,  develops  a  pneumonia,  the  dysp- 
noea that  may  have  accompanied  the  previous  condition  diminislies.  He 
simply  feels  exhausted,  and  usually  dies  suddenly. 

Pain  follows  the  chill  ;  it  is  situated  underneath  the  nipple  of  the  af- 
fected side.  It  is  sharp  and  stabbing,  often  located  over  the  pneumonic 
spot,  and  is  intensified  by  coughing,  sneezing  and  deep  inspirations.  In 
central  pneumonia  there  is  no  pain  ;  it  is  the  pleurisy  that  causes  it.  Pneu- 
monia itself  is  a  painless  disease.  Pain  in  the  affected  side  rarely  continues 
beyond  the  third  or  fourth  day.  If  it  continues  beyond  the  eighth  day  it 
is  evidence  of  pleuro-pneumonia.  It  is  present  in  85  per  cent,  of  all  cases. 
In  old  age  pain  is  never  severe.  It  is  rather  a  dull,  uneasy  feeling  referred 
to  the  whole  chest  or  to  the  abdomen. 

Cough  is  present  in  over  90  per  cent,  of  the  cases.  It  comes  on  within 
twenty-four  hours  after  the  advent  of  the  disease.  At  first  it  is  short, 
'Slacking "in  character.  It  may  entirely  cease  just  before  a  fatal  issue. 
It  is  more  constant  in  children  than  in  adults;  it  is  sometimes  parox- 
ysmal. Old  people  with  pneumonia  often  have  no  cough.  When  present 
it  may  be  so  slight  as  to  escape  the  notice  of  both  patient  and  physician. 
Should  bronchitis  or  asthma  have  preceded  the  pneumonia,  the  cough 
diminishes,  and  may  wholly  disappear  on  the  advent  of  the  latter.  The 
expectoration  is  characteristic.  In  the  first  forty-eight  hours  of  the  dis- 
ease it  is  simply  frothy  mucus.  Then  it  becomes  semi-transparent,  viscid, 
gelatinous  and  tenacious,  but  never  opaque.  So  tenacious  is  it  that  the 
cup  containing  it  may  be  inverted  without  spilling  the  mass.  It  can  be 
drawn  out  between  the  thumb  and  finger  into  thin  strings.  This  tenacity 
in  great  part  causes  the  difficulty  of  expectoration.  Its  color  varies.  About 
the  second  day  the  "brick-dust"  or  "rusty"  sputa  may  be  observed. 
This  color  is  due  to  the  presence  of  blood.  The  sputa  may  be  creamy  and 
yellow,  or  of  a  very  dark  or  prune-juice  color  ;  the  latter  is  indicative  of  a 
depraved  blood  state,  and  occurs  especially  in  alcoholic  subjects.  As  death 
approaches  the  sputa  become  scanty,  less  tenacious,  more  diffluent  and 
often  of  a  greenish  hue.  Greenish  sputa  may  occur  in  the  middle  of  the 
6 


82 


DISEASES   OF  THE   RESPIRATORY   ORGAKS. 


pneumonia  and  during  resolution,  and  in  "bilious  pneumonia."  When  res- 
olution occurs  the  sputum  becomes  abundant,  and  of  a  yellow,  creamy  color. 
There  may  be  no  sputum  throughout ;  or  it  may  not  appear  until  the 
sixth  or  even  the  twelfth  day.  The  sputum  may  remain  brick-dust  till 
the  ninth  or  tenth  day.  In  pneumonia  of  the  apex  and  in  that  compli- 
cating acute  articular  rheumatism  the  sputa  are  often  entirely  wanting. 
In  children  sputa  are  usually  absent ;  but  brick-dust  masses  may  be  de- 
tected in  the  matters  vomited.  In  senile  pneumonia  expectoration  is  never 
an  early  symptom,  and  is  liable  to  cease  suddenly  during  any  period  of 
the  disease.  Rusty  sputa  are  present  in  about  33  per  cent,  only  of  such 
cases  ;  frothy  or  "catarrhal"  sputa  are  the  rule.  A  chocolate-looking 
serous  sputum,  appearing  soon  after  the  onset  of  a  pneumonia,  shows  a 
depraved  condition  and  indicates  "typhoid  pneumonia."  Examined  under 
the  microscope  the  sputum  is  found  to  contain  swollen  spheroidal  red  and 
white  blood  discs,  minute  fat  spherules  and  the  other  elements  described 
under  morbid  anatomy.^  In  about  75  per  cent,  of  cases  there  will  be  found 
in  the  sputa  (when  floated  in  water)  casts  of  the  alveoli  and  bronchioles. 
The  chemical  constituents  of  the  sputa  are  albumen  and  mucin.  Tyrosin 
and  sugar  are  sometimes  found  in  it.     There  are  two  explanations  of  the 

acid  reaction  of  the  sputa  :  Verdeil 
thought  it  due  to  excess  of  pneumic 
acid  ;  Bamberger  claims  that  it  is  due 
to  deficiency  in  alkaline  phosphates.* 
Early  in  pneumonia  there  is  an  increase 
in  the  chloride  of  sodium  in  the  serum, 
and  it  has  been  thought  that,  from  the 
rapid  and  excessive  cell-transformation 
in  the  lung,  chloride  of  sodium  is  at- 
tracted to  that  organ. ^  The  expired  air 
in  pneumonia  is  colder  than  normal, 
and  there  is  a  diminution  in  the  amount 
of  carbonic  acid  excreted. 

The  temperature-range  of  a  typical 
case  of  lobar  pneumonia  indicates  that 
it  belongs  to  a  remittent  or  sub-remit- 
tent type,  rather  than  to  the  class  of  feb- 
rile disorders  marked  by  a  continuously 
high  temperature.  Earely,  it  is  inter- 
mittent. The  temperature  rises  sud- 
denly during  the  initial  chill,  and  in 
two  to  three  hours  after  it  may  range  from  102°  to  105°  F.  After  the  first 
iwenty-four  hours  the  temperature  is  subject  to  morning  and  evening  exacer- 


FiG.  20. 

Temperature  Record  in  a  case  of  Acute  Lobar 
Pneumonia,  ending  in  Recovery. 


'  Dr.  Walshe  affirms  that  pus  cells  are  not  found  in  the  brick-dust  sputum. 

^  Catarrhal  sputa  contain  10  to  14  per  cent,  of  alkaline  phosphates  :  pneumonic  sputa  none.  In  catarrh, 
soda  is  to  potash  as  31  to  20  :  in  pneumonia,  15  to  41.  There  is  .5  per  cent,  more  sulphuric  acid  in  pneu- 
monic sputa  than  in  catarrhal. 

3  In  one  case  where  there  was  no  chloride  of  sodium  in  the  urine,  10  per  cent,  of  the  solid  material  of 
the  sputa  consisted  of  that  sail. 


ACUTE    LOBAR   PNEUMOJSriA. 


83 


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Fig.  21. 

Temperature  Record  in  a  case  of  Acute  Lobar  Pneu- 
monia, with  observations  every  six  liours.  Re- 
covery. 


bations  and  remissions ;  but  the  morning  temperature  is  rarely  2°  F.  lower 
than  the  evening — the  difference  in  the  .SMZ>-remittent  type  may  amount  to 
only  -^-°  or  1°  F.  At  midnight  a  second  exacerbation  may  occur,  but  not  so 
marked  as  that  occurring  early  in 
the  evening.  Rarely,  remissions 
occur  in  the  evening  and  exacerba- 
tions in  the  morning.  The  tem- 
j)erature  is  usually  highest  on  the 
evening  of  the  third  day.  In  some 
cases  the  maximum  is  not  reached 
till  a  few  hours  before  the  crisis. 
Just  before  death  the  tempera- 
ture may  rise  very  high,  even  to 
1091°  F.  If,  after  the  fourth  day, 
a  marked  remission  is  followed  by 
a  high  temperature,  it  indicates 
either  an  extension  of  the  pneu- 
monia, or  the  occurrence  of  some 
active  complication.  If,  in  a  mild 
pneumonia,  the  temperature  sud- 
denly rises,  it  indicates  a  grave 
complication.  The  sudden  fall  of 
temperature  on  the  fifth  or  sixth 

day  indicates  a  crisis,  and  the  beginning  of  convalescence  :  it  may  occur  in 
the  morning  or  after  the  evening  exacerbation.  In  a  typical  case  it  is  usual 
to  find  the  temperature  on  the  morning  of  the  fifth,  sixth,  or  seventh  day 
two  or  more  degrees  lower  than  on  the  preceding  night.  Then  it  falls 
gradually  until  a  normal,  often  a  subnormal  temperature  is  reached.  The 
crisis  may  show  itself  by  successively  increasing  remissions,  while  the  tem- 
perature during  the  exacerbations  rises  to  the  same  height  as  before.  It  is 
usual  for  the  remission  to  be  exaggerated  just  before  the  crisis ;  again, 
the  fever  may  reach  its  highest  point  Just  before  the  final  fall.  When 
the  temperature  declines  gradually  {"lysis"),  a,  normal  point  is  visu- 
ally reached  by  the  ninth  day,  sometimes  not  until  the  twelfth  or 
fourteenth.  A  protracted,  slow  fall  is  met  with  oftenest  in  the  weak, 
debilitated,  and  in  those  who  have  been  bled  or  depressed  by  treatment. 
A  continuously  high  temperature  after  the  tenth  day  indicates  purulent 
infiltration.  (See  Fig.  19.)  Pneumonia  at  the  apex  has  the  highest 
temperature  range.  The  fifth  and  seventh  are  the  days  of  crisis  in  the 
majority  of  uncomplicated  cases.  Of  867  cases,  677  ended  before  the 
eighth  day.  Neither  the  height  of  the  fever  nor  the  amount  of  lung  in- 
volved influences  the  day  of  crisis.  In  hilious  pneumonia  occurring  in  mi- 
asmatic regions,  the  temperature  is  paroxysmal.  In  children  the  tempera- 
ture rises  very  rapidly,  sometimes  reaching  106°  in  the  first  twelve  hours. 
The  highest  recorded  temperatures  are  in  the  pneumonias  of  children.  The 
critical  fall  is  remarkable,  the  temperature  quite  often  reaching  2°  to  2^** 
5e?ow  normal.     This  low  temperature  may  continue  two  or  three  days.     In 


84 


DISEASES    OF   THE   KESPIRATOKT   OEGAN"S. 


old  age  it  is  mainly  by  the  temperature  that  the  exact  time  of  invasion  ia 
determined.  The  rectal  temperature  may  be  103°  to  104''  on  the  first  days, 
and  then  continue  at  the  initial  point  for  three  or  four  days^  with  morning 
and  evening  oscillations  of  a  degree  or  l|-°.  The  temperature  does  not  be- 
gin to  rise  until  several  hours  after  the  chill,  if  the  chill  occur.  (See  Fig. 
21. 

^he  pulse  varies  with  the  severity,  extent  and  stage  of  the  pneumonia. 
In  mild  cases  it  ranges  from  90  to  120  ;  if  it  continues  above  120  the  case  is 

severe.     The  pulse  is  soft 

full 


l^a.y 


xof 


J03. 


^r 


/ 


5 


n 


^ 


z^ 


^ 


m 


Z=?5 


^23^ 


/O 


// 


/-2 


^    Later   it 


and 


Fig.  22. 


at    the    onset. 

becomes  small 
and  feeble.  In  severe 
cases,  and  when  the  ner- 
vous system  is  markedly 
implicated,  it  is  rapid, 
small  and  feeble,  and  may 
be  130  to  140  or  160  at 
the  onset.  High  temper- 
ature is  usually  accom- 
panied by  a  rapid  pulse, 
and  vice  versa.  When  the 
critical  fall  of  tem|)era- 
ture  occurs,  the  pulse 
falls  correspondingly. 
After  the  third  or  fourth 
day    the    pulse    exhibits 

Temperature  Record  in  a  case  of  Acute  Lobar  Pneumonia  passing   dlCroHsm    IXi    many  CaSCS  I 
into  purulent  infiltration  and  ending  in  Death  on  the  12th  day.         • ,  ,  .     ■, 

it  may  be  jerky,  very 
compressible  and  intermittent.  Just  before  death,  it  becomes  markedly 
slow  in  many  instances.  It  is  not  the  most  extensive  pneumonia  that 
is  accompanied  by  the  greatest  flagging  of  the  heart.  Heart-failure  may 
exist  before,^  or  just  as  hepatization  is  commencing.  The  pneumonia 
with  the  highest  temperature  is  not  the  one  where  heart  failure  is 
most  marked  or  occurs  earliest.  When  the  heart  is  failing,  the  pulse 
shows  that  the  artery  is  unequally  filled  by  each  beat.  First,  the  force 
varies  ;  then  waves  occur,  and  finally  true  intermission.  I  have  been  able 
to  detect  heart-insufficiency  by  these  variations  in  the  pulse  within  twenty- 
four  hours  after  the  onset  of  the  pneumonia,  and  occasionally  during  the 
initial  chill.  In  children  the  pulse-rate  is  greatly  increased  :  it  may  be  200 
per  minute.  It  is  small,  unequal  and  irregular,  but  never  intermittent.  In 
senile  pneumonia  the  pulse  is  not  a  reliable  indication.  Its  average  rate  is 
73  to  78  ;  rarely  does  it  reach  120.  In  old  age,  both  in  health  and  disease, 
the  pulse  has  a  fictitious  hardness,  on  account  of  arterial  rigidity.  It  may 
not  be  irregular  or  intermittent  when  the  heart  is,  and  vice  versd.  Inter- 
mittence  of  the  pulse  in  senile  pneumonia  is  common,  independent  of  any 
cardiac  disturbance.  In  all  cases  of  senile  pneumonia,  the  pulse  should  he 
counted  at  the  heart. 


ACUTE   LOBAR   PNEUMONIA.  85 

The  shin  is  often  hot  and  dry  until  the  crisis  ;  but  it  may  be  bathed  in 
perspiration  from  the  onset.  A  moist  surface  is  regarded  as  a  favorable 
sign,  but  when,  at  the  acme  of  the  disease,  the  parched  skin  becomes  moist 
and  the  patient  is  not  relieved,  it  is  an  unfavorable  symjDtom.  In  most 
cases,  the  expression  of  the  countenance  is  characteristic.  The  face  is  anx- 
ious, and  over  the  malar  bones  is  a  mahogany  flush,  not  diffused  as  in  ty- 
phus fever,  but  well  defined  and  circumscribed  ;  it  is  called  the  ^^pneu- 
monic sjjot."  The  rest  of  the  face  is  pale.'  Usually,  one  cheek  is  more 
flushed  than  the  other ;  this  is  due  to  disturbance  of  the  vaso-motor  sys- 
tem. When  there  is  a  great  disturbance  of  the  circulation,  or  when  vaso- 
motor disturbance  is  excessive,  the  lips  become  cyanosed.  At  the  time  of 
the  crisis  the  lips  become  pale.  In  about  50  per  cent,  of  cases,  pneumonia 
is  attended  by  an  herpetic  eruption  upon  the  cheeks,  nose,  li2)s  or  eyelids. 
It  is  rare  before  the  second  or  third  day,  and  it  may  not  occur  until  the 
crisis  is  reached.  Herpes  occurs  with  varying  frequency  in  different  years, 
and  is  more  commonly  met  with  in  pneumonia  than  in  any  other  febrile 
disease.  One  winter,  nearly  every  case  of  pneumonia  in  Bellevue  Hospital 
was  accompanied  by  "herpes  labialis."  Sudamina  may  accompany  profuse 
sweatings.  In  children,  while  the  surface  of  the  body  is  hot  and  dry,  the 
extremities  are  cool,  and  the  pneumonic  flush  is  bluish  or  violet-colored. 
Cyanosis  of  the  extremities  is  more  frequent  than  in  adults,  and  herpes  la- 
bialis is  more  constant.  All  the  cutaneous  symptoms  are  exaggerated  in 
children.  In  old  age  the  pneumonic  flush  is  often  the  first  objective  sign 
of  pneumonia.  The  eyelids  alone  are  cyanotic.  If  the  face  is  at  first 
dusky,  it  later  assumes  a  sallow  hue,  and  the  surface  heat  is  succeeded 
by  a  cold,  clammy  perspiration. 

The  cerebral  symptoms  are  not  very  significant  in  the  early  stages  of 
pneumonia.  Headache  is  the  first  to  occur,  and  may  continue  throughout 
the  entire  course  of  the  disease.  It  usually  diminishes  after  the  third  day. 
When  severe  in  the  evening  there  will  be  slight  delirium  at  night,  so  slight 
as  often  to  escape  notice.  Delirium  and  convulsions  rarely  occur  except 
in  the  debilitated  and  in  those  of  dissipated  habits.  It  is  most  frequently 
met  with  in  drunkards,  and  then  assumes  the  character  of  delirium  tre- 
mens. Sometimes  in  non-alcoholic  pneumonia  the  delirium  assumes  an 
active,  violent  character.  Whenever  delirium  is  present  it  is  important 
to  make  diligent  search  into  the  former  habits  of  the  patient.  Pneumonia 
of  the  apex  is  oftenest  accompanied  by  severe  cerebral  symptoms.  The 
delirium  may  pass  into  coma.  When  delirium  and  headache  are  marked 
symptoms,  muscular  tremors  ("subsultustendinum")  are  very  apt  to  occur 
with  insomnia  and  frightful  hallucinations.  These  cerebral  symptoms 
occur  so  early  and  are  so  marked  in  alcohol  drinkers  that  they  mask  the 
pneumonia  ;  a  physical  exploration  alone  reveals  the  disease.  When  de- 
lirium is  present  in  the  weak  and  feeble  it  is  of  the  low,  muttering, 
"  typhoid "  type,  and  soon  passes  into  a  state  of  stupor.     Photophobia, 

'  Bouillard  regards  the  flush  as  best  mai-ked  in  pneumonia  of  the  apex.  Some  regard  the  flush  as  best 
marlied,  or  existing  solely,  on  the  cheek  corresponding  to  the  affected  side  ;  others  us  on  the  opposite 
side.  —Juccoud. 


86  DISEASES   OF   THE   KESPIRATORY    ORGANS. 

disturbances  of  vision,  and  deafness  are  rare.  In  cliildren  the  cerebral 
symptoms  are  more  prominent  than  in  adults.  Stupor  and  restlessness  on 
the  one  hand,  or  headache,  delirium  and  convulsions  on  the  other,  may 
usher  in  pneumonia  in  children,  and  they  may  rapidly  pass  into  a  semi- 
comatose condition.  Convulsions  are  as  common  in  children  as  they  are 
rare  in  adults.  They  may  be  general,  resembling  those  of  epilepsy 
("Eclamptic  Pneumonia"),  or  they  may  attack  single  muscles  or  groups. 
Tetanus  and  opisthotonos  are  uncommon.  Delirium  and  coma  occurring 
late  are  usually  followed  by  fatal  coma.  The  cerebral  disturbances  often 
strikingly  resemble  those  of  acute  meningitis.  In  senile  pneumonia  head- 
ache may  persist  throughout  the  disease.  It  is  usually  accompanied  by 
mild  delirium,  especially  when  the  pneumonia  is  at  the  apex.  It  is  a  busy, 
active  delirium,  and  the  patient  has  a  constant  desire  to  get  out  of  bed. 

The  symptoms  referable  to  the  digestive  tract  are  not  important. 
Nausea  and  vomiting  are  among  the  initial  symptoms,  and  occur  in 
about  75  per  cent,  of  cases.  At  first  the  tongue  is  covered  with  a  white 
fur ;  later  it  becomes  dry.  Anorexia  is  marked,  and  thirst  is  intense. 
The  lips  and  tongue  may  become  brown,  dry  and  cracked,  and  sordes 
collect  on  the  teeth.  Diarrhoea  may  be  an  initial  symptom  ;  it  usually 
accompanies  nausea  and  vomiting.  The  bowels  are  usually  constipated. 
In  children  nausea  and  vomiting  are  not  only  common,  but  in  25  per 
cent,  usher  in  the  pneumonia.  They  usually  cease  by  the  second  day. 
Persistent  diarrhcea  often  precedes  death.  In  senile  pneumonia  the  tongue 
early  becomes  dry,  brown  and  shrivelled,  and  is  protruded  with  difficulty. 
Although  these  patients  may  not  complain  of  thirst,  they  drink  with 
avidity  when  fluid  is  placed  to  their  lips.  Dysphagia  is  frequent.  At  the 
crisis  critical  diarrhoea  is  more  frequent  than  critical  sweats.  Loss  of 
strength  occurs  early,  and  is  more  marked  in  pneumonia  tlian  in  any  other 
acute  disease  except  typhus  fever.  Eecovery  is  rapid  when  convalescence 
begins. 

The  wrme  in  pneumonia  is  scanty,  high  colored  and  of  high  specific  grav- 
ity. The  amount  of  urea  and  uric  acid  excreted  is  two  or  three  times 
more  than  normal ;  it  increases  until  the  crisis,  and  then  suddenly  dimin- 
ishes, falling  below  normal.  Inorganic  salts,  chloride  of  sodium  especially, 
are  constantly  diminished  and  may  be  wholly  absent.  Eeappearance  of  the 
chlorides  marks  the  approach  of  convalescence.  At  the  crisis  they  are 
present  in  excess.  Urea  and  uric  acid  are  also  sometimes  retained  in  the 
system  ;  and  at  the  crisis  there  will  then  be  a  critical  diarrhoea  followed 
by  prolonged  convalescence.  Bile  pigment  and  sometimes  the  bile  acids 
appear  in  the  urine.  Slight  albuminuria  is  present  in  35  per  cent,  of  the 
cases.     The  severer  the  pneumonia  the  more  marked  the  albuminuria. 

Epistaxis  may  occur  at  any  time,  but  is  most  frequent  at  the  onset  and 
at  the  crisis.  Swelling  of  the  veins  of  the  hands  in  children  is  an  unfavor- 
able symptom .  When  pneumonia  is  to  terminate  fatally  dyspnoea  greatly 
increases,  the  patient  suddenly  "  sinks,"  the  pulse  becomes  small,  rapid, 
intermittent  and  dicrotic  ;  moist  rales  are  heard  in  the  larger  bronchi  or 
trachea,  and  there  are  physical  evidences  of  pulmonary  oedema.     The  sputa 


ACUTE   LOBAE   PNEUMONIA.  87 

become  frothy,  liquid,  and  blood-stained  ;  they  may  be  entirely  suppressed. 
The  respirations  are  more  and  more  hurried,  and  the  radial  pulse  becomes 
imperceptible.  The  face  is  sunken  and  livid ;  the  extremities  become 
cold,  and  the  capillary  circulation  more  and  more  imperfect.  Tlie  body  is 
bathed  in  a  profuse  cold  sweat.  Death  is  usually  preceded  by  a  semi-coma- 
tose state.  The  temperature  may  steadily  rise  up  to  the  time  of  death,  or 
there  may  be  "  defervescence."  Death  may  occur  at  any  period  of  the  dis- 
ease. In  alcoholic  pneumonia  death  is  preceded  by  active  brain  symptoms. 
In  children  death  is  often  preceded  by  convulsions  or  coma ;  sometimes 
exhaustion  or  collapse  is  most  marked.  Cyanosis  and  extreme  rapidity  of 
pulse  are  common  in  children  before  death. 

Senile  jpneumonia  may  end  fatally  within  a  few  hours  after  the  onset 
in  a  most  unexpected  and  quiet  manner.  In  other  cases  sallowness  of  the 
skin,  cold,  clammy  sweat,  working  of  the  auxiliary  muscles  of  respiration, 
a  feeble,  rapid,  irregular  and  intermittent  pulse,  and  a  sudden  rise  or  fall  of 
the  temperature  may  precede  the  fatal  issue. 

Abscess. — Acute  pneumonia  terminates  in  abscess  in  \\  to  3  per  cent,  of  all 
cases.  It  is  met  with  oftenest  in  debilitated  weak  subjects.  The  sputa  are 
copious  and  fetid,  yellowish  in  color,  consisting  almost  wholly  of  pus.  The 
fever  is  of  the  hectic  type,  and  is  accompanied  by  rigors  and  sweats.  The 
patient  grows  weak  and  emaciated,  death  resulting  from  exhaustion,  from 
asphyxia,  or  from  discharge  of  the  abscess  into  some  neighboring  cavity  or 
organ. ^  The  physical  signs  of  the  cavity  are  the  most  reliable  evidences 
of  an  abscess.  Abscess  is  rare  in  children.  In  old  age  there  are  no  well- 
marked  signs. 

Gangrene  as  a  termination  of  pneumonia  has  been  found  in  about  14 
per  cent,  of  cases.  This,  however,  is  an  exceptionally  high  percentage. 
Its  occurrence  is  marked  by  signs  of  sudden  collapse.  The  pulse  is  raj^id, 
feeble  and  intermittent ;  the  face  is  pale  and  "death-like  ;  "  there  is  pro- 
fuse expectoration  of  blackish-green  masses  containing  shreds  of  decom- 
posed lung  substance  having  a  gangrenous  odor.  The  breath  is  offen- 
sive and  the  body  has  a  cadaverous  smell.  The  sickening  odor  of  pul- 
monary gangrene  is  most  perceptible  after  coughing.  Gangrene  has  its  seat 
in  the  lower  lobes  of  the  lung,  and  it  is  here  we  must  search  for  its  ill-defined 
physical  signs.  In  old  age  when  pneumonia  is  to  terminate  in  gangrene 
typhoid  symptoms  are  present  early  and  death  occurs  in  collapse,  usually 
within  five  days  from  the  onset. 

Purulent  infiltration  has  symptoms  that  differ  but  slightly  from  those 
of  the  third  stage  of  pneumonia.  When  resolution  does  not  take  place  at 
the  period  of  crisis  and  the  temperature  remains  high,  accompanied  by 
symptoms  of  prostration  and  profuse  purulent  expectoration,  purulent 
infiltration  may  be  suspected.  Somnolence  and  mild  delirium  'are  quite 
frequent  during  "  purulent  infiltration."  The  sputum  contains  a  large 
number  of  cells  in  various  stages  of  fatty  degeneration.  The  fever  has 
regular  evening  exacerbations,  and  it  may  range  higher  than  at  any  other 

1  Fox  and  Green  state  that  abscess  is  located  preferably  at  the  apex  ;  Da  Costa  says  at  the  base.— Guy's 
Hospital  Reports.    Ser.  VII.  1848. 


88  DISEASES   OF   THE    RESPIRATORY    ORGANS. 

period  in  the  disease.  The  tongue  becomes  brown  and  dry,  and  sorde* 
collect  on  the  teeth  and  mouth.  Eecovery  is  slow  and  convalescence 
tedious.     Death  results  from  exhaustion. 

Typlioid  pneumonia  is  a  term  that  has  been  applied  to  a  pneumonia 
attended  by  tyj)hoid  symptoms.  It  has  also  been  called  ''asthenic," 
*'  low,"  or  "nervous  "  pneumonia.  It  is  marked  by  extreme  prostration  that 
may  exist  from  the  onset.  In  the  majority  of  cases,  well-marked  pneumonic 
symptoms,  after  having  been  present  for  a  short  time,  soon  give  place  to 
intense  nervous  prostration  and  adynamic  symptoms.  There  is  no  sputa, 
no  dyspnoea,  no  pain,  no  cough.  Sordes  collect  on  the  teeth  and  gums. 
The  tongue  is  thickly  coated,  and  later,  covered  with  black  crusts.  There 
is  incontinence  or  retention  of  urine.  The  pulse  is  small  and  rapid.  There 
is  stupor,  somnolence,  and  continual  low,  muttering  delirium.  This  form 
is  common  in  the  aged.  In  some  cases  there  is  marked  disturbance  of  the 
special  senses — the  speech  being  most  affected.  Tremor  and  subsultus 
tendinum  are  frequent.  Typhoid  pneumonia  may  be  accompanied  by 
glandular  swellings,  sharp  and  darting  muscular  pains,  arthritic  symptoms 
or  vomiting.  It  is  not  infrequent  in  epidemics,  and  it  may  follow 
Bright's  disease,  erysipelas,  alcoholismus,  or  phlebitis.  Eecovery  is  always 
possible,  but  is  slow  and  tedious,  and  may  not  begin  until  the  twelfth  or 
fourteenth  day.  A  modification  of  typhoid  pneumonia  sometimes  accom- 
panies dysentery,  intestinal  catarrh  or  phlegmonous  gastritis.  There  is 
great  sweating,  profuse  colliquative  diarrhoea  and  high  fever. 

Bilious,  or  gastric  pneumonia,  is  lobar  pneumonia  occurring  in  mala- 
rial districts,  and  accompanied  by  gastro-enteritis  with  hepatic  symptoms. 
It  is  sometimes  called  "malarial  pneumonia."  It  has  the  characteristics 
of  a  severe  pneumonia,  but  the  fever  is  paroxysmal.  The  tongue  is  heavily 
coated ;  nausea  and  vomiting  are  common  and  may  be  persistent.  The 
epigastrium  is  distended  and  tender,  the  skin  more  or  less  jaundiced  ;  the 
liver  is  enlarged,  and  there  is  constipation  or  exhausting  diarrhoea ;  the 
latter  is  accompanied  by  greenish-black,  viscid  and  inodorous  discharges. 
"  Bilious"  pneumonia  may  be  sthenic  or  asthenic  ;  but  prostration  is  apt 
to  be  nearly  as  marked  as  in  the  typhoid  variety.  The  symptoms  of  bilious 
pneumonia  have  frequently  led  to  the  diagnosis  of  ^^  typlioid  gastric 
fever.''"'  It  runs  a  much  more  protracted  course  and  has  a  much  longer 
period  of  convalescence  than  the  typhoid  variety  ;  vomiting  is  "bilious," 
and  somnolence  and  stupor  may  indicate  a  fatal  issue. 

Latent  pneumonia  seldom  occurs  in  adults  unless  it  complicates  some 
disease  whose  symptoms  are  so  severe  that  the  pneumonia  is  obscured. 
Inter-current  senile  pneumonia  is  always  latent;  and  Grisolle  states  that 
a  physical  exploration  gives  negative  results  in  the  majority  of  instances. 
Senile  pneumonia  may  run  its  course  without  expectoration,  dyspnoea, 
flushed  face  or  physical  signs.  Its  diagnosis  is  then  difficult.  It  is  to  be 
remembered  that  of  all  phlegmasia  of  advanced  life,  pneumonia  is  the 
most  frequent ;  and  of  all  the  acute  diseases  of  advanced  life  it  causes  the 
highest  temperature  range  and  the  greatest  prostration.  When  an  old 
person  has  a  slight  rigor,  followed  by  a  febnle  movement  attended  by  great 


ACUTE    LOBAR   PNEUMONIA.  89 

prostration  for  which  there  is  no  explanation,  pneumonia  may  be  suspected 
even  though  all  its  usual  signs  are  absent. 

Intermittent  'pneumonia,  which  is  by  some  described  as  a  distinct  type, 
is  a  form  of  acute  pneumonia  in  which  a  malarial  element  is  so  pronounced 
that  all  the  subjective  and  even  the  physical  signs  undergo  distinct  inter- 
missions, returning  each  day  with  increased  severity.  It  may  assume  the 
quotidian  or  the  tertian  type.  During  the  intermission  the  temperature 
may  fall  to  the  normal.  Recurring  chills  and  sweats  are  often  present ; 
and  the  pneumonia  is  not  infrequently  double.  By  some  it  is  regarded  as 
peculiar  to  old  age ;  it  is  very  rare  at  any  other  period.  Those  malarial 
influences  that  give  rise  to  this  type  of  pneumonia  are  more  frequently  met 
with  in  our  Southern  and  Western  States  than  in  any  other  part  of  the 
world. 

Physical  Signs. — First  Stage,  or  Stage  of  Congestion.— The  physical  signs 
indicative  of  the  first  stage  of  lobar  pneumonia  are  usually  present  within 
twenty-four  hours  after  its  invasion.  If  the  pneumonia  commences  in  the 
central  portion  of  the  lung  their  appearance  may  be  delayed  till  the  third 
day.  By  studying  these  signs  in  connection  with  tlie  anatomical  stages  of 
the  disease  their  importance  in  diagnosis  and  prognosis  can  best  be  appre- 
ciated. 

Inspection. — The  movements  of  the  affected  side  are  more  or  less  re- 
stricted. The  unaffected  side  moves  as  in  health.  In  double  pneumonia 
the  respiratory  movements  will  assume  the  costal  type,  attended  by  increase 
in  the  abdominal  breathing. 

Palpation. — There  is  more  or  less  marked  increase  m  the  vocal  fremitus 
over  the  affected  lung;  the  degree  of  increase  corresponding  to  the  extent 
of  the  congestion. 

Percussion. — There  is  slight  dulness  over  that  portion  of  the  chest 
which  corresponds  to  the  affected  portion  of  the  lung.  It  is  not  well  marked 
until  the  end  of  this  stage,  although  the  pulmonary  capillaries  are  engorged 
with  blood  from  the  very  first.  Even  at  the  end  of  this  stage  there  some- 
times remains  a  slight  tympanitic  note.  Very  extensive  central  pneumonia 
may  fail  to  give  any  signs  until  the  second  stage  is  reached.  Absolute 
dulness  in  this  stage  is  very  rare. 

Auscultation. — During  the  ^^dry"  stage — which,  according  to  some, 
precedes  the  exudation — there  will  be  noticed  a  feebleness  and  unnatural 
dryness  of  the  respiratory  murmur.  This  murmur  is  sometimes  harsh, 
sometimes  weaker  than  normal,  losing  the  '^ breezy,"  rustling  quality  of 
normal  breathing.  Elsewhere  it  is  exaggerated.  As  soon  as  the  conges- 
tion is  well  marked,  fine  crackling  sounds  are  neard  at  the  end  of  inspira- 
tion— ''  crepitant  rdles  " — which  have  been  regarded  as  characteristic  of 
this  first  stage,  but  which  are  usually  pleuritic  crepitation.  These  sounds 
resemble  those  produced  by  throwing  salt  on  hot  coals  or  rubbing  the  hair 
between  the  fingers.  They  are  as  numerous  as  they  are  minute,  are  un- 
affected by  coughing,  and  remain  audible  for  from  twelve  to  twenty-four 
hours.  This  rale  is  of  an  unvarying  character,  and  continues,  i.  e.,  is  not 
inter-  or  remittent.     If  the  pneumonic  stages  succeed  each  other  in  rapid 


90  DISEASES   OF   THE   EESPIRATORT   ORGANS. 

succession,  the  crepitant  rale  may  not  be  heard.  They  are  rare  in  pneumonia 
developed  with  acute  articular  rheumatism.  The  respiratory  murmur  is 
feeble  or  assumes  a  broncho-vesicular  character.  Bronchial  breathing  may 
be  heard  in  this  stage  {Traube).  The  voice  sounds  are  slightly  increased 
in  intensity  over  the  engorged  spot.  In  children  the  "  pneumonic  crepita- 
tion ■'  is  usually  absent ;  and  though  it  may  be  heard  at  the  end  of  a  full 
inspiration  after  crying,  it  is  never  as  fine  or  as  distinct  as  in  adults.  There 
will  be  no  marked  increase  in  vocal  fremitus.  In  old  age  the  physical 
signs  are  modified  by  a  more  complete  bony  union  of  the  chest  walls,  by 
curvature  of  the  spine,  rigidity  of  the  bronchial  tubes,  by  the  rounded 
form  of  the  chest,  and  by  senile  rarefaction  of  the  lungs. 

Second,  or  Stage  of  Red  Hepatization. — The  physical  signs  of  this  stage  are 
more  diagnostic  than  those  of  either  of  the  other  stages. 

Inspection  shows  the  expansive  movements  of  the  affected  side  more 
markedly  diminished  than  in  the  first  stage  ;  while  those  of  the  other  side 
are  increased.     There  may  be  absolute  loss  of  motion  over  the  affected  lung. 

Palpation. — There  is  usually  marked  increase  in  the  vocal  fremitus  over 
the  consolidation.  In  some  instances  this  is  so  slight  that  no  difference  can 
be  detected.  Very  rarely  it  is  less  than  on  the  normal  sid«.  The  heart 
may  be  slightly  displaced.  Earely  can  pulsation  be  felt  over  th^^i  inflamed 
lung.  The  majority  of  authorities  regard  this  pulsation  as  due  to  increased 
pulsation  in  the  arteries  of  the  inflamed  spot,  but  there  is  ne  reason  to 
doubt  that  the  cardiac  impulse  itself  can  be  transmitted  through  t)io  solid- 
ified lung  as  well  as  the  arterial  impulse  or  the  vibrations  from  the  ^Jiordm 
vocales.  In  central  pneumonia,  vocal  fremitus  may  be  normal.  Pleuritic 
effusions  mask  the  signs. 

Percussion. — There  is  marked  dulness  over  that  portion  of  the  lung- 
which  is  the  seat  of  the  pneumonia.  Over  the  unaffected  lung  there  is  ex- 
aggerated resonance.  The  nearer  the  hepatization  to  the  surface  the  more 
marked  the  dulness.  There  is  a  sense  of  resistance  accompanying  the  per- 
cussion. A  pneumonic  lung  is  more  resistant  than  any  other  form  of  con- 
solidated lung.  When  an  entire  lobe  is  consolidated  its  exact  outlines  can 
be  defined.  The  percussion  may  have  a  tympanitic  quality  anteriorly, 
but  there  will  always  be  dulness  posteriorly.  There  may  be  slight  tympa- 
nitis Just  around  the  pneumonic  spot.  When  an  entire  upper  lobe  is  con- 
solidated a  tympanitic  percussion  sound  may  be  caused  by  vibration  of  the 
air  in  a  large  bronchus.  The  "  cracked-pot  sound  "  is  occasionally  met 
with  in  pneumonia  over  the  relaxed  and  permeable  parts  of  the  lung  in  the 
immediate  vicinity  of  the  consolidation.  When  heard  over  the  condensed 
portion  it  is  caused  by  the  sudden  expulsion  of  air  from  the  large  bron- 
chus. This  occurs  most  frequently  in  the  young  with  thin  chest  walls.  In 
basic  pneumonia  the  percussion  note  under  the  clavicle  of  the  affected  side 
may  be  amphoric. 

Auscultation. — As  soon  as  the  air-cells  are  completely  filled  with  the 
pneumonic  exudation  the  crepitant  rdles  cease,  and  bronchial  respiration 
is  heard  over  the  affected  lung.  It  often  has  a  metallic  character  ;  or  it  may 
sound  like  tearing  a  piece  of  linen.     Bronchial  respiration  is  more  intense 


ACUTE    LOBAR    PNEUMONIA 


91 


in  pneumonia  than  in  any  other  disease.^  At  the  commencement  of  the 
second  stage  tubular  breathing  attends  expiration  only.  Later,  it  accom- 
panies both  acts.  Pleuritic  exudation  may  mask  the  auscultatory  signs. 
Plugging  of  a  large  bronchus  will  prevent  tubular  breathing  ;  a  violent  fit 
of  coughing  may  allow  it  to  occur  when  the  mucus  is  dislodged.  The 
voice  sounds  are  increased  in  intensity,  and  bronchophony  is  heard  over 
the  whole  of  the  consolidated  lung.  Bronchophony  has  the  same  diagnos- 
tic significance  as  bronchial  respiration  because  it  is  produced  by  the  same 
physical  condition  of  the  lung.  When  the  pleural  cavity  is  partly  filled 
with  fluid,  bronchophony  is  indistinct  or  absent  below  the  level  of  the  fluid; 
while  at  the  level  the  voice  sounds  may  be  asgophonic.     Pectoriloquy  may 


First  stage. 


Diminished  respiratory  movements 

Slight  diilness  on  percussion 

Broncho-vesicular  breathing 

Crepitant  rales 

.  Slight  increase  of  vocal  resonance  .. 


Second  stage.   - 


I^st  movement 

Increased  vocal  fremitus 

Complete  dulness  on  percussion. 

Bronchial  respiration 

.  Bronchophony 


f  Returning  respiratory  movemen'-. 
Diminishing  dulness 


Third  stage. 


Bronchial,  giving  place  to 
Broncho-vesicuiar  breathing 

EaZeredux 


Pig.  23. 


Diagram  Illustrating  the  Physical  Signs  in  the  Three  Stages  of  Lobar  Pneumonia, 

be  heard  independent  of  fluid  in  the  pleural  cavity.  The  heart  sounds  are 
abnormally  intense.  In  children  dulness  is  especially  marked  in  the  infra- 
clavicular region.  Some  speak  of  a  feeling  of  greater  solidity  below  than 
above  the  scapula  which  can  be  perceived  before  the  ear  can  detect  dulness 
on  percussion.  Vocal  fremitus  may  be  increased,  but  this  is  not  always 
to  be  expected.  In  old  age,  inspection  and  palpation  give  negative  results. 
What  is  dull  on  percussion  in  old  age  might  be  regarded  as  resonant  in 


1  Laennec  taught  that  bronchial  respiration  was  due  to  the  superior  conducting  power  of  condensed 
lung.  Skoda  combats  this  view,  and  s.iys  that  bronchial  respiration  is  generated  or  magnified  in  caverns 
and  in  the  bronchi  of  condensed  lung  substance  by  the  air  in  the«e  cavities  and  bronchi  vibrating  in  con- 
sonance with  that  of  the  trachea  ;  the  condition  necessary  for  this  consonMnce  is  provided  in  the  circunk- 
stance  that  the  air  is  pent  up  in  confined  spaces  whose  solid  walls  reflect  the  sonorous  undulations. 


92  DISEASES    OF    THE    EESPIRATOEY    ORGANS. 

adults.  Hence  dulness  on  percussion  is  a  relative  term  in  senile  pneumo- 
nia. When  the  pneumonia  is  superficial  there  is  actual  dulness.  Tubu- 
lar or  bronchial  breathing  marks  the  second  stage,  and  is  even  more  intense 
than  in  adult  life.  Small  gurgles  or  mucous  rales  are  heard  in  this  stage. 
Bronchophony  is  not  very  common,  and  never  distinct,  ^gophony  is  fre- 
quent. By  causing  the  aged  patient  to  cough  and  expire  violently  tubular 
breathing  may  be  heard. 

Third,  or  Stage  of  Oray  Hepatization. — There  is  no  abrupt  transition 
from  the  second  to  the  third  stage  ;  the  physical  signs  of  early  gray  hepati- 
zation are  the  same  as  in  the  second  stage. 

Inspection. — As  resolution  progresses,  expansive  motion  on  the  affected 
side  becomes  more  and  more  apparent. 

Palpation. — Vocal  fremitus  gradually  diminishes. 

Percussion. — Dulness  becomes  less  and  less  marked.  Of  all  the  signs 
this  is  the  last  to  disappear.  As  the  percussion  sound  becomes  more  and 
more  resonant  the  tympanitic  note  is  again  heard  in  spots.  It  is  a  long 
while  before  normal  pulmonary  resonance  is  re-established.  The  dulness 
may  disappear  in  patches.  As  the  dulness  diminishes  the  pitch  of  the 
percussion  note  rises. 

Auscultation. — The  bronchial  respiration  that  was  present  in  the  second 
stage  gives  place  to  broncho-vesicular  breathing,  which  soon  becomes 
*^ blowing,"  then  indeterminate,  dindi  finally  normal.  Bronchophony  gives 
way  to  exaggerated  vocal  resonance.  In  connection  with  these  changes  in 
the  respiratory  and  vocal  sounds  the  crepitant  rale  returns,  but  is  soon 
obscured  by  larger  and  moister  crepitating  sounds — the  ''resolving  sub- 
crepitant  rale  "  of  pneumonia — the  "rale  redux.''^  Large  and  small  mucous, 
sibilant,  and  sonorous  rales  accompany  the  sub-crepitant  sounds,  to  disap- 
pear only  when  resolution  is  complete.  Not  infrequently  the  bronchial 
rdles  that  are  developed  during  the  stage  of  resolution  are  "  consonant  "  or 
ringing.^ 

The  physical  signs  of  this  stage  are  all  retrogressive,  and  they  disappear  in 
the  opposite  order  to  that  in  which  they  appeared.  In  rare  cases  resolution 
is  so  rapid  that  the  sub-crepitant  rale  is  not  developed.  In  this  class  of 
cases  bronchial  breathing  and  dulness  on  percussion  continue  for  some 
time  after  the  crisis. 

If  the  consolidated  lung  becomes  the  seat  of  purulent  infiltration,  the 
temperature  remains  high  and  symptoms  of  great  prostration  are  developed. 
Bronchial  breathing  continues,  and  becomes  more  intense,  dulness  persists, 
and  when  rales  occur  they  are  high-pitched,  sharp,  and  resemble  fine 
gurgles.  The  occurrence  of  aiscess  and  gangrene  is  indicated  by  the 
physical  signs  which  attend  the  formation  of  a  cavity  in  consolidated  lung 
substance,  No  one  of  the  physical  signs  present  during  a  pneumonia  is 
sufficient  for  a  diagnosis ;  but  the  manner  and  order  of  their  occurrence 
and  their  relation  to  the  subjective  symptoms  enable  one  to  reach  a  positive 
diagnosis  in  all  typical  cases.     The  only  diagnostic  symptom  is  the  sputum. 

In  children  bronchial  breathing  rarely  disappears  before  the  seventh  day  ; 

J  Skoda  and  Traube. 


ACUTE   LOBAR    PNEUMONIA.  93 

it  IS  often  accompanied  by  the  sub-crepitant  rale.  When  resolution  takes 
place,  bronchial  breathing  and  the  sub-crepitant  rdle  will  disappear  simul- 
taneously. If  purulent  infiltration  occurs,  large  gurgling  crepitation  will 
be  heard.  "Vesicular  breathing  is  rarely  heard  before  the  eighth  or  ninth 
day. 

In  old  age,  inspection,  palpation  and  percussion  give  similar  results  to 
those  in  adult  life.  Auscultation  shows  the  crepitating  sounds  to  be  louder, 
and  gurgles  large  and  loud  are  often  heard  at  a  distance  from  the  chest. 
The  rdle  redux  is  not  distinctive  of,  or  j)eculiar  to  the  third  stage  of  senile 
pneumonia.  The  sound  heard  afc  this  stage  is  a  muco-crepitating  sound, 
i.  e.,  a  sound  produced  in  bronchi  of  medium  size.  The  physical  signs  of 
pulmonary  abscess  in  the  aged  are  very  generally  wanting.  Distinctly  local- 
ized gurgling  and  cavernous  respiration  may,  with  the  rational  signs  of 
abscess,  suffice  for  a  diagnosis.  The  sputa  will  also  aid,  but  the  diagnosis 
is  only  approximate.  In  old  age  the  physical  signs  are  subject  to  greater 
variations  than  in  adult  life. 

Differential  Diagnosis. — Lobar  pneumonia  may  be  confounded  with  pul- 
monary congestion  and  oedema,  capillary  bronchitis,  j)leurisy,  hypostatic  con- 
gestion, catarrhal  pneumonia  (in  children),  pulmonary  infarction,  incipi- 
ent phthisis  (especially  in  children),  meningitis  and  typhoid  fever. 

Pneumonia  begins  with  a  chill,  followed  by  a  rapid  rise  in  temperature 
and  pain  in  the  side  ;  in  pulmonary  congestion  and  oedema,  there  is  no  chill 
or  rise  in  temperature,  and  no  pain.  The  sputum  of  pneumonia  is  viscid, 
rusty  and  (microscopically)  diagnostic  ;  in  pulmonary  congestion  and  oedema 
there  is  profuse  watery,  blood-stained  expectoration.  Pneumonia  is  com- 
monly unilateral,  and  may  occur  in  any  portion  of  the  lung ;  pulmonary 
oedema  is  bilateral,  and  usually  occurs  in  the  most  dependent  portions  of 
the  lungs.  In  pneumonia  there  is  complete  dulness  on  percussion,  crep- 
itant rales  and  bronchial  respiration  ;  in  pulmonary  oedema  the  dulness  is 
not  complete,  there  is  no  bronchial  breathing,  and  there  occur  numerous 
large,  liquid,  sub-crepitant  rales. 

The  resolving  stage  of  pneumonia  may  be  mistaken  for  acute  capillary 
'bronchitis  ;  but  in  the  latter  the  sub-crepitant  rale  is  heard  all  over  the 
c?iest ;  while  in  pneumonia  it  is  usually  limited  to  a  small  area.  The  ex- 
pectoration is  muco-purulent  in  bronchitis,  and  the  temperature  range  is 
lower  than  in  pneumonia.  There  is  no  dulness  on  percussion,  no  bronchial 
breathing  in  capillary  bronchitis ;  the  vesicular  murmur  is  feeble,  and 
cyanosis  is  more  marked.  The  breathing  is  labored  in  bronchitis,  and  pant- 
ing in  pneumonia. 

Pneumonia  is  ushered  in  by  a  distinct  chill  folloAved  by  fever  ;  acute  pleu- 
risy begins  with  chilliness  or  several  rigors,  and  the  temperature  rarely 
rises  above  100°  F.  The  dry,  hacking  cough  of  pleurisy  is  accompanied  by 
slight  mucous  expectoration,  and  the  characteristic  j)neumonic  sputum  is 
absent.  In  pleurisy  the  face  is  pale  and  anxious,  and  the  pulse  is  firm, 
small,  tense  and  wiry  ;  in  pneumonia  the  face  has  a  mahogany  flush,  and 
the  pulse  is  full  and  compressible.  The  breathing  in  pleurisy  is  "catch- 
ing ;"  in  pneumonia  it  is  "panting."     There  are  no  critical  days  in  pleu- 


94  DISEASES   OF   THE    RESPIRATOEY    ORGANS, 

risy.  Vocal  fremitus  is  diminished  or  absent  in  pleurisy  with  effusion, 
there  is  flatness  on  percussion,  and  the  sound  of  the  percussion  changes 
with  a  change  in  position  of  the  patient.  In  pneumonia  vocal  fremitus  is  in- 
creased, and  there  is  dulness — not  flatness — on  percussion.  In  pleurisy  the 
respiratory  sounds  are  feeble,  and  a  grazing,  rubbing  or  sticky  friction- 
sound  is  heard ;  in  pneumonia  there  are  crepitant  rales  and  bronchial 
breathing.  Bronchophony  and  bronchial  breathing  may  exist  in  pleurisy, 
but  they  are  always  diffuse — never  sharp  and  tubular  as  in  j^neumonia. 

Hypostatic  congestion  is  accompanied  by  copious,  loatery,  blood-stained 
expectoration ;  it  occurs  in  the  most  dependent  portions  of  the  lungs,  dis- 
appears when  the  patient  sits  up,  and  is  accompanied  by  no  rational  symp- 
toms except  dyspnoea  and  expectoration. 

Lobular  pneumonia  in  children  is  always  secondary  ;  it  is  not  ushered  in 
by  a  chill,  usually  follows  n  bronchitis,  and  is  developed  in  both  lungs. 
There  are  no  days  of  crisis,  and  the  physical  signs  of  pneumonia  are  lim- 
ited to  circumscribed  spots.  The  range  of  temperature  in  the  two  forms 
of  pneumonia  differ ;  the  two  curves  represented  by  Figs.  20  and  25  show 
the  differences. 

Pulmonary  infarction  is  rarely  met  with  independent  of  cardiac  disease 
or  pyemia.  It  is  a  non-febrile  disease,  and  intense  dyspnoea,  coming  on 
abruptly,  is  its  prominent  symptom.  In  pneumonia  dyspnoea  comes  on 
slowly.  The  expectoration  in  infarction  consists  of  small  black  coagula  ;  in 
pneumonia  it  is  viscid  and  contains  few  blood-globules.  The  dulness  of 
an  infarction  is  circumscribed,  and  around  it  moist  rales  are  heard  ;  in 
pneumonia  the  area  of  dulness  is  extensive,  and  there  are  no  moist  rales. 
There  is  a  peculiar  garlic-like  odor  to  the  breath,  in  pulmonary  infarction, 
never  present  in  pneumonia.. 

When  lobar  pneumonia  has  its  seat  at  the  apex,  it  may  be  confounded 
with  the  first  stage  of  phthisis.  But  the  history  of  a  well-marked  chill, 
followed  by  the  characteristic  pneumonic  symptoms,  will  enable  one  to 
exclude  phthisis.  Moreover,  the  fever  in  phthisis  is  subject  to  irregular 
exacerbations  and  remissions.  If  the  signs  of  consolidation  persist  with  lit- 
tle or  no  change,  if  the  temperature  at  no  time  falls  to  normal,  if  there  are 
night  sweats,  if  emaciation  is  progressive — then  the  case  is  to  be  regarded 
as  one  of  phthisis,  even  though  pneumonia  may  have  complicated  it. 

In  children  pneumonia  is  so  often  accompanied  by  cerebral  symptoms  that 
it  may  be  mistaken  for  meningitis.  Meningitis  comes  on  insidiously,  the 
temperature  rarely  rises  above  103°  F.,  the  pulse  is  often  lower  than  nor- 
mal, there  are  no  thoracic  symptoms,  no  dyspnoea,  the  face  is  pale  and  anx- 
ious, and  the  physical  signs  of  pneumonia  are  absent. 

Sometimes  latent  pneumonia  may  be  mistaken  for  typhus  fever,  especially 
when  typhus  is  prevailing.  While  in  charge  of  the  typhus  fever  patients 
on  Blackwell's  Island,  I  frequently  saw  cases  where  such  a  mistake  had  been 
made  during  a  typhus  epidemic.  In  these  cases  there  will  be  dry  tongue, 
delirium,  and  high  temperature.  The  countenance  resembles  that  of  pneu- 
monia, but  the  presence  of  the  typhus  eruption  and  the  absence  of  the 
physical  signs  of  pneumonia  will  establish  the  diagnosis. 


ACUTE   LOBAR   PNEUMONIA.  95 

Pneumonia  with  typhoid  symptoms  is  sometimes  mistaken  for  typhoid 
fever.  The  differential  diagnosis  is  not  difficult,  if  one  remembers  that  the 
pneumonia  which  complicates  typhoid  fever  does  not  come  on  until  late  in 
the  fever,  and  the  regular  history  of  typhoid  fever  precedes  its  development. 
On  the  other  hand,  when  the  typhoid  symptoms  are  present  from  the  be- 
ginning, or  come  on  at  the  end  of  the  second  stage  of  pneumonia,  the  phys- 
ical signs  of  pneumonia  will  precede  the  typhoid  symptoms.  If  a  patient 
over  sixty  years  of  age,  with  this  type  of  pneumonia,  is  not  seen  until  the 
second  or  third  week  of  his  sickness,  although  evidences  of  lung  consolida- 
tion maybe  found,  it  will  be  very  difficult  to  decide  whether  the  pneumonia 
is  or  is  not  complicating  a  typhoid  fever,  and  under  these  circumstances 
the  diagnosis  will  be  difficult  if  not  impossible. 

Prognosis. — The  phenomena  of  the  crisis  of  pneumonia  are  a  sudden  fall 
of  temperature  followed  by  profuse  sweats  and  a  diminution  in  frequency 
of  respirations  and  pulse.  The  cough  becomes  loose,  the  dyspnoea  abates, 
the  flush  disappears  from  the  face,  the  sputum  is  more  copious,  loses  its 
rusty  hue,  diminishes  in  viscidity  and  becomes  ''creamy,"  thin  and  watery. 
Thirst  decreases,  the  appetite  returns,  pain  ceases  and  the  patient 
falls  into  a  quiet  sleep,  waking  extremely  exhausted.  Epistaxis,  hge- 
maturia  and  hemorrhage  from  the  bowels  may  occur  at  the  cri- 
sis. After  the  crisis  the  amount  of  urea  in  the  urine,  which  was  aug- 
mented before,  becomes  normal  and  the  chloride  of  sodium  reappears.  The 
crisis  in  children  is  marked  by  a  greater  fall  in  temperature  and  by  a  more 
profuse  sweat.  When  children  have  been  restless  or  delirious  the  crisis  is 
marked  by  a  state  of  stupor.  In  old  age  the  crisis  is  marked  by  a  critical 
diarrhoea  rather  than  by  a  sweat. 

The  fatality  of  pneumonia  is  shown  by  the  following  statistics :  of 
12,431  cases  treated  in  the  hospitals  at  Stockholm,  11  per  cent.  died.  In 
the  Vienna  hospitals  24  per  cent.  died.  The  Basle  Hospital  Reports  for 
thirty-two  years  give  23  per  cent,  of  deaths.  Grisolle  reports  59  per  cent,  of 
deaths  in  those  over  sixty.  In  the  "  U.  S.  Medical  Reports,"  May  1st, 
1861,  to  July,  1866,  of  61,202  cases  which  occurred  among  the  white  troops, 
14,738  died— more  than  24  per  cent.  ;  and  of  16,133  among  colored  troops, 
nearly  33  per  cent.  died.  The  deaths  from  all  other  inflammatory  diseases 
of  the  respiratory  system  for  the  same  time  were  only  one-seventh  as  many 
as  from  pneumonia.'  Of  255  cases  treated  in  Bellevue  Hospital  during  a 
period  of  four  years  the  rate  of  mortality  was  34  per  cent.  The  statistics  of 
private  practice  are  very  different :  of  Lebert's  205  cases,  only  TyVper  cent. 
died.  Ziemssen  lost  only  3^^  per  cent,  of  his  cases.  Rennet  lost  none  of 
his  105  cases.  (He  says,  however,  that  no  complications  existed.)  Brundes, 
of  Copenhagen,  lost  over  21  per  cent,  of  his  142  cases.  Fox  gives  to  pneu- 
monia the  fifth,  and  Walshe  the  third  place  among  fatal  diseases.  The 
average  mortality-rate  from  all  the  published  reports  to  which  I  have  had 
access  gives  20^o  P^^  cent,  of  deaths.  But  the  rate  varies  in  different 
years. 

1  The  Confederate  Hospitals'  Reports  give  over  30  per  cent,  of  deaths  from  pneumonia  for  the  same 
period. 


96  DISEASES   OP   THE   KESPIKATORY    ORGANS. 

The  prognosis  depends  more  on  the  age  than  on  any  other  single  ele- 
ment. In  infancy  the  mortality  is  greater  than  in  early  childhood.  Be- 
tween the  ages  of  forty  and  sixty  the  death-rate  is  from  10  to  25  per 
cent.,  while  from  ten  to  thirty  years  almost  all  of  the  uncomplicated  cases 
recover.  After  sixty  the  prognosis  is  always  unfavorable.  Pneumonia  is 
the  most  fatal  of  all  acute  diseases  at  this  period  of  life ;  most  "  sud- 
den deaths"  in  the  old.  are  from  acute  lobar  pneumonia.  Some  of  the  most 
reliable  modern  authorities  state  that  nine-tenths  of  deaths  after  the  seventy- 
fifth  year  are  from  acute  pneumonia.  It  is  more  fatal  in  females  than  in 
males.  In  some  years  the  proportion  of  deaths  is  far  greater  in  summer 
than  either  in  the  spring  or  winter  ;  and  certain — as  yet  unknown — atmos- 
pheric influences  are  of  the  utmost  imj)ortance  in  determining  the  death- 
rate.  The  extent  of  lung  involved  influences  the  prognosis  ;  double  pneu- 
monia is  rarely  recovered  from.  When  an  entire  lung  is  involved,  the 
prognosis  is  not  as  good  as  when  only  a  single  lobe  is  involved.  Apical 
pneumonia — esjoecially  in  the  old  and  very  young — is  more  often  fatal  than 
basic.     The  feebler  the  patient  the  more  unfavorable  the  prognosis. 

Complications  render  the  prognosis  unfavorable  :  of  225  of  my  own  cases, 
87  Avere  fatal  and  168  recovered.  Of  these,  124  were  complicated  and  131 
uncomplicated.  Of  the  complicated  cases,  75  died;  of  the  uncom]3licated, 
12  died.^  The  most  dangerous  complications  are  those  which  exert  a 
direct  influence  on  the  heart,  diminishing  its  power  and  obstructing  the 
flow  of  blood  from  the  right  ventricle.  Acute  infectious  diseases  are 
dangerous  complications  because  they  hasten  heart  failure. 

Pneumonia  may  be  regarded  as  mild  when  the  temperature  is  below  104°. 
When  the  fever  ranges  above  106°  for  two  days,  the  case  is  unfavorable. 
A  gradual  rise  in  temperature  after  the  fourth  day  is  always  an  unfavor- 
able sign.  A  low  temperature  is  dangerous  only  when  the  respirations 
are  greatly  accelerated.  When  the  pulse  is  120  to  130  for  two  or  three 
days,  the  prognosis  is  bad.  If  the  pulse  reach  150  per  minute,  or  if  it 
becomes  irregular,  intermitting,  or  dicrotic,  the  patient  rarely  recovers.  In 
children  a  rapid  pulse  is  of  less  significance,  and  in  old  age  the  pulse  is 
never  a  reliable  guide.  Prune-juice  expectoration  is  an  unfavorable  sign, 
indicating  extensive  blood  changes.  When  expectoration  is  absent  in 
the  second  or  third  stage,  or  if  it  become  scanty  and  difficult,  the  prog- 
nosis is  unfavorable.  Sudden  suppression  of  the  sputa,  with  coincident 
tracheal  rales,  indicates  impending  death.  Delirium  coming  on  after  the 
sixth  day,  convulsions  in  children,  with  jactitation  and  subsultus,  or,  in 
the  aged,  a  tendency  to  coma,  are  unfavorable  signs.  Exhaustion  and 
prostration,  accompanied  by  a  sunken  pallid  face  and  cold,  clammy  sweat, 
are  always  dangerous.  In  children,  bronchial  breathing,  after  the 
seventh   day,  numerous  subcrepitant  rdles,   copious  and  persistent   diar- 

-  Lebert  states  that  he  lost  only  5>^  per  cent,  of  hisimcomplicated,andaZ^of  his  complicated  cases.  Huss 
lost  6  per  cent,  of  uncomplicated  and  20  per  cent,  of  complicated  cases.  Fox  states  that  pneumonia  com- 
plicated by  endocarditis  is  fatal  in  75  percent,  of  cases  ;  by  pericnrditis,in  54  per  cent.;  by  Bright's  disease, 
in  50  per  cent.;  and  by  alcoholismus,  in  25  per  cent.  Brundes  (of  Copenhagen),  in  120  uncomplicated  cases, 
lost  6%  per  cent.;  of  22  complicated,  he  lost  all.  The  danger  of  complications  is  markedly  shown  by 
these  statistics. 


ACUTE   LOBAR   PNEUMONIA.  97 

rhoea,  and  swelling  of  the  veins  of  the  hands  are  bad  symptoms.  In 
old  age  a  sudden  rise  or  fall  in  temperature,  apathy,  somnolence,  and  a 
sallow,  anxious  countenance  are  dangerous  symptoms.  Pulmonary  con- 
gestion and  oedema  in  the  unaffected  part  of  the  lung  often  precede  a  fatal 
issue.  The  occurrence  of  purulent  infiltration,  abscess,  or  gangrene  ren- 
ders the  prognosis  unfavorable. 

In  pneumonia  the  fibrin-factors  of  the  blood  are  increased  (often  400 
per  cent,  more  than  normal),  the  heart-power  is  diminished,  so  that 
the  ventricles  cannot  empty  themselves,  the  columns  and  cords  whip 
Tip  the  residual  blood  (already  prepared  for  clotting),  and  ''heart 
clots"  always  form  when  the  death  struggle  is  prolonged  and  cardiac 
contractions  feeble.  The  "  heart  failure "  is  the  beginning  of  death. 
Post-mortem  results  can  never  give  all,  or  the  true  causes  of  death, 
but  only  the  modes  of  death.  If,  on  account  of  heart  failure,  pulmonary 
oedema  and  congestion  occur  and  heart  clots  form,  these  clots  cannot  be 
called  causes  of  death.  Jiirgensen  states  that  in  fatal  cases  of  pneumonia 
oedema  of  the  lungs  is  probably  always  present,  and  heart  clots  are  fre- 
quent. Death  may  occur,  then,  from  heart-insuflficiency,  from  complica- 
tions (cardiac  especially),  or  from  asphyxia.  Fatal  collapse  may  follow  an 
apparently  regular  and  well-marked  crisis. 

Treatment. — If  we  regard  pneumonia  as  a  general  disease  with  a  charac- 
teristic local  lesion,  the  treatment  must  be  modified  by  the  constitutional 
condition  of  each  patient  and  by  the  type  of  the  pneumonia.  If  it  is  un- 
complicated and  occurs  at  certain  periods  of  life,  it  will  terminate  spon- 
taneously in  recovery  by  crisis  ;  but  when  certain  complications  exist,  when 
certain  conditions  are  present,  and  at  certain  ages,  it  is  almost  necessarily 
fatal. 

Any  plan  of  treatment  in  such  a  disease,  if  resorted  to  indiscriminately, 
will  prove  unsatisfactory.  Although  a  large  proportion  of  cases  will  re- 
cover without  treatment,  yet  well-directed  therapeusis  will  save  lives  and 
render  convalescence  less  tedious.  The  pneumonic  lung  no  more  requires- 
treatment  than  the  intestinal  ulcers  of  typhoid  fever.  It  is  i\ie  ge7ieral  con- 
dition of  the  patient,  not  the  local  changes,  which  is  to  govern  us  in  the 
management  of  each  case.  Agents  for  the  arrest  of  local  inflammation 
have  no  place  here ;  hence  venesection,  once  generally  practised,  has  been 
almost  entirely  abandoned.  A  careful  study  of  the  pathology  of  pneumo- 
nia not  only  leads  to  the  conclusion  that  bleeding  does  harm,  but  it 
strongly  contra-indicates  the  use  of  all  those  agents  which  have  been  em- 
ployed for  the  arrest  of  simple  pulmonary  inflammation.  Hence  veratrum 
viride,  aconite,  antimony,  calomel,  the  tartrate  of  potash  and  antimony, 
iodide  of  potassium,  and  all  so-called  "cardiac  sedatives"  have  been  dis- 
carded, for  it  is  evident  that  they  add  a  new  load  to  an  already  overburdened 
heart.  They  may,  for  a  time,  lower  temperature  and  pulse-rate,  but  this 
wiU  be  accomplished  at  the  expense  of  heart-power.  Cardiac  insufficiency 
will  therefore  appear  earlier  and  be  more  profound. 

Counter -irritafAon  by  blisters,  or  other  irritants,  to  the  chest  (in  the 
early  stages)  is  apt  to  do  harm  ;  but  blisters  may  be  applied  during  the  third 
7 


98  DISEASES    OF    THE    EESPIRATOET    OEGAKS. 

stage,  to  hasten  resolution.  The  application  of  leeches,  followed  by  a  lin- 
seed-meal poultice  or  other  soothing  fomentation,  will  relieve  the  pain  in 
the  side,  which  is  often  so  urgent  at  the  onset,  and,  if  the  condition  of  the 
patient  will  allow,  may  be  of  service.  If  extensive  pulmonary  oedema  oc- 
curs, dry  cups  applied  to  the  chest  will  relieve  the  dyspnoea,  and  for  a 
time  dispel  the  oedema.  It  has  come  to  be  a  rule  to  incase  the  chest  in 
a  cotton-batting  or  flannel  jacket,  covered  with  oiled  silk.  This  has  no 
influence  over  the  course  of  the  pneumonia,  but  it  promotes  diaphoresis, 
protects  the  surface  from  sudden  clianges  of  temperature,  and  it  is  always 
grateful  to  the  patient.     The  "  Jacket  "  is  especially  beneficial  in  children. 

Absolute  rest  is  important ;  the  patient  should  be  moved  as  little  as 
possible,  and  should  not  be  kept  in  a  constrained  posture.  If  signs  of 
heart  failure  occur,  he  should  not  be  allowed  to  sit  up  or  talk.  The  sick 
room  should  be  large,  cheerful  and  well  ventilated,  and  its  temperature 
should  range  between  65°  and  70°  Fahr.  A  most  important  adjuvant  is 
a  carefully-regulated  diet.  The  food  should  be  fluid  or  semi-fluid,  and 
highly  nutritious,  e.  g.,  milk,  eggs,  beef -tea,  and  concentrated  broths. 
Milk  is  preferable  to  all  other  nourishment. 

The  nervoiis  slioclc  which  attends  the  onset  of  acute  lobar  pneumonia  is 
greater  than  in  any  other  acute  disease,  except,  perhaps,  acute  peritonitis, 
and  the  important  question  presents  itself:  what  measures  shall  be  em- 
ployed to  counteract,  or  mitigate,  the  impression  made  on  the  nerve  centres 
by  the  morbific  agent  which  is  operating  to  produce  the  jDneumonia  ?  The 
exiDcrience  of  the  last  five  years  leads  me  to  the  conclusion  that  during  the 
developing  period  of  the  disease,  when  the  pneumonic  blow  is  first  struck, 
and  until  the  infiltration  is  complete  (usually  for  the  first  four  days),  the 
patient  is  to  be  brought  under  the  full  influence  of  opium  and  held  in  a 
state  of  comparative  comfort,  by  hypodermic  injections  of  morphia,  re- 
peated at  regular  intervals  ;  and  that  by  this  course  a  pneumonic  patient 
is  placed  in  the  best  condition,  not  only  for  sustaining  the  primary  shock, 
but  for  resisting  the  pneumonia.  Thus  given,  opium  does  not  interfere 
with  the  employment  of  any  stimulating  or  anti-pyretic  measures  which 
may  be  demanded.  And  not  only  does  it  diminish  the  chances  of  the 
occurrence  of  heart  failure,  but  the  great  relief  and  comfort  which  it  gives 
to  the  sufferer  in  the  first  four  days  of  his  struggles  are  sufficient  to  com- 
mend its  use.  After  the  pneumonic  infiltration  is  completed,  opium  should 
be  discontinued,  for  paralysis  of,  and  a  consequent  accumulation  of  secretion 
in  the  bronchi  may  greatly  increase  the  already  deficient  respirations. 

In  all  severe  types  of  pneumonia  there  are  two  prominent  sources  of 
danger — heart-insufficiency  and  high  temperature.  The  two  prominent 
indications  for  treatment  are,  therefore,  to  sustain  the  heart  and  to  reduce 
the  temperature.  A  large  proportion  of  deaths  in  pneumonia  directly  result 
from  heart  failure ;  alcohol,  judiciously  used,  is  the  most  efficient  means 
for  preventing  or  overcoming  it,  but  its  indiscriminate  use  is  more  dangerous 
than  indiscriminate  bleeding.  Only  a  few  ounces  of  brandy  may  be  re. 
'quired  to  carry  a  pneumonic  patient  through  a  critical  period  ;  or  its  free 
administration  may  be  demanded  to  save  life.     In  the  old  and  feeble,  apd 


ACUTE   LOBAR   PNEUMONIA.  99 

in  those  who  have  been  accustomed  to  the  use  of  alcohol,  stimulation  may 
be  necessary  from  the  very  onset.  The  indications  in  each  case  demand 
careful  study ;  in  no  disease  is  so  much  discretion  required  in  the  admin- 
istration of  stimulants.  The  pulse  is  the  indicator  of  the  heart's  con- 
dition. A  frequent,  feeble,  irregular  or  intermitting  pulse  calls  for 
stimulants.  The  quantity  required  in  any  case  is  to  be  determined  by  its 
effects  on  the  pulse.  It  is  best  to  begin  with  small  quantities,  and  care- 
fully note  the  effect  of  the  first  few  doses.  If  it  acts  beneficially,  a  favor- 
able effect  will  be  seen  in  a  few  hours  ;  and  then  the  quantity  administered 
must  be  varied  to  suit  each  case.  It  is  seldom  necessary  to  use  more  than 
six  or  eight  ounces  of  brandy  in  twenty-four  hours  ;  but,  when  demanded, 
it  is  to  be  unsparingly  given.  A  dicrotic  pulse  is  always  an  indication  for 
its  use.  The  period  immediately  following  the  crisis  is  the  time  when 
stimulants  are  usually  most  required.  Delirium,  muscular  tremor  and  sub- 
sultus  are  indications  for  their  use.  Critical  collapse  in  the  aged  must  be 
combated  by  a  very  free  use  of  stimulants.  Carbonate  of  ammonia  is 
extensively  employed  as  a  stimulant  in  pneumonia  ; — it  is  claimed  that 
its  use  diminishes  the  danger  of  heart  clot,  but  there  is  no  evidence  in 
support  of  this  statement; — and  if  given  in  sufficiently  large  doses  to  act 
as  a  stimulant  it  irritates  the  stomach.  It  is  unquestionably  inferior  to 
alcohol  as  a  cardiac  stimulant.  Camphor  and  musk  are  also  inferior  to 
alcohol,  and  digitalis  is  only  of  service  when  there  are  evidences  of  extensive 
renal  congestion. 

There  are  two  plans  of  treatment  advocated  for  reducing  temperature 
in  pneumonia  :  (1)  the  application  of  cold  in  various  ways  to  the  surface 
of  the  body  ;  and  (2)  the  internal  administration  of  the  sulphate  of  quinine. 
It  is  claimed  that  the  temperature  can  be  reduced  by  applying  cold  com- 
presses to  the  chest  :  a  cloth  of  some  thickness  is  to  be  wrung  from  cold 
water  and  applied  every  ten  or  fifteen  minutes  to  the  affected  side.  This 
not  only  relieves  the  local  symptoms,  but  it  lowers  the  body  temperature 
and  hastens  the  day  of  crisis.  Some  prefer  the  "  Esmarch  ice-bag "  to 
the  cold  compress.  There  is  no  doubt  but  that  the  pain  in  the  side  and 
fever  will  be  relieved  by  this  means,  but  the  relief  is  only  temporary  ;  and 
my  own  experience  leads  to  the  belief  that  pneumonia  treated  in  this  way 
is  more  likely  to  extend,  and  that  there  is  great  danger  of  chilling  the 
patient.  The  other  methods  of  applying  cold  to  the  surface  for  the  reduc- 
tion of  temperature  in  pneumonia  are  the  cold  bath,'  the  cold  pack  and 
cold  sponging. 

'  The  rules  for  administering  the  bath  are  as  follows  :  as  soon  as  the  axillary  temperature  rises  above 
104°  F.,  place  the  patient  in  a  water-bath  having  a  temperature  of  70°  F.  or  80°  F.,  and  gradually  lower  the 
temperature  by  the  addition  of  cold  water  or  ice  until  the  temperature  of  the  patient  begins  to  fall.  When 
the  patient's  temperature  begins  to  fall  the  thermometrical  observations  must  be  taken  every  two  or  three 
minutes  in  the  rectum.  If  it  falls  rapidly,  the  patient  must  be  removed  from  the  bath  as  soon  as  the  tem- 
perature has  reached  102°  F.  ;  (if  it  falls  slowly,  as  soon  as  it  reaches  101°  F.,)  and  immediately  placed  in 
bed.  While  in  the  bath  cold  must  be  applied  to  the  head  by  means  of  sponges  or  ice-bags.  The  cold  pack 
consists  in  wrapping  the  patient  in  a  sheet  wrung  out  of  tepid  water,  and  applying  over  this  sheet  one 
wrung  out  of  cold  water.  The  latter  is  to  be  removed  as  often  as  it  becomes  warm.  Its  application  and 
removal  must  be  continued  until  the  desired  fall  in  temperature  is  obtained.  To  keep  the  temperature  at 
the  desired  point,  the  baths  or  packs  must  be  repeated  and  continued  night  and  day  whenever  the  tem- 
perature rises  above  104°,  until  the  crisis  is  reached. 


100  DISEASES   OF  THE   RESPIRATOEY   OEGAITS. 

The  experience  of  American  practitioners  is  against  the  cold  bath  and 
the  cold  pack.  The  shock  of  cold  causes  depression,  which  the  feeble  or 
old  cannot  rally  from.  And  though  fever  is  lessened,  heart-failure  more 
rapidly  follows,  and  is  more  difficult  to  overcome.  My  own  experience  is 
decidedly  against  the  use  of  cold  on  the  surface  for  the  reduction  of  tem- 
perature in  pneumonia.  Cold  "sponging"  may  be  practised  when  it  is 
grateful  to  the  patient. 

It  is  claimed  that  sulphate  of  quinine  is  an  arterial  sedative  ;  that  it  has 
a  peculiar  tonic  effect  on  the  capillary  circulation  ;  that  it  arrests  cell-devel-- 
opment,  and  checks  the  amoeboid  movement  of  the  white  blood  corpuscles. 
Theoretically,  therefore,  its  use  is  indicated  in  lobar  pneumonia  ;  and,  clin- 
ically, it  is  found  to  reduce  temperature  more  permanently  and  with  greater 
certainty-than  any  other  agent.  To  act  antipyreticaily  it  must  be  given  in 
doses  of  from  gr.  x.  to  gr.  xx.  within  a  period  of  not  more  than  two  hours. ^ 
The  very  large  antipyretic  doses  of  quinine  which  have  been  recommended 
seem  to  me  to  be  attended  with  danger,  for  in  such  large  doses  it  appears 
to  act  as  a  cardiac  depressant,  and  I  believe  that  with  gr.  x.-xv.  given  in 
one  dose  we  obtain  as  certain  an  antipyretic  result  as  with  much  larger  doses. 

If  there  is  great  restlessness  or  wakefulness  during  the  third  stage,  small 
hypodermatics  of  morphia,  or,  better,  hydrate  of  chloral,  can  be  given.  If 
there  is  even  slight  evidence  of  cyanosis,  these  remedies  should  be  used 
with  great  care.  When  the  pupils  are  small,  belladonna  or  hyoscyamus  may  be 
given.  For  the  relief  of  the  distressing  cough  which  is  sometimes  present, 
five  grains  of  hydrate  of  chloral  combined  with  one-twentieth  of  a  grain  of 
morphia,  or  twenty-five  drops  of  chlorodyne  every  two  hours,  may  be  given. 
If  expectoration  is  difficult  from  loss  of  muscular  power,  stimulating 
*' expectorants,"  such  as  senega  and  turpentine,  are  useful.  But  if  this 
diJBBculty  arises  from  great  viscidity  of  the  sputum,  alkalies  will  be  found 
of  service,  and,  as  alkalies  and  neutral  salines  also  have  a  diuretic  and 
diaphoretic  action,  they  are  especially  indicated  just  before  the  crisis.  For 
the  relief  of  the  delirium  of  chronic  alcoholism,  tartar  emetic  and  digitalis 
are  highly  recommended  by  English  authorities. 

In  the  first  stage  of  senile  pneumonia  an  emetic,  when  not  specially  con- 
tra-indicated, is  given  in  the  "  Salpetriere  Hospital."  Ipecacuanha  is  re- 
garded as  especially  indicated.  The  nitrate  of  potash  and  the  hydro- 
chlorate  of  ammonia  are  also  highly  recommended  in  senile  pneumonia. 

In  children  the  chest  should  be  thoroughly  protected,  the  diet  carefully 
regulated.  Leeching  and  blistering  are  both  harmful,  and  should  never 
be  employed.  Stimulating  expectorants  are  often  indicated,  and  the  mod- 
erate use  of  stimulants  in  feeble  children  is  always  required.     During  con- 

•  Liebermeister  gives  quinbie  until  the  temperature  has  been  reduced  by  it  to  within  \°  of  the  normal. 
Few  American  practitioners  carry  the  antipyretic  effects  of  quinine  so  far.  In  Ringer  and  Gill's  experi- 
ments upon  "  The  Influence  of  Quinine  on  Temperature^''  m  health,  it  took  at  least  gr.  xx.  to  produce  a  fall 
of  1°.  From  fifty  to  eighty  minutes  elapsed  before  the  fall  occurred,  and  the  effects  lasted  from  forty -five 
minutes  to  three  hours.  Ringer  states  that  in  pneumonia  (and  some  other  diseases)  quinine  does  not 
readilj'  pass  out  with  the  urine,  but  is  delayed  in  the  system  for  considerable  time,  and  its  antipyretic 
effects  are  continued  longer  than  in  other  diseases.  Prof.  Flint  states  that  he  has  seen  pneumonia  rendered 
abortive  in  a  certain  proportion  of  cases  by  xs.  to  xl.  grains  of  qninine  daily,  and  even  when  this  result  has 
not  followed,  the  disease  has  often  been  favorably  modified  in  a  greater  degree  than  by  smaller  doses. 


LOBULAR   PN"EUMONIA.  101 

yalescence,  iron,  quinine,  mineral  acids,  cod-liver  oil,  and  blood-making 
wines,  should  be  given. 

Very  recently  there  has  been  advocated  an  antiseptic  treatment  of  pneu- 
monia, the  origin  of  which  is  to  be  found  in  the  notion,  which  somewhat 
extensively  prevails,  that  pneumonia  is  a  zymotic  disease.  Klebs  even 
advocates  injection  of  carbolic  acid  to  kill  or  render  inert  the  "  monas  pul- 
monale," which  he  claims  to  be  the  contagious  element  found  in  the  sputum. 
It  cannot  be  denied  that  a  septic  element  exists  in  some  if  not  in  all  cases ; 
hence  the  sulphites  and  hyposulphites  (30  grain  doses  every  three  hours) 
are  rceommended.  Carbolic  acid,  from  1  to  5  grains,  sulpho-carbolate  of 
soda  (5  to  20  grains  every  two  hours),  have  both  been  used  quite  extensively 
as  antiseptics  in  the  treatment  of  pneumonia.  Thymol  and  salicylic  acid 
have  risen  into  favor  because  they  are  powerfully  antiseptic  and  are  almost 
physiologically  inert.  Quinine  has  also  been  advocated  for  its  antiseptic 
power.  The  antiseptic  treatment  of  pneumonia  has  not  yet  assumed  a 
definite  aspect  or  been  sufficiently  tried  for  any  definite  statements  to  be 
made  concerning  it. 

LOBULAR   PNEUMONIA. 

Lobular,  catarrhal,  or  hroncho-pneumonia,  is  always  secondary,  being 
preceded  by,  or  associated  with,  inflammation  and  obstruction  of  the  smaller 
bronchi,  which  lead  to  the  consolidated  lobules.  It  may  run  an  acute,  sub- 
acute or  chronic  course,  and  differs  very  decidedly  both  in  its  clinical  and 
pathological  history  from  acute  lobar  pneumonia. 

Morbid  Anatomy. — The  anatomical  changes  in  lobular  pneumonia  are 
confined  to  scattered  groups  of  air-vesicles,  hence  the  gross  appearance  of 
the  portion  of  lung  involved  will  vary  with  the  duration  and  extent  of  the 
pneumonic  process.  In  well-marked  cases  there  will  be  found  scattered 
throughout  one  or  both  lungs,  small,  circumscribed  nodules  of  a  light, 
deep-red,  or  bluish  color,  which  do  not  inflate  when  the  lung  is  inflated. 
If  they  are  situated  near  the  surface  of  the  lung,  they  cause  small,  rounded 
elevations.  When  they  are  of  minute  size  they  resemble,  and  may  be  con- 
founded with,  tubercles.  When  they  are  of  considerable  size,  a  reddish 
fluid  oozes  from  their  cut  surfaces  on  section,  and  a  small  quantity  of  dark 
blood  can  be  pressed  from  them.  They  are  less  tough  than  healthy  lung 
substance  and  break  down  easily  on  pressure.  These  nodules  shade  off  into 
the  surrounding  zones  of  lung-tissue,  which  may  be  the  seat  of  oedema, 
congestion,  or  emphysema.  The  nodules  vary  in  size  from  that  of  a  pea  to 
that  of  a  hazelnut,  and  are  very  rarely  granular.'  When  the  lung  is  in- 
flated these  spots  of  consolidation  are  rendered  more  prominent,  so  that 
they  stand  out  sharply  defined  from  the  adjacent  lung-tissue.  In  some  in- 
stances these  isolated  spots  of  consolidation  become  confluent  and  involve 
a  large  portion  of  lung — perhaps  a  whole  lobe — and  become  pale,  firm  and 
dry,  resembling  in  color  the  gray  hepatization  of  lobar  pneumonia.  The 
smaller  bronchi  are  congested ;  their  walls  are  often  thickened,  and  they 
may  contain  a  thick,  tenacious,  puriform  secretion  which,  later,  may  be- 

*  Jtlrgensen  says  :  "  Granulation  is  never  obseired." 


102 


DISEASES    OE    THE    EESPIRATORY    ORGANS. 


come  dry  and  inspissated.  When  a  section  of  the  lung  is  made  they  often 
stand  out  prominently  or  even  rise  a  little  above  the  level  of  the  cut  sur- 
face. A  peri-lroncJiitis  i&'^Qvy  often  associated  with  these  changes.  Cy- 
lindrical and  fusiform  dilatations  of  the  tubes  are  not  infrequent.  Often, 
when  a  small  patch  of  consolidation  is  cut  across  there  will  be  found  at  its 
centre  a  dilated  bronchiole  filled  with  pus.  Discoloration  begins  at  this 
point  and  extends  towards  the  periphery.  The  connective-tissue  of  the 
portion  of  lung  involved  is  increased,  and  this,  in  long-standing  cases,  is 
often  pigmented.     Bronchiectasis  may  occur  at  various  points. 

A  microscopical  examination  of  an  affected  lobule  may  distinguish  three 
stages  in  the  inflammatory  process.  First,  the  air  vesicles  may  be  more  or 
less  completely  filled  with  pus  and  serum,  containing  swollen  and  granular 

epithelium.  The  capillaries  in 
the  walls  of  the  air  vesicles  are 
usually  elongated,  and  red  globules 
may  escape  into  the  air-sacs.  In 
the  unaffected  portions  of  lung- 
tissue  the  epithelial  cells  appear 
large  and  more  distinct  than  in 
healthy  lungs.  In  the  second  stage 
the  affected  lobules  become  solid 
and  airless.  Their  color  changes 
to  a  pinkish  gray.  The  other 
changes  are  similar  to  those  that 
take  place  in  the  stage  of  red 
hepatization  in  lobar  pneumonia, 
except  that  no  fibrillated  fibrin  is 
found  in  the  exudation,  the  pus 
and  epithelial  cells  are  more  abun- 
dant and  there  are  fewer  red  blood 
globules.  The  anatomical  differ- 
ences between  the  second  stages 
of  acute  lobar  and  acute  lobular  pneumonia  are  as  follows  :  acute  lobar 
pneumonia  involves  a  whole  lobe ;  acute  lobular  only  portions  of  a 
lobe.  Lobar  pneumonia  advances  steadily  and  uninterruptedly  from  one 
point,  usually  from  the  base  upwards,  until  the  whole  lobe  is  involved ;  while 
lobular  begins  simultaneously  in  several  lobules  remote  from  one  another. 
Moreover,  these  lobules  are  in  different  stages  of  the  inflammatory  process, 
e.  g.,  one  is  dark,  red  and  moist  ;  another  is  grayish  and  quite  firm.  In  lob- 
ular pneumonia  the  small  bronchi  are  more  or  less  filled  with  catarrhal  pro- 
ducts ;  while  in  lobar  pneumonia  the  exudation  is  fibrinous  and  does  not 
extend  beyond  the  infundibula  and  minute  bronchioles. 

The  third  stage  is  the  stage  in  which  occurs  either  resolution,  cheesy 
degeneration,  or  purulent  infiltration.  Abscess  and  gangrene  may  both 
occur,  but  they  are  very  rare.  When  resolution  occurs  the  contents  of  the 
alveoli  become  fatty  and  granular  and  are  absorbed,  and  the  pulmonary 
epithelium  is  restored.     Large  confluent  spots  of  catarrhal  pneumonia  may 


FiQ.  S>4. 

Alveolus  from  a  Lung  in  Lobular  Pneumonia. 

The  capillaries  are  distended  with  blood,  and  within  the 
alveolus  are  seen  swollen  epithelia  (a,  a)  and  pus  cells 
b.    X  250. 


LOBULAR   PKEUMONIA.  103 

undergo  clieesy  degeneration.  And  even  solitary  lobules  may  remain  pale 
and  yellow,  looking  like  so-called  cheesy  tubercles  ;  when  cut  into,  a  fluid 
escapes  from  their  centres.  Some  lobules  that  look  like  cheesy  masses  are 
soft,  never  granular,  and  a  purifonn  fluid  flows  from  their  cut  surfaces. 
While  the  contents  of  the  alveoli  are  undergoing  cheesy  changes,  hyper- 
plasia of  the  interstitial  connective-tissue  is  taking  place,  which  leads  to 
more  or  less  fibroid  induration  or  "  sclerosis'^  of  the  lung.  On  the  pleura 
covering  the  superficial  nodules  an  exudation  of  plastic  lymph  occurs ; 
the  bronchial  glands  are  swollen  and  hyperaemic'  Catarrhal  pneumonia 
in  adults  occurs  independently  of  lobular  collapse  or  atelectasis. 

Etiology. — Lobular  pneumonia  is  always  secondary  to  obstruction  in  the 
air  passages,  especially  those  of  capillary  size.  It  may  be  excited  either  by 
the  gradual  extension  of  inflammatory  processes  from  the  tubes  to  the  air- 
cells,  or  by  the  entrance  of  inflammatory  products  from  the  tubes  into  the 
air-cells.  It  is  most  frequently  met  with  between  the  ages  of  one  and  three. 
The  senile  period  also  seems  to  predispose  to  it.  The  more  imperfectly 
nourished  the  child,  the  more  anti-hygienic  the  air,  surroundings  and  food, 
the  more  liable  is  it  to  develop  lobular  pneumonia.  Debility  and  a  long- 
continued  recumbent  posture  predispose  to  it.  Indirectly,  any  cause  of 
bronchial  irritation  is  a  predisposing  cause.  The  bronchitis  of  measles, 
whooping-cough,  influenza,  and  that  which  accomjDanies  the  acute  infec- 
tious diseases,  often  leads  to  lobular  pneumonia.  It  occurs  in  lung-tissue 
adjacent  to  spots  of  hemorrhage,  or  pyaemic  infarctions;  traumatism  may 
induce  it.  It  is  intimately  associated  with  all  varieties  of  acute  and  chronic 
phthisis. ' 

Symptoms. — The  phenomena  which  attend  this  form  of  pneumonia  are 
always  more  or  less  obscured  by  those  of  the  disease  by  which  it  has  been 
preceded.  It  has  no  early  distinctive  symptoms.  From  an  anatomical 
standpoint  it  is  evident  that  its  symptoms  should  resemble  those  of  capillary 
bronchitis.  It  rarely  runs  a  regular  course, — terminating  after  a  definite 
period  in  either  death  or  resolution, — but  may  be  protracted  for  weeks  or 
months.  A  large  number  of  cases  occur  in  the  course  of  whooping-cough 
and  measles  or  other  diseases  complicated  by  bronchitis.  The  acute  form 
is  met  with  almost  exclusively  in  children.  In  adults  the  disease  usually 
runs  a  sub-acute  or  chronic  course. 

After  a  diffuse  capillary  bronchitis  has  existed  for  a  variable  period, 
attended  by  its  ordinary  symptoms,  such  as  a  cough  with  muco-purulent 
expectoration,  slight  rise  in  temperature  and  labored  breathing,  if  lobular 
pneumonia  is  developed  the  labored  breathing  becomes  panting  and  ac- 
celerated ;  the  respiration  may  be  100  per  minute.  Dyspnoea  is  greatly 
increased.  It  is  rarely  ushered  in  by  a  rigor  or  a  distinct  chill.  The  tem- 
perature will  gradually  rise  to  104°-105°,  unlike  the  sudden  rise  of  lobar 
pneumonia.  It  runs  no  typical  course  ;  though  exacerbations  and  remis- 
sions are  marked,  they  have  no  regularity ;  sometimes  the  morning,  some- 

•  Many  patholoj^ists  claim  that  the  pulmonary  alveolar  epithelium  takes  no  active  part  in  the  processes 
that  result,  in  the  above  described  consolidation.    Rindfleisch  assorts  an  active  proliferation. 

^  "  EUrat.or  pneum.onia  "  is  a  name  given  to  catarrhal  pneumonia  caused  by  inhalation  of  the  dust  of 
grain  elevators  in  our  Western  cities. 


104 


DISEASES   OP   THE   EESPIRATORY   ORGANS. 


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Fig.  25. 

Temperature  Record  in  a  case  of  Acute  Lobular 

Pneumonia  in  a  child.     (Recovery.) 


times  the  evening  temperature  is  the  higher.  It  varies  with  the  extent  of 
lung  involved,  and  also  with  the  rapidity  with  which  consolidation  is  de- 
veloped. This  steady  rise  in  tempera- 
ture, occurring  in  any  disease  in  which 
lobular  pneumonia  is  liable  to  be  devel- 
oped, is  one  of  its  most  valuable  diag- 
nostic suggestive  symptoms.  When 
death  occurs  early  the  temperature 
may  rise  to  1 08°.  The  pulse  rate  often 
reaches  140  to  150.'  In  twenty-four 
to  forty-eight  hours  it  becomes  small, 
compressible  and  feeble,  though  at 
fii-st  it  is  full  and  hard.  The  cough, 
which  during  the  bronchitis  was  loose, 
*'  bronchial,"  and  paroxysmal,  now 
becomes  dry,  hacking  and  non-par- 
oxysmal. It  is  usually  very  painful. 
The  expectoration  is  seldom  seen  in 
children ;  but  we  may  find  in  the  matters  vomited  clumps  of  tenacious, 
often  blood-streaked  muco-pus. 

After  a  time  the  dyspnoea  becomes  constant.  The  breathing  is  shallow, 
inspiration  is  short,  the  chest  expanding  but  very  slightly.  The  auxiliary 
muscles  are  called  into  play,  and  there  is  marked  expansion  of  the  nares 
during  inspiration.  The  pale  and  anxious  face  becomes  cyanotic,  and  the 
restlessness  and  jactitation  give  place  to  a  lethargic  semi-comatose  state, 
interrupted  by  occasional  but  ineffectual  attempts  to  cough.  Towards  the 
end  the  cough  almost  entirely  ceases.  Diarrhoea  frequently  increases  the 
exhaustion ;  and  vomiting  which  may  accompany  or  follow  the  cough, 
while  rare  at  the  onset  of  the  disease,  is  frequent  in  its  advanced  stages. 
Anorexia  is  an  early  symptom,  though  young  children  will  take  the  breast, 
while  older  children  cannot  be  made  to  swallow  even  the  blandest  liquids. 
The  tongue  may  become  dry  ;  sordes  collect  on  the  lips  and  teeth  ;  aphthous 
stomatitis  is  common.  Emaciation  is  rapid.  The  sub-acute  form  often 
occurs  in  the  bronchitis  of  strumous  children,  and  in  that  which  accom- 
panies measles  and  whooping-cough.  Its  occurrence  is  marked  by  an 
elevation  of  temperature,  but  the  rise  is  not  so  great  nor  so  sudden  as  in 
acute  cases ;  it  rises  gradually  until  it  reaches  103°  F.  or  104°  F.  The 
cough  becomes  more  severe  and  metallic  in  character,  and  the  respira- 
tion changes  from  the  labored  respiration  of  bronchitis,  to  the  rapid 
panting  respiration  of  pneumonia.  The  patient  begins  to  lose  flesh, 
becomes  pale,  has  profuse  sweatings  and  fits  of  exhaustion  ;  the 
appetite  becomes  capricious  or  is  entirely  lost;  loss  of  strength  and 
emaciation  are  progressive  ;  the  face  appears  bloated,  small  indolent  ab- 
scesses appear  on  the  nates  and  back,  the  patient  assumes  the  appearance 
of  extreme  anaemia,  and  finally  death  slowly  comes  from  wasting  and 
exhaustion. 


^  Jiirgensen  states  that  he  has  found  the  pulse  often  over  200  a  minute. 


LOBULAR   PNEUMONIA.  105 

Perhaps,  when  hope  of  recovery  has  been  abandoned  after  a  prolonged 
illness,  resolution  of  the  consolidated  lung  takes  place,  and  a  slow  though 
complete  recovery  is  reached.  When  the  disease  is  to  end  fatally  the  tem- 
perature rises  rapidly,  cyanosis  increases,  the  respiration  becomes  irregular 
in  rhythm,  and  the  comatose  state  is  interrupted  by  convulsions  in  which 
death  occurs.  Death  may  occur  suddenly  in  the  midst  of  a  violent  fit  of 
coughing.  The  disease  may  terminate  with  symptoms  which  resemble  those 
of  well-marked  tubercular  meningitis.  When  recovery  occurs,  it  is  very  slow, 
pulse-rate,  temperature,  cough,  and  dyspnoea  all  imperceptibly  diminish- 
ing. There  is  no  rapid  fall  in  temperature,  such  as  occurs  in  croupous 
pneumonia.  In  a  few  cases,  especially  in  older  children,  slight  delirium 
will  occur  at  night.  The  urine  contains  chlorides  and  slight  traces  of 
albumen. 

Chronic  lobular  pneumonia  differs  from  acute  in  the  severity  rather 
than  the  character  of  its  symptoms.  When  it  supervenes  upon  some  ca- 
tarrhal affection  of  the  bronchi  of  moderate  severity — a  whooping-cough  or 
an  attack  of  measles — the  temperature  gradually  rises  until  it  reaches  102° 
or  103°  Fahr.  Exacerbations  and  remissions  then  occur  which  are  more 
irregular  than  in  the  acute  or  sub-acute  variety.  The  respirations  increase 
in  frequency.  The  increase  in  the  pulse-rate,  the  dyspnoea,  the  anorexia, 
the  loss  of  flesh  and  strength — all  are  more  marked  than  in  the  acute  form 
and  much  more  persistent.  The  interference  with  respiration  is  greater 
than  in  lobar  pneumonia.  As  muscular  weakness  increases  the  auxiliary 
and  normal  respiratory  muscles  become  more  and  more  enfeebled,  and  the 
supply  of  oxygen  becomes,  in  some  cases,  so  much  diminished  as  to  cause 
complete  muscular  paralysis.  From  all  of  these  causes,  and  perhaps  from 
the  prolonged  fever,  the  heart  becomes  feeble.  Should  recovery  occur,  the 
fall  of  temperature  and  the  decline  of  the  other  symptoms  are  gradual,  and 
there  is  great  liability  to  a  second  attack  during  the  protracted  convalescence. 
A  spot  of  consolidation  often  remains  after  recovery  is  apparently  complete. 
Bronchiectasis,  fibroid  induration  of  the  lung  and  emphysema  are  frequent 
sequelae  ;  and  in  children  as  well  as  in  adults,  phthisis  is  a  not  infrequent 
sequela.  The  pneumonic  symptoms  are  much  less  pronounced  in  adults 
than  in  children,  except  when,  in  the  latter,  the  disease  suj)ervenes  upon 
diphtheria.  In  the  old  and  feeeble,  especially  when  they  have  lain  in  one 
position  for  a  long  time,  lobular  pneumonia  occurs  as  the  result  of  hypo- 
stasis, independent  of  bronchial  catarrh.  In  senile  bronchial  catarrhs 
gravitation  determines  the  lobular  pneumonia,  and  it  is  not  infrequently 
unilateral.  If  epidemic  influenza  is  complicated  by  lobular  pneumonia 
the  sputa,  in  adults,  may  be  quite  free  and  blood-streaked,  but  never 
rusty. 

Physical  Signs. — Inspection.  In  well-marked  cases  the  expansive  move- 
ment of  the  chest  is  diminished  ;  the  diaphragmatic  depression  is  deepened 
and  the  lower  ribs  may  appear  retracted.  Should  there  be  extensive  pul- 
monary collapse  the  chest  walls  will  be  retracted. 

Palpation. — Slight  increase  in  vocal  fremitus  may  exist  over  isolated 
spots,  if  the  pneumonic  nodules  are  large  and  near  the  surface. 


106  DISEASES   OF   THE   EESPIRATOKY   OEGANS. 

Percussion. — There  is  slight  dulness  over  the  consolidated  spots.  The 
diminished  pulmonary  resonance  in  lobular  pneumonia  is  not  easily  distin- 
guished from  lobular  collapse,  and  since  collapse  is  symmetrical,  usually 
involving  both  posterior  bases,  the  difficulty  is  increased.  One  should 
therefore  percuss,  in  succession,  over  similar  areas  on  either  side  of  the 
chest,  for  if  a  spot  of  dulness  on  one  side  has  no  counterpart  on  the  other, 
one  may  be  sure  that  it  corresponds  to  a  spot  of  pneumonic  consolidation, 
and  not  to  collapse.  The  upper  part  of  the  chest  may  be  extra  resonant 
and  even  tympanitic  if  there  is  mucli  emphysema. 

Auscultation. — On  auscultation,  small  mucous  rales  resembling  sub-crep- 
itant  rales,  having  a  fine,  crackling  and  metallic  character,  are  heard  over 
the  spots  where  there  is  dulness.  These  rdles  are  audible  both  with  inspi- 
ration and  expiration.  They  are  not  as  fine  as,  and  are  more  suj)erficial 
than  ordinary  pneumonic  crepitation.  In  children,  during  and  after  a  fit 
of  crying,  fine  crepitating  sounds  may  be  heard  which  were  not  audible 
during  quiet  respiration.  The  breathing  is  less  vesicular  and  may  even  be 
broncho-vesicular.  There  is  increased  vocal  resonance  and  perhaps  bron- 
chophony. The  respiration  in  unaffected  portions  of  the  lung  is  more  or 
less  exaggerated.  When  there  is  an  extensive  bronchitis  with  the  pneumo- 
nia, moist,  dry  and  bubbling  rales,  varying  from  the  finest  to  the  coarsest, 
may  be  heard  all  over  the  chest. 

Differential  Diagnosis. — Lobular  pneumonia  may  be  confounded  with 
croupous  pneumonia,  capillary  ironchitis,  acute  tuberculosis  and  pulmo- 
nary collapse. 

The  differentiation  between  lobar  and  lobular  pneumonia  has  been 
given. 

Capillary  bronchitis  may  be  primary ;  lobular  pneumonia  is  always 
secondary.  The  range  of  temperature  in  capillary  bronchitis  is  lower  than 
in  lobular  pneumonia.  The  breathing  is  labored  in  capillary  bronchitis  and 
panting  in  pneumonia.  Capillary  bronchitis  is  marked  by  exaggerated 
resonance  on  percussion  ;  lobular  pneumonia  by  dulness.  In  capillary 
bronchitis  rt4,les  are  heard  all  over  the  chest  and  there  is  no  bronchial 
character  to  the  breathing  ;  while  in  pneumonia  fine  rdles  are  heard  over 
the  dull  spots  accompanied  by  broncho-vesicular  respiration. 

Acute  tuberculosis  is  accompanied  by  a  higher  temperature  than  lob- 
ular pneumonia  and  the  pyrexia  precedes  the  physical  signs  of  bronchitis  ; 
whereas  in  lobular  pneumonia  the  signs  of  a  bronchitis  precede  the  physical 
evidences  of  consolidation.  Lobular  pneumonia  occurs  oftenest  in  the 
child  (1  to  4  years) ;  tuberculosis  occurs  in  early  adult  life.  Acute  tuber- 
culosis is  attended  by  more  rapid  exhaustion  and  emaciation,  and  haemop- 
tysis is  not  infrequent.  The  presence  of  brain  symptoms  is  in  favor  of 
tuberculosis.  The  history  of  an  inherited  tendency  to  tubercular  disease  is 
rarely  absent  in  tuberculosis. 

In  collapse  of  the  lung  there  is  a  tympanitic  quality  to  the  percussion 
note  over  the  unaffected  portions.  The  affected  side  is  more  retracted, 
and  sinking  of  the  ribs  and  elevation  of  the  diaphragm  are  more  marked 
than  in  pneumonia.    In  collapse  the  respiratory  murmur  is  feeble  or  absent 


LOBULAR   PKEUMONIA.  107 

and  has  no  bronchial  character.  Eales  are  rare  in  a  collapsed  portion  of 
lung.     Vocal  resonance  and  fremitus  are  diminished.' 

Prognosis. — The  prognosis  in  lobular  pneumonia  is  determined  almost 
entirely  by  the  conditions  which  precede  and  attend  its  development.  In 
children  under  five  the  average  mortality  is  one  in  five.  The  younger  and 
feebler  the  subject,  the  more  unfavorable  the  prognosis.  The  prognosis 
is  better  when  it  follows  measles  than  when  it  occurs  after  whooping- 
cough  and  scarlatina  or  when  it  complicates  renal  or  heart  disease.  When 
the  initial  bronchitis  is  severe  and  extensive,  when  the  temperature  rises 
rapidly  to  305°  to  106°  Fahr.,  when  there  is  cyanosis,  muscular  paralysis, 
and  the  pulse  is  feeble  and  frequent,  the  prognosis  is  very  unfavorable. 
Lobular  pneumonia  occurring  in  a  rachitic  subject  is  always  grave.  The 
greater  the  extent  of  lung  involved  the  more  unfavorable  the  prognosis. 
The  more  abrupt  the  onset  the  better  the  prognosis.  The  average  duration 
of  acute  lobular  pneumonia  is  from  ten  to  fourteen  days  ;  death  may  occur 
within  the  first  week.  Chronic  lobular  pneumonia  may  be  complicated  by 
capillary  bronchitis,  fibroid  induration  of  the  lung,  tuberculosis,  jDleurisy, 
emphysema  and  pneumothorax.  A  very  frequent  complication  is  acute 
intestinal  catarrh.  It  may  be  complicated  by  pyaemia  and  pulmonary 
infarcts  non-pymnic  in  origin.  Death  may  result  from  asthenia,  asphyxia, 
or  from  complications. 

Treatment. — It  must  be  borne  in  mind  in  the  treatment  of  this  affection, 
that  it  is  a  secondary  disease  and  that  its  occurrence  indicates  that  the  pa- 
tient is  in  an  enfeebled  condition.  All  depressing  remedies  must  be  avoided; 
even  when  the  disease  assumes  a  very  active  form  depletion  is  not  allow- 
able. When  the  bronchitis  is  extensive,  vapor  inhalations  and  the  internal 
use  of  muriate  of  ammonia  are  to  be  employed  in  accordance  with  the  plan 
proposed  in  the  treatment  of  capillary  bronchitis  in  children.  The  patient 
should  be  kept  in  a  warm  room,  the  temperature  of  which  should  never 
fall  below  60°  F.  The  ventilation  should  be  as  thorough  as  possible,  but  all 
draughts  and  sudden  changes  of  temperature  should  be  avoided.  The  air 
should  be  kept  moist  and  the  body  should  be  covered  with  flannel.  Some 
recommend  cold  compresses  to  the  chest ;  the  cold  pack  is  likewise  advocated. 
Cold  baths  or  baths  from  77°  to  86°,  which  are  subsequently  lowered  to  60° 
Fahr.,  are  also  advocated  even  for  young  children.  Jiirgensen  recommends 
that  a  small  stream  of  cold  water  be  thrown  just  over  the  upper  part  of  the 
back  of  the  neck,  the  irrigation  of  which  produces  the  most  violent  respira- 
tory efforts.  My  experience  has  been  altogether  against  cold  applications  ; 
and  I  regard  the  application  of  counter-irritants,  blisters,  etc.,  especially  to 
young  children,  as  productive  of  more  harm  than  good.  I  prefer  that  the 
chest  should  be  enveloped  in  linseed  or  mild  mustard  poultices.  Or,  in 
very  young  children,  it  may  be  rubbed  two  or  three  times  a  day  with  a 
stimulating  liniment  and  wrapped  in  cotton-batting  covered  with  oiled 
silk. 

1  Jiirgensen  states  that  the  differential  diagnosis  between  collapse  and  catarrhal  i)neumonia  can  be 
determined  only  in  two  ways  :  the  diminution  in  volume  of  a  certain  portion  of  the  lung,  if  distinctly 
demonstrated,  is  evidence  of  simple  collapse,  an  increase  in  volume  is  evidence  of  infiltration.  In  pulmo- 
nary collapse  there  is  not  the  rise  of  temperature  which  always  attends  broncho-pneumonia 


108  DISEASES   OF   THE   KESPIRATORY    ORGANS. 

During  the  whole  course  of  the  disease  the  food  should  be  fluid,  nutri* 
tious,  and  administered  in  sniall  quantities  and  at  short  intervals.  Brandy 
or  gin  in  milk,  ten  to  twenty  drops  every  three  or  four  hours,  may  be  given 
to  a  very  young  infant,  and  the  quantity  may  be  increased  until  the  pulse 
is  increased  in  force,  the  respirations  become  less  frequent,  and  the  distress 
and  cyanosis  diminish.  As  a  rule  stimulants  must  be  commenced  at  the 
very  onset  of  the  disease  and  continued  throughout  its  entire  course;  the 
quantity  to  be  administered  is  to  be  determined  by  the  necessities  of  each 
case.  The  drug  which  has  most  power  in  reducing  temperature  and  com- 
bating asthenia  is  the  sulphate  of  quinine,  which  may  be  given  in  full  doses 
during  the  period  of  fever ;  and  as  an  aid  to  resolution  it  is  most  serviceable 
during  the  active  period  of  the  disease.  From  ten  to  twenty  grains  may 
be  administered  daily  to  a  child  three  years  of  age.  If  the  attendant 
bronchitis  is  extensive  and  the  accumulation  in  the  tubes  obstructs  the 
entrance  of  air  into  the  lungs,  emetic  doses  of  ipecacuanha  will  often 
afford  great  relief.  Apomorphia  is  advocated  by  some,  but  the  danger  of 
its  producing  collapse  is  very  great  in  young  children.  Under  no  consid- 
eration is  opium  to  be  given.  Oil  of  turpentine,  five  drops  every  four 
hours,  is  often  beneficial  in  chronic  cases.  While  a  patient  with  acute  lob- 
ular pneumonia  should  always  be  kept  in  bed,  it  cannot  be  too  constantly 
borne  in  mind  that  he  should  not  constantly  lie  upon  his  back,  for  collapse 
and  hypostasis  are  apt  to  occur  in  a  lung  whose  power  of  resistance  is 
diminished.  Convalescence  should  be  managed  with  the  greatest  care,  for 
fatigue  and  exposure  may  induce  bronchitis,  a  second  attack  of  lobular 
pneumonia,  and  quite  probably  the  advent  of  phthisis  will  be  hastened,  if 
a  tendency  to  that  disease  exists.  If  the  disease  is  prolonged  and  emacia- 
tion is  marked,  cod -liver  oil,  iron  by  hydrogen,  or  the  syrup  of  the  iodide 
of  iron  should  be  given,  with  a  change  of  air. 


INTEESTITIAL   PJSTEUMONIA. 

Interstitial  pneumonia  is  a  fibroid  induration  of  the  lung  due  to  chronic 
Inflammation  involving  its  fibrous  framework.  Multiplication  of  the  con- 
nective-tissue elements  in  the  pulmonary  septa  takes  place,  which  leads  to 
progressive  obliteration  of  the  alveolar  cavities  and  conversion  of  portions 
of  the  lung  into  callous  fibrous  masses.  It  has  been  called  chronic  fibroid, 
and  chronic  interstitial  pneumonia  ;  also  scirrhus  and  cirrhosis  of  the 
lung.  ^ 

Morbid  Anatomy. — The  new  tissue  formation  in  this  variety  of  pneumo- 
nia may  involve  the  walls  of  the  air- vesicles,  the  bronchi,  the  blood-vessels, 
and  the  pleura.  It  may  be  arranged  in  the  form  of  nodules,  bands,  or  ir- 
regular patches,  and  it  may  involve  an  entire  lobe.  The  lung  is  sometimes 
shrunken  from  one-third  to  one-quarter  its  normal  size.    The  first  change  is 

1  Chomel  and  Grisolle  state  that  it  is  very  rare.  Fox  (Reynolds'  Practice^  p.  245)  says  it  is  rare  except 
in  connection  with  tubercles  ;  but  Niemeyer  (Practice  Medicine,  vol.  i.  p.  195)  states  that  it  is  one  of  tha 
most  frequent  pulmonary  diseases. 


INTERSTITIAL   PNEUMONIA. 


109 


hyperaemia  of  the  intercellular  and  interlobular  tissue,  followed  by  the  de- 
velopment of  fibro-nucleated  tissue  from  the  alveolar  and  bronchial  walls, 
and  from  the  interlobular  connective-tissue.  At  the  same  time  the  alveo- 
lar epithelium  undergoes  more  or  less  pro- 
liferation. As  the  new  tissue  contracts,  it 
slowly  replaces  and  obliterates  the  alveolar 
structure.  As  a  consequence,  the  calibre  of 
the  air-cells  is  diminished.  The  new  tissue 
development  may  reach  such  an  extent  that  all 
of  the  air-cells  of  that  portion  of  the  lung 
which  is  the  seat  of  the  process  may  be  oblit- 
erated, and  no  trace  of  lung-tissue  remain. 
This  is  not  infrequently  observed  in  the  sub- 
pleural  tissue,  and  at  the  apex  of  the  lung 
in  chronic  pleuritis.  The  alveolar  cavities, 
when  not  obliterated,  are  empty  or  contain  ex- 
udation products.  Frequently,  dense  fibrous 
bands  pass  in  from  a  thickened  pleura, 
and  the  changes  are  more  localized.  The 
nuclei  of  the  capillaries  participate  in  these 
fibroid  changes.  *  In  a  few  instances  the  proc- 
ess begins,  and  is  chiefly  located,  in  the 
tissue  about  the  bronchi  and  the  blood- 
vessels. 

On  section  of  a  lung  or  portion  of  a  lung  that  is  the  seat  of  interstitial 
pneumonia,  there  is  a  creaking  sound  with  the  movement  of  the  knife,  ac- 
companied by  a  sense  of  resistance  that  normal  lung  never  offers.  The 
lung  substance  tears  with  difiiculty.  The  cut  portion  is  firm,  dry,  hard, 
solid  and  shining,  its  color  varying  :  at  times  it  is  of  a  dull,  glistening, 
slaty  blue  ;  at  others  whitish,  resembling  an  amyloid  organ  ;  or  it  may  be 
yellowish  red.^  The  bluish-colored  lung  is  called  by  some  "gray  black- 
fibroid  induration."  ^  Sometimes  the  cut  surface  presents  a  marbled  appear- 
ance, due  to  the  irregular  pigmentation  of  the  interstitial  tissue.  The  bron- 
chi are  usually  dilated  in  those  portions  where  the  fibroid  changes  are  well 
marked.  The  dilated  tubes  may  form  cavities  of  considerable  size,  and 
their  mucous  surfaces  are  often  ulcerated,  or  the  seat  of  intense  passive 
hyperemia.  Bronchial  dilatations  rarely  occur  unless  there  has  been  a  pre- 
ceding pei'i-bronchitis,  which  has  diminished  the  elasticity  of  the  bronchial 
tubes.  As  the  new  connective-tissue  develops  at  different  points,  the  weak- 
ened bronchi  become  constricted,  and  as  a  result  of  this  constriction  bron- 
chiectases form,  the  dilatation  being  increased  by  the  violent  inspiratory 
efforts  that  attend  the  fits  of  coughing  which  are  so  common  in  interstitial 
pneumonia.  It  has  been  maintained  that  with  the  diminution  in  size  of 
the  lung,  there  is  compensatory  retraction  of  the  chest-walls  ;  but  that  this 


Fig.  26. 
Interstitial  Pneumonia. 

Section  of  Lung  thrauyh  one  of  the 
inletiobular  septa  with  the  contiguous 
vesicular  structure. 

A  A.  Band  of  neiv  connective-tissue 
from  an  interlobular  septum — mnch 
thickened  and  containing  many  lym- 
phoid and  large  nucleated  cells. 

B  B  B.  Pulmonary  alveoli  on  one  side 
of  the  lobular  septum  with  walls 
thickened  and  infiltrated.  Changed 
epilhelia  are  seen  crowding  the  air- 
vesicles.     X  200. 


'  Fox  in  "Reynolds'  System." 

2  "  Red  induration  of  chronic  pneumonia." — Fox. 

3  Reynolds'  System.    Art.  Pneumonia. 


110  DISEASES   OF   THE   KESPIRATOKY   OEGANS. 

compensation  being  inadequate  to  the  loss  in  size,  dilatation  of  the  Ironchi 
occurs,  to  restore  the  equilibrium.' 

Microscopically ,  the  new  tissue  is  seen  as  a  dense  homogeneous,  or  ob- 
scurely fibrillated  mass,  containing  comparatively  few  cells.  Pigmentation 
is  especially  marked  about  the  vessels,  and  shades  off  gradually  into  the 
new  tissue.  The  arteries  are  not  obliterated,  but  when  cut  across  stand 
gaping  in  the  section.^  The  pleura  of  the  affected  lung  is  thickened  and 
adherent.  The  bronchial  lymphatic  glands  may  be  hypertrophied,  indu- 
rated, or  cheesy.  The  heart  is  somewhat  hypertrophied,  and  nearly  always 
displaced  when  there  is  considerable  retraction.  Granular  kidney  and 
granular  or  cirrhotic  liver  are  frequent  accompaniments ;  and  all  these 
changes  are  ascribed  to  the  existence  of  a  "fibroid  diathesis."  ^ 

Etiology. — Interstitial  pneumonia  is  always  secondary — a  conservative 
process  in  many  instances.  All  protracted  inflammatory  processes  in  the 
lungs  are  attended  by  more  or  less  interstitial  pneumonia.  All  pulmonary 
phthisis,  unless  it  run  a  very  acute  course,  is  attended  by  it.  It  is  the 
limit  of  progression  in  many  cases  of  peri-bronchitis,  and  occurs  in  all  lung 
tissue  which  is  the  seat  of  neoplasms,  infarctions,  encapsulated  abscesses, 
etc.  Chronic  bronchitis  inducing  a  dry  pleurisy,  with  the  gradual  devel- 
opment of  thickenings  and  adhesions,  is  a  frequent  determining  cause  of 
interstitial  pneumonia  ;  it  progresses  more  rapidly  when  starting  from  the 
pleura,  than  from  any  other  centre.  Interstitial  pneumonia  is  more  apt  to 
develop  in  the  gouty  and  rheumatic,  after  pleurisy  or  bronchitis,  than  in 
any  other  class.  Niemeyer  states  that  it  may  result  from  simple  "col- 
lapse." 

Symptoms. — The  subjective  symptoms  of  interstitial  pneumonia  are  at 
no  time  well  defined  ;  and  it  is  impossible  to  determine  the  exact  period  of 
its  commencement,  for  in  the  majority  of  cases  its  symptoms  are  continu- 
ous with  those  of  the  pre-existing  disease.  If,  after  a  lobular  or  pleuro- 
pneumonia, the  dulness  on  percussion,  bronchial  breathing,  absence  of  the 
vesicular  respiration,  slight  elevation  of  temperature,  cough  and  dysp- 
noea continue  beyond  the  period  at  which  resolution  should  occur,  the  de- 

1  Sir  D.  Corrigan.  Ziems?en  records  a  case  where  dilatation  of  the  bronchi  occurred  in  both  lungs, 
while  induration  was  found  only  in  one.  Secondary  inflammation  of  the  indurated  parts  is  regarded  by 
Traube  as  one  of  the  most  common  causes  of  gangrene  of  the  lung.  In  100  cases  of  bronchiectasis  gangrene 
occurred  in  eight. 

2  Comil  and  Ranvier  describe  a  senile  (?  physiological)  condition  of  lung  called  slaly  wduration  of 
the  apex.  The  tissue  is  hard,  elastic,  non-crepitant  and  black ,  upon  the  surface  it  sometimes  presents  de- 
pressed cicatrices  of  the  pleura  and  dense  fibrous  adhesions.  Upon  section  there  is  seen  a  dense  tissue 
formed  of  thickened  septa,  limiting  retracted  alveoli  ;  or  there  are  emphysematous  dilatations  surrounded 
by  a  dense  fibrous-tissue  which  is  infiltrated  with  black  pigment.  Caseous  or  calcareous  nodules  lodged  in 
minute  cystic  cavities  are  also  formed  in  the  midst  of  this  fibrous-tissue.  The  nodules  are  altered  pus. 
Here  we  also  find  spiculfe  of  bone  at  the  apex  in  some  cases. 

3  Rokitansky,  in  his  Pathological  Anatomy,  thus  describes  a  bronchiectatic  cavity  :  ''We  find  a  bron- 
chial tube  widened  into  a  fusiform  or  rounded  pouch  :  in  the  latter  case  the  dilatation  often  being  greater 
one  side  than  on  another,  so  that  a  greater  part  of  the  bronchial  sac  lies  out  of  the  axis  of  the  bronchial 
tube.  In  rare  cases  the  size  of  such  apoucii  may  equal  that  of  a  hen's  egg.  They  will  often  contain  a  bean, 
a  hazel-nut,  or  a  walnut.  We  further  find,  either  that  any  one  of  the  bronchial  tubes  may  become  ex- 
panded into  a  pouch  of  this  kind,  the  tube  retaining  its  normal  calibre  on  either  side  of  the  dilatation  ;  or 
else  quite  a  large  tract  of  the  bronchial  ramifications  may  undergo  enlargement.  Then  many  such  Bacs  of 
different  size  are  so  grouped  together  that  they  form,  as  it  were,  a  vast  sinuous  case  with  many  branches, 
whose  individual  pouches  are  bounded  and  separated  from  one  another  by  ledges  or  valvular  folds  of  the 
bronchial  wall." 


INTERSTITIAL  PNEUMOiflA.  Ill 

velopment  of  interstitial  pneumonia  may  be  suspected.  Dyspnoea  is  a  con- 
stant symptom,  and  is  increased  by  active  exercise,  and  by  lying  on  the 
unaffected  side.  Cough  is  rarely  absent,  and,  as  the  disease  progresses,  it 
becomes  paroxysmal.  It  may  be  accompanied  by  a  copious  muco-purulent 
or  gray-black  fetid  expectoration.  Sometimes  it  will  separate,  on  standing, 
into  three  layers: — the  lowest  contains  the  solid  matter,  and  is  yellow  in  color; 
the  middle  is  a  greenish  fluid  ;  and  the  surface  is  frothy,  containing  mucus 
iind  fat-granules.  If  there  are  deep-seated  bronchiectases,  the  cough  is  har- 
assing and  painful  ;  when  ulceration  of  the  bronchial  mucous  membrane 
exists,  haemoptysis  is  not  infrequent.  The  pyrexia  has  no  regular  or  typ- 
ical course  ;  the  temperature  is  often  highest  in  the  evening,  rarely  rising 
above  102°  F.  The  morning  temperature  may  be  normal.  The  respira- 
tions and  pulse  are  but  slightly  accelerated,  there  will  be  gradual  loss  of 
flesh  and  strength,  night-sweats,  dyspeptic  symptoms,  and  not  infrequently 
diarrhoea.  The  fever  assumes  a  hectic  type,  and  the  consequent  ansemia 
and  interference  with  the  pulmonary  circulation  lead  to  general  dropsy.  In 
some  instances  a  large  portion  of  lung  may  remain  indurated  for  a  long 
time,  without  giving  rise  to  any  symptoms  except  dyspnoea.  The  jjatient 
always  lies  on  the  affected  side  ;  any  other  position  increases  dyspnoea  and 
cough. 

Physical  Signs. — Inspection.  After  retraction  of  the  lung  has  occurred, 
inspection  will  show  retraction  of  the  chest-walls  over  the  indurated  por- 
tion of  lung,  with  marked  loss  of  expansion  on  the  affected  side.  With- 
out these  signs  the  diagnosis  of  interstitial  pneumonia  cannot  be  made. 
The  younger  the  patient,  the  more  the  chest-walls  are  retracted.  There 
will  be  bulging  of  the  healthy  side,  and  increased  respiratory  movement. 
The  apex-beat  will  be  displaced  to  the  right  or  left,  according  as  the  right 
or  left  lung  is  the  seat  of  induration.  In  some  rare  instances  it  is  so  dis- 
placed as  to  be  seen  under  the  right  nipple  or  under  the  left  clavicle.'^ 

Palpation. — Vocal  fremitus  is  usually  increased  over  the  affected  portion 
of  the  lung,  but  it  may  be  diminished. 

Percussion  elicits  a  dull  note,  '"'toneless"  or  ''wooden  "in  character. 
The  note  is  high  pitched,  and  somewhat  tubular.  A  sense  of  resistance  is 
imparted  to  the  hand  in  percussing.  The  normal  lung  may  overlap  its 
shrunken,  indurated  fellow  ;  hence,  dulness  will  not  be  as  well  marked  an- 
teriorly as  posteriorly.  It  may  even  be  normal  in  front  and  dull  and  wooden 
behind.     The  percussion  note  over  the  opposite  lung  is  extra-resonant. 

Auscultation. — There  is  a  loss  of  vesicular  quality  in  the  respiration  over 
the  affected  portions  of  lung,  and  the  breathing  is  more  or  less  bron- 
chial in  character.  The  bronchial  sounds  are  loud  and  sometimes  am- 
phoric. Bronchophony  and  pectoriloquy  are  not  infrequently  present. 
Rales  are  heard,  varying  from  the  large,  moist,  metallic,  to  the  high-pitched 
bubbling.  The  rales  may  only  be  audible  after  coughing.  The  respiration 
in  the  unaffected  side  will  be  exaggerated. 

Differential  Diagnosis. — Interstitial  pneumonia  may  be  confounded  with 

'  Niemeycr  states  that  the  "  depression  of  the  infra-  and  Mipra-clavicnlar  regions  which  accompanies 
pulmonary  consumption  is  due  to  interstitial  pneumonic  induration." 


112  DISEASES   OF  THE  EESPIEATOKY  ORGAN'S. 

nleurisy  with  retraction,  cancer  of  the  lung,  collapse  of  one  lung,  and  puU 
monary  phthisis.  It  is  often  difficult  to  distinguish  fibroid  pneumonia 
from  pleurisy  with  retraction,  and  without  the  aid  of  an  intelligent  history 
it  is  impossible.  There  will  be  retraction  of  the  chest-walls  in  both.  The 
retraction  from  pleurisy  is  uneven,  the  ribs  are  twisted,  and  the  spine  more 
or  less  curved.  In  interstitial  pneumonia  the  retraction  is  uniform,  and 
there  is  a  general  diminution  in  size  of  the  affected  side.  Hgemoptysis,  fetid 
expectoration,  and  pyrexia  may  be  present  in  induration  of  the  lung,  but 
not  in  pleurisy  with  retraction.  Bronchial  respiration  is  usually  present  in 
pneumonia,  while  the  respiratory  sounds  are  feeble  or  entirely  absent  over 
the  affected  side  in  pleurisy. 

In  distinguishing  fibroid  induration  of  the  lung  from  cancer  of  the  lung, 
although  the  physical  signs  of  the  two  conditions  are  similar,  the  history  of 
the  two  diseases  is  so  different  that  by  it  alone  a  differential  diagnosis  can 
be  made.  Then  the  existence  or  non-existence  of  cancer  in  other  parts 
of  the  body  is  important,  for  primary  cancer  of  the  lung  or  pleura  is  rarely 
met  with.  After  the  cancer  has  become  sufficiently  extensive  to  simulate 
the  physical  signs  of  pneumonia,  there  can  be  but  little  difficulty  in  the 
diagnosis.  For,  at  that  late  period,  the  constitutional  disturbances  attend- 
ing the  development  of  a  cancer,  as  manifested  by  the  cachectic  look  and 
the  glandular  enlargements,  will  make  the  way  to  a  correct  diagnosis  quite 
plain.     If  the  disease  has  lasted  two  years  or  over,  cancer  is  excluded. 

Collapse  of  an  entire  lung  is  exceedingly  rare,  and  can  only  be  caused  by 
a  tumor  pressing  on  a  main  bronchus.  In  collapse  the  respiratory  sounds 
would  be  feeble  or  absent,  and  there  would  be  no  cough,  expectoration,  or 
constitutional  symptoms.  If  pressure  on  the  trachea  or  a  main  bronchus 
is  long  continued,  the  lung  supplied  by  the  compressed  bronchus  will  be 
studded  with  hepatized  lobules,  collapsed  lobules,  and  interstitial  pneumo- 
nia ;  the  diagnosis  will  be  determined,  not  by  the  physical  signs,  but  by  the 
presence  of  the  tumor. 

Prognosis. — Interstitial  pneumonia  is  never  a  direct  cause  of  death. 
Such  patients  live  for  years,  and  suffer  only  from  dyspnoea.  As  it  is  a  sec- 
ondary disease,  the  prognosis  will  be  determined  by  the  primary  disease. 
Extensive  induration  of  the  lung,  following  a  slowly  resolving  croupous 
pneumonia  and  accompanying  a  chronic  bronchitis,  may  continue  for  years 
after  bronchial  dilatations  have  occurred.  The  dangers  and  causes  of 
death  are  intercurrent  pulmonary  affections,  marasmus,  haemoptysis,  and 
secondary  right  heart  dilatation^  accompanied  by  tricuspid  regurgitation. 
If  gangrene  occurs  in  indurated  tissue,  it  rapidly  extends,  and  causes  death 
by  exhaustion  or  septicisemia.  Some  cases  of  sudden  and  unexpected  death 
occur  from  thrombosis  of  the  pulmonary  artery. 

Treatment. — Advanced  interstitial  pneumonia  is  incurable.  Cicatricial 
tissue,  once  formed  in  the  lungs,  remains  during  the  life  of  the  patieiit. 
Something  may  be  done  to  prevent  its  further  development ;  if  it  is  devel- 
oped from  a  bronchitis  or  a  pleurisy,  it  is  important  to  guard  against  the 
recurrence  of  the  bronchitis  or  pleurisy.  Under  these  circumstances,  the 
hygienic  and  climatic  conditions  are  all  important,  and  the  individual 


HYPEE^MIA   OF   THE    LUNGS.  113 

should  live  in  the  climate  which  is  best  suited  to  his  condition ;  high 
altitudes  are  always  indicated.  Besides  residence  in  a  proper  climate,  the 
patient  should  be  warmly  clad,  and  efforts  should  be  made  to  improve  the 
general  health.     Ood-liver  oil  and  iron  are  serviceable  in  most  cases- 

HYPERJEMIA    OF   THE    LUNGS. 

Hyperaemia  of  the  lungs  is  a  condition  in  which  there  is  an  excess  of  blood 
in  the  lungs  ;  it  may  be  local  or  general,  active  or  passive.  Active  hyper- 
semia,  or  fluxion,  is  not  of  so  frequent  occurrence  as  passive  hyperaemia  or  con- 
gestion. The  former  is  due  to  increased  afflux  of  blood  ;  the  latter  to  ob- 
structive causes  which  slow  the  current  and  favor  accumulation  of  the  blood 
in  the  pulmonary  capillaries.  Active  pulmonary  hyperemia  may  be  associ- 
ated with  violent  and  accelerated  action  of  the  heart.  It  may  be  developed 
in  young  persons  with  contracted  chest  by  violent  exercise,  like  running  or 
jumping.  It  may  follow  sudden  checking  of  an  habitual  flow,  mental  ex- 
citement, or  the  drinking  of  large  quantities  of  alcohol.  Sudden  diminution 
of  the  atmospheric  pressure  (as  during  a  violent  inspiration),  e.  g.,  in  croup, 
laryngitis,  or  whooping-cough,  may  cause  active  hyperaemia.  It  may  be 
developed  by  the  inhalation  of  stimulating  gases  or  a  highly  rarefied  atmos- 
phere such  as  is  met  with  at  high  elevations. 

Passive  hyperaemia,  or  pulmonary  congestion,  depends  upon  an  obstruc- 
tion to  the  return  circulation.  It  occurs  with  varying  appearances  and 
anatomical  characteristics  that  have  led  to  its  subdivision  into  splenization, 
Irown  induration,  and  hypostatic  congestion.  A  form  of  active  hyperaemia 
has,  because  of  its  physiological  cause  and  situation,  been  called  compensa- 
tory JiypercBmia.  Other  divisions  are  sometimes  made,  but  all  the  varieties 
can  properly  be  classified  under  these  heads. 

Morbid  Anatomy. —In  active  hyperaemia  the  lungs  contain  more  blood 
than  normal.  On  section  a  bright  red  frothy  fluid  flows,  and  if  the  active 
hypersemia  be  local  and  compensatory,  extensive  oedema  may  result.  The 
mucous  membrane  of  the  bronchial  tubes  may  be  minutely  injected.  The 
alveolar  epithelium  undergoes  nutritive  changes,  and  becomes  swollen  and 
granular.  The  pulmonary  capillaries  stand  out  turgid  and  distinct  in  the 
alveolar  wall. 

In  passive  hyperaemia  the  lungs,  wholly  or  in  part,  are  distended,  of  a 
dark  blue  or  dark  red  color,  crepitating  little,  and  are  heavier  and  less  elas^ 
tic  than  normal.  The  process  begins  in  the  lower  lobes  and  then  becomes 
general.  On  section,  dark  blood,  often  in  considerable  quantity,  flows  freely 
from  the  cut  surface,  but  the  lung-tissue  retains  its  dark  color  because  much 
blood  still  remains  in  the  capillary  vessels.  The  interstitial  tissue  is  often 
oedematous  and  studded  with  points  of  extravasation.  The  bronchial  tubes 
and  pleura  ^ow  post-mortem  staining.  Epithelial  changes  are  very  com- 
mon, and  the  alveoli  may  contain  many  swollen  and  granular  cells  that  have 
become  detached.  Even  fibrin  and  leucocytes  are  found  in  the  air-cells  in 
simple  congestion.^ 

'  Comil  and  Ranvier. 


114  DISEASES    OF   THE   RESPIRATORY   ORGANS. 

8plenization  is  a  form  of  congestion  whicii  has  received  its  name  from 
the  close  resemblance  which  the  affected  portion  of  lung-tissue  bears  to  the 
spleen.  The  portion  of  lung  which  is  the  seat  of  this  form  of  congestion 
is  of  a  darker  color  than  normal,  and  scattered  throughout  its  substance 
will  be  seen  little  red  or  yellowish-white  points  ;  these  little  points  are  sim- 
ply blood  extravasations.  Lung-tissue,  in  a  condition  of  splenization,  is  of 
a  dark  reddish-blue,  brown,  or  black  color,  airless,  firmer  than  normal, 
crepitates  less  freely,  has  a  more  uniform  homogeneous  appearance  upon  its 
cut  surface,  and  is  less  moist  than  normal  lung-tissue  ;  a  dark  fluid  will 
sometimes  ooze  from  its  cut  surface,  but  not  so  freely  as  in  the  other  forms 
of  hyperaemia,  and  the  fluid  is  more  watery  in  appearance.  In  splenization 
there  is  swelling  of  the  alveolar  walls,  dilatation  and  tortuosity  of  the 
vessels,  and  a  more  or  less  collapsed  state  of  the  lung  ;  and  when  a  con- 
gested lung  is  also  deprived  of  air  it  looks  like  muscle,  and  the  condition  is 
then  called  "  carnification  of  the  lung."  In  the  development  of  this  con- 
dition hyperemia  occurs  and  is  followed  by  interstitial  oedema  ;  it  is 
this  interstitial  oedema  that  distinguishes  splenization  from  hypersemia.  It 
occurs  in  connection  with  typhoid  and  typhus  fever,  measles  or  any  disease 
in  which  there  are  certain  blood  changes,  and  it  is  always  developed 
slowly. 

Hypostatic  congestion  is  a  term  applied  to  that  form  of  hyperaemia  which 
occurs  in  the  most  dependent  parts  of  the  lungs  ;  it  is  usually  bilateral  in 
those  dying  of  diseases  which  have  confined  them  in  bed  for  a  long  time. 
It  very  closely  resembles  splenization,  but  the  lung-tissue  is  very  friable  in- 
stead of  doughy,  and  the  little  whitish  or  reddish  points  which  are  seen  in 
splenization  are  absent  in  hypostatic  congestion.  The  lung  texture  itself  is 
but  little  altered.  Low  forms  of  pneumonia  are  liable  to  occur  iil  hypostatic 
congested  parts  of  the  lung,  and  hence  some  call  it  ''hypostatic  pneumo- 
nia," and  others  again  call  it  splenification  (differing  from  the  above  de- 
scribed splenization). 

Compensatory,  or  collateral,  congestion,  is  that  form  of  congestion  which 
occurs  in  one  portion  of  the  lungs,  because  of  obstructed  circulation  in  some 
other  portion.  The  pulmonary  congestion  in  unaffected  portions  of  the  lung 
in  pneumonia  and  pleurisy  is  an  example  of  this  form.  The  same  kind 
■occurs  in  collapsed  lung-tissue,  and  about  points  of  venous  obstruction, 
tumors,  emphysema,  etc.,  etc. 

Broion,  or  pigment,  induration^,  by  some  called  the  pneumonia  of  heart 
disease,  is  a  form  of  congestion  especially  connected  with  obstruction  or  re- 
gurgitation at  the  mitral  orifice.  The  lung  is  distended,  firm,  heavy,  seldom 
Very  moist,  of  a  dark  brown  or  red  color,  and  usually  contains  only  a  moder- 
ate amount  of  air.  It  is  dotted  with  yellowish  or  brownish  spots,  usually 
of  small  size,  while  its  own  color  is  generally  red.  The  capillaries  of  the 
lung  are  exceedingly  enlarged,  both  in  width  and  length  ;  sometimes  they 
;are  three  times  as  long  as  normal,  and  encroach  on  the  lumen  of  the  al- 
veoli. The  brown  or  yellow  spots  are  due  to  old  blood  extravasations  which 
have  undergone  granular  and  pigment  degenerations  ;  red  spots  from  recent 

1  First  described  by  Virchow,  in  1847. 


BROWN   INDURATION    OF   THE   LUNGS. 


115 


extrarasations  are  often  found  beside  the  old  ones.  Some  parts  of  the  lung 
may  present  these  changes  very  markedly,  while  others  are  but  little 
affected.  Within  the  air-cells  are  usually  found  large  cells  which  have  un- 
dergone more  or  less  pigmentation.  In  and  around  the  connective-tissue  cells 
are  seen  these  pigment  granules  in  great  number.  All  of  these  changes 
result  from  prolonged  interference 
with  the  return  circulation.  Inter- 
stitial connective-tissue  thicken- 
ings occur  in  this  form.  The 
pigmentation  which  is  present  is 
the  result  of  the  long-continued 
retention  of  blood  in  the  parts, 
and  the  consequent  changes  in  the 
blood  itself.  Minute  blood  extra- 
vasations, or  even  diffuse  pulmo- 
nary hemorrhage,  may  occur  with 
brown  induration.  The  pulmo- 
nary arteries  and  veins  are  enlarged 
and  congested,  and  the  smooth 
muscular  fibres  of  the  parenchyma 
of  the  lung  may  undergo  hypertro- 
phy. A  brownish  fluid  sometimes 
flows  from  the  cut  surface  (Yir- 
chow's  "  brown  oedema  "). 

Etiology. — The  causes  of  the  dif- 
ferent varieties  of  pulmonary  hy- 
pergemia  I  have  sutficiently  considered  in  connection  with  their  morbid 
anatomy,  so  that  they  do  not  require  separate  consideration. 

Symptoms.  —It  is  difficult  to  distinguish  the  symptoms  of  pulmonary  con- 
gestion from  those  of  pulmonary  oedema,  and  also  from  those  of  diseases 
in  which  it  is  liable  to  occur  as  a  complication.  If  the  congestion  is  con- 
siderable, there  is  more  or  less  dyspnoea,  cough,  and  expectoration.  Blood- 
stained, watery  expectoration  is  the  prominent  objective  symptom  of  pul- 
monary congestion.  The  advent  of  active  hypermraia  is  usually  very 
sudden.  Dyspnoea,  more  or  less  marked,  is  present  in  both  active  and 
passive  hypersemia ;  it  arises  from  decreased  alveolar  capacity  and  conse- 
quent diminished  supply  of  oxygenated  blood  to  the  system.  The  dyspnoea 
is  often  urgent  if  the  congestion  is  extensive,  but  in  many  cases  of  passive 
hyperaemia  there  will  be  little  change  in  the  respiration ;  the  patient  be- 
comes accustomed  to  habitual  dyspnoea  and  suffers  no  special  inconven- 
ience except  moderate  shortness  of  breath  on  physical  exertion;  especially  is 
this  the  case  in  brown  induration  of  the  lungs; — a  feeling  of  tightness  or 
oppression  is  often  experienced  in  the  chest,  but  pain  is  rarely  present.  In 
extreme  cases  of  passive  hyperaemia  there  is  usually  lividity  of  the  lips  and 
extremities,  and  a  sense  of  prostration ;  all  the  symptoms  which  attend 
imperfect  aeration  of  the  blood  are  developed,  and  the  patient  dies  as  in 
pulmonary  oedema.     The  temperature  may  be  elevated ;  in  pigment  indu- 


Section  of  Lung  showing  a  single  Alveolus  in  Brown 
Induration. 

W.  Wall  of  alveolus  thickened  and  containing  masses 

of  pigment.    Pq. 
VV.  Cajnllay^es,  sit'otlen,  tortuous ;  at  B,  the  vessel 
rupturing.,  blood  escapes  into  the  alveolus. 
P.  Infiltration  of  pus. 
E.  Epithelium,,  swollen,  distorted  and  pigmented. 

X  350. 


116  DISEASES   OF  THE  EESPIRATOET   OEGANS. 

ration  it  may  be  100°  to  102°,  according  to  Fox,  and  even  in  other  simple 
forms  slight  pyrexia  is  not  uncommon. 

The  Physical  Signs  of  pulmonary  hypersemia  are  not  well  marked ;  the 
movements  of  the  chest  are  increased  and  the  respiration  more  or  less  la- 
bored in  character.  The  percussion  sound  is  at  first  abnormally  resonant, 
perhaps  tympanitic,  but  as  oedema  is  developed  in  the  congested  portion  and 
in  brown  induration  of  the  lung,  it  becomes  somewhat  dull.  On  ausculta- 
tion, the  respiratory  murmur  is  feeble  or  harsh ;  in  brown  induration  of 
the  lung  there  is  a  feebleness  of  the  normal  vesicular  murmur,  the  inspira- 
tory sound  becomes  harsh,  and  the  expiratory  becomes  prolonged.  Abundant 
small,  bubbling  rales  are  heard  when  oedema  accompanies  the  hypersemia, 
as  is  almost  always  the  case  when  it  is  active.'  The -physical  signs  in  hy- 
postatic congestion  depend  on  the  position  of  the  patient,  but  are  best 
marked,  as  a  rule,  behind  and  in  the  infrascapular  spaces. 

Differential  Diagnosis. — The  diagnosis  of  pulmonary  congestion  is  not 
difficult  if  one  considers  the  circumstances  under  which  it  occurs,  and  the 
two  prominent  symptoms,  viz.:  the  dyspnoea,  and  the  copious,  watery, 
blood-stained  expectoration.  If,  in  the  progress  of  acute  pneumonia,  watery, 
blood-stained  expectoration  is  present,  and  the  dyspnoea  is  severe,  pulmo- 
nary congestion  and  oedema  may  be  recognized  as  having  occurred  in  that 
portion  of  lung  not  involved  by  the  pneumonia.  There  is  a  blood-stained 
expectoration  present  in  pneumonia,  but  it  is  of  a  tenacious  character,  and 
entirely  unlike  the  copious,  watery,  blood-stained  sputum  of  pulmonary 
congestion  and  oedema.  The  existence  of  pulmonary  oedema  being  estab- 
lished, it  is  impossible  to  determine,  either  by  the  rational  or  physical  signs, 
whether  the  attendant  hypersemia  is  active  or  passive  in  character  ;  but  in 
the  majority  of  cases  the  circumstances  under  which  it  occurs  will  decide 
the  question.  Pulmonary  congestion  is  readily  distinguished  from  spas- 
modic asthma  by  the  absence  of  the  characteristic  rales  of  asthma. 

Prognosis. — Active  pulmonary  hypersemia  is  usually  rapid  in  its  course, 
and  either  terminates  in  complete  recovery,  in  pneumonia  and  pulmonary 
hemorrhage,  or  destroys  life  in  a  few  hoars.  Eecovery  from  acute  hyper- 
semia is  attended  by  sero-frothy  sputa.  Patients  suffering  from  the  disease 
can  generally  be  relieved  at  its  onset  from  the  dangers  which  attend  it. 
The  prognosis  in  passive  hypersemia  depends  altogether  upon  the  condition 
with  which  it  occurs.  When  it  occurs  with  heart  disease  the  prognosis 
will  vary  according  to  the  exact  condition  of  the  heart,  it  may  then  last  for 
years,  or  if  the  patient  is  in  the  advanced  stages  of  heart  disease,  and  an 
intense  pulmonary  congestion  comes  on  suddenly,  the  prognosis  is  unfavor- 
able ;  in  brown  induration,  the  prognosis  is  uncertain.  Extensive  pulmo- 
nary congestion  in  the  form  of  splenization  leads  to  unfavorable  results. 
As  a  rule,  pulmonary  congestion  and  oedema  are  very  serious  affections, 
because  they  complicate  already  existing  dangerous  conditions. 

Treatment. — In  cases  of  active  hypersemia  coming  on  abruptly,  and  rap- 
idly assuming  a  threatening  aspect,  an  effort  must  be  made  to  lessen  the 

'  Powell  says  a  fine  inspiratory  crepitant  rale  is  heard  in  heart-disease  congestion,  and  that  there  are 
repeated  bronchial  catarrhs. 


PULMONARY  (EDEMA.  11? 

quantity  of  blood  in  the  pulmonary  vessels.  This  is  best  accomplished  by 
the  application  of  wet  or  dry  cups  over  the  entire  chest,  or  over  the  seat  of 
the  congestion,  or,  perhaps,  in  extreme  cases,  by  opening  a  vein  in  the 
arm  ;  these  remedies  to  be  followed  by  steam  inhalations,  poultices,  and 
warmth  to  the  extremities  ; — saline  purges  are  beneficial.  Digitalis  may  be 
given  in  active  hyperaemia  from  alcohol.  In  congestion  the  attention  must 
be  turned  to  the  condition  in  connection  with  which  it  occurs,  and  the 
pulmonary  circulation  must  be  regulated  by  overcoming  or  controlling  the 
cause  of  the  congestion.  If  it  depends  on  feeble  action  of  the  heart,  adminis- 
ter stimulants ;  as  stimulants,  ammonia,  quinine  and  ether  are  especially 
valuable  in  addition  to  alcohol.  Stimulants  are  especially  demanded  in 
hypostatic  congestion,  and  the  position  of  the  patient  must  be  constantly 
varied.  Deep,  full  inspirations  are  of  service.  If  the  hyperaemia  is  caused 
by  forcible  heart's  action  (the  organ  being  diseased),  give  aconite  in  full 
doses.  Hydragogue  cathartics  are  indicated  when  pulmonary  oedema  is  also 
present.  When  dependent  on  valvular  lesions,  the  treatment  indicated  for 
these  lesions  must  be  employed. 

PULMOITAEY   (EDEMA. 

Pulmonary  oedema  is  a  secondary  affection  which  may  be  complicated 
by  pulmonary  congestion  or  may  occur  independently  of  it. 

Morbid  Anatomy. — The  anatomical  lesion  of  pulmonary  oedema  consists 
in  the  presence  of  serum  in  the  cavity  of  the  alveoli  and  in  the  interstitial 
tissue  of  the  lungs  ;  if  it  is  associated  with  pulmonary  congestion  the  serum 
will  be  blood-stained;  if  there  is  no  pulmonary  congestion  present,  the 
serum  in  the  cavity  of  the  alveoli  and  interstitial  tissue  will  be  light  colored. 
Lungs  which  are  the  seat  of  pulmonary  oedema  do  not  collapse  when  the 
thoracic  cavity  is  opened.  Unless  congestion  is  present,  that  portion  of  the 
lung  which  is  the  seat  of  the  oedema  is  paler  than  normal  lung-tissue. 
When  the  oedematous  portion  is  pressed  upon  with  the  finger  the  indenta- 
tion remains.     The  weight  of  the  lung  is  increased. 

On  section,  serum  exudes  or  can  be  easily  expressed  from  the  cut  surface. 
The  serum  is  usually  frothy  unless  the  air  cel'ls  are  filled  with  serum.  By 
this  means  we  are  able  to  determine  the  amount  of  oedema  present. 
(Edema  may  occur  in  any  portion  of  the  lung,  but  it  is  most  frequently 
met  with  in  the  most  dependent  portion.  The  pleural  surfaces  are  moist, 
and  the  pleur.al  cavities  may  contain  some  serum.  When  oedema  of  the 
lungs  is  found  at  a  post-mortem  examination,  it  is  impossible  to  decide,  by 
simple  inspection,  whether  it  occurred  before  or  after  death.  In  order  to 
determine  its  exact  import  it  is  necessary  to  know  the  physical  signs  and 
symptoms  present  previous  to  death. 

Etiology. — Pulmonary  oedema,  as  has  already  been  stated,  is  a  secondary 
affection.  It  may  be  caused  by  hydraemia  resulting  from  general  dropsy 
depending  upon  Bright's  disease,  scorbutus,  purpura,  anaemia,  etc.  It 
occurs  in  portions  of  lung  which  are  the  seat  of  pulmonary  hyperaemia 
(active  or  passive),  but  especially  when  the  hyperaemia  is  due  to  heart-fail- 


118  DISEASES   OF   THE   EESPIRATORY   ORGAKS. 

ure.  It  may  be  found  in  lung- tissue  which  is  adjacent  to  parts  that  are 
the  seat  of  inflammatory  or  irritative  processes,  as  pneumonia,  capillary 
bronchitis,  miliary  tuberculosis,  etc.  When  the  circulation  has  been 
obstructed  in  one  portion  of  the  lung,  oedema  ^  may  arise  in  another  portion 
of  the  same  lung ;  its  occurrence  in  connection  with  pneumonia  is  not 
infrequent  under  such  circumstances,  and  is  often  an  early  indication  of 
the  necessity  of  prompt  and  careful  attention  in  order  to  avert  its  fatal  ten- 
dencies. Want  of  "  tone  "  in  the  vessels,  from  pressure  on  the  vagus  or  the 
pulmonary  plexus,  may  cause  it.  It  occurs  in  the  course  of  acute  general 
diseases,  such  as  typhoid,  typhus,  and  scarlet  fevers,  with  feeble  heart 
action,  especially  in  the  aged  and  feeble.  Under  such  circumstances  the 
posterior  portion  of  the  lungs  is  usually  the  seat  of  the  oedema,  and  its  pro- 
duction is  aided  by  gravitation. 

Symptoms. — The  prominent  rational  symptoms  of  oedema  of  the  lungs 
are  increased  frequency  in  the  respiration  and  dyspnoea.  Frequently  the 
dyspnoea  is  sudden  in  its  advent  and  extreme,  amounting  to  orthopnoea. 
The  temperature  remains  normal.  The  pulse,  if  increased  in  frequency, 
is  feeble.  There  is  more  or  less  cough  attended  by  a  frothy,  watery  expec- 
toration, which  is  colorless  unless  pulmonary  congestion  is  present ;  then 
it  is  more  or  less  blood-stained.  The  cough  often  has  a  peculiar  "retch- 
ing "  character.  If  the  oedema  is  extensive,  or  if  it  complicates  some  pul- 
monary disease,  the  lips  become  blue,  the  extremities  livid  and  cold,  and 
the  patient  presents  a  more  or  less  cyanosed  appearance. 

Physical  Signs. — The  signs  furnished  by  insjjection  and  palpation  are 
negative.  There  is  more  or  less  dulness  on  percussion  (never  complete), 
over  the  seat  of  the  oedema :  usually  the  dulness  is  equally  diffused  over 
the  posterior  surface  of  the  chest  on  both  sides,  and  is  best  marked  at  the 
most  dependent  portion  of  the  lungs.  It  is  usually  more  extensive  at  one 
base  than  at  the  other.  On  auscultation  the  respiratory  murmur  is  feeble, 
sometimes  entirely  absent,  or  harsh  in  character.  With  inspiration  and 
the  commencement  of  ex]3iration,  small-sized  bubbling  rales  are  heard  over 
the  seat  of  the  oedema.  Sometimes  these  rdles  greatly  resemble  pneumonic 
crepitation,  but  they  may  generally  be  distinguished  from  it  by  their 
liquid  character.  The  absence  of  any  bronchial  character  to  the  respira- 
tory sound  excludes  the  presence  of  pneumonic  consolidation.  Vocal 
fremitus  and  resonance  may  be  increased  or  diminished  ;  both  are  quite 
unreliable  as  a  means  of  diagnosis. 

Differential  Diagnosis. — CEdema  of  the  lungs  may  be  confounded  with  the 
first  stage  ot pneumonia,  with  Jiydrotliorax,  and  with  capillary  hronchitis. 
It  is  distinguished  from  pneumonia  by  the  absence  of  a  chill  followed  by 
febrile  symptoms,  by  the  liquid  character  of  the  rdles,  and  by  its  occurrence 
on  both  sides  at  the  most  dependent  portion  of  the  lungs.  A  patient  in 
the  last  stage  of  Bright's  disease  may  suddenly  develop  high  temperature 
and  a  cough,  but  in  such  a  ease  the  absence  of  a  chill,  as  well  as  the  bub- 
bling character  of  the  rdles,  will  enable  one  to  recognize  the  condition  as 

1  Cohnheim  states  that  it  is  the  inflammatory  state  of  the  vessels,  rather  than  increase  in  blood  press- 
ure (compensatory),  that  causes  oedema  in  this  (third)  class. 


PULMONARY   (EDEMA.  119 

pulmonary  cedema,  not  pneumonia.     The  expectoration  in  the  two  diseases 
is  very  dissimilar. 

The  physical  signs  of  pulmonary  oedema  and  hydrotJtorax  are  quite 
distinctive.  CEdema  may  be  distinguished  from  hydrothorax  by  the 
presence  of  rdles,  and  by  the  fact  that  the  level  of  dulness  is  not  changed 
by  a  change  in  the  position  of  the  patient,  while  in  hydrothorax  tlie 
upper  border  of  the  area  of  dulness,  recognized  by  percussion  while  the 
patient  is  sitting  or  standing,  will  immediately  shift  its  position  when  the 
patient  stoops  forward. 

The  onset  of  the  capillary  bro/ichitis,  from  which  pulmonary  oedema 
is  to  be  distinguished,  is  almost  always  accompanied  by  fever.  The 
expectoration  differs  in  character  from  that  of  pulmonary  oedema.  In 
capillary  bronchitis  it  is  at  first  scanty  and  tenacious,  and  even  when 
the  disease  is  fully  established,  although  it  may  be  abundant,  it  is  still 
tenacious.  In  pulmonary  oedema  the  expectoration  is  always  frothy 
and  watery  in  character  and  abundant.  In  oedema  there  is  always  some 
dulness  on  percussion,  often  it  is  well  marked ;  in  capillary  bronchitis 
there  is  no  percussion  dulness,  but,  on  the  contrary,  exaggerated  resonance. 
In  both  affections  the  rales  closely  resemble  each  other ;  they  are  usually 
more  abundant  in  capillary  bronchitis  than  in  oedema.  The  two  diseases 
are  liable  to  occur  together  ;  but  the  presence  or  absence  of  fever,  and  the 
character  of  the  expectoration,  are  generally  sufficient  to  enable  one  to 
make  a  correct  diagnosis. 

Prognosis. — This  mainly  depends  upon  the  condition  of  the  patient  at  the 
time  of  the  occurrence  of  the  oedema.  A  large  number  of  persons  die 
(often  suddenly)  from  pulmonary  oedema  in  connection  with  general 
'dropsy  ;  especially  is  there  danger  when  it  occurs  with  the  general  dropsy 
depending  upon  renal  or  cardiac  disease.  When  one  lung  is  the  seat  of 
pneumonic  inflammation,  not  infrequently  oedema  is  suddenly  developed 
in  the  other  lung  and  destroys  life.  In  continued  fevers,  phthisis,  and 
other  exhausting  diseases,  pulmonary  oedema  due  to  cardiac  insufficiency 
often  occurs  as  the  immediate  cause  of  the  fatal  issue.  Extensive  pulmo- 
nary oedema,  sufficient  to  give  rise  to  extreme  dyspnoea  and  a  cyanosed  con- 
dition of  the  face  and  extremities,  is  of  serious  import  and  should  not  be 
lightly  regarded  ;  it  necessitates  a  very  guarded  prognosis. 

Treatment. — The  treatment  of  this  affection  will  depend  almost  exclus- 
ively upon  the  condition  with  which  it  is  associated.  If  it  occurs  in  con- 
nection with  Bright's  disease,  the  excretory  function  of  the  kidneys  must 
be  increased,  and  the  vicarious  excretory  power  of  the  bowels  and  skin 
brought  into  active  operation  with  hydragogue  cathartics,  diuretics  and 
diaphoretics  ;  all  of  these  eliminating  forces  must  be  crowded  to  their  ut- 
most. Dry  cups  must  be  applied  over  the  thoracic  and  lumbar  regions  as 
often  as  the  patient  will  bear  them,  in  numbers  varying  from  twenty  to  fifty 
at  each  application.  If  it  occurs  in  connection  with  typhus  or  typhoid  fever, 
stimulants  are  indicated,  for  it  does  not  generally  make  its  appearance  in  con- 
nection with  these  diseases  until  symptoms  of  heart  exhaustion  are  present. 
If  the  heart's  action  is  feeble,  its  power  must  be  increased  ;  under  such  cir- 


120  DISEASES   OF  THE  EESPIEATORT  ORGAN'S. 

cumstances,  tlie  administration  of  digitalis  will  be  of  service.  When  the 
oedema  occurs^in  connection  with  pulmonary  congestion,  counter-irritation, 
regulation  of  the  heart's  action,  or  any  means  which  will  have  a  tendency 
to  relieve  or  arrest  the  congestion,  should  be  employed.  In  those  diseases  in 
which  there  are  feebleness  of  the  circulation  and  depression  of  the  vital 
powers,  it  is  important  that  the  patient  should  not  remain  constantly  in  one 
position.  He  should  frequently  be  moved,  in  order  to  prevent  gravitation 
of  the  blood  to  the  most  dependent  portion  of  the  lungs.  Care  must 
also  be  taken  that  the  lungs  are  filled  and  emptied  as  frequently  and  fully 
as  possible. 

PIJLMONAEY    ESTFARCTION". 

{Embolic  Pneumonia.) 

There  are  two  well-defined  varieties  of  hemorrhage  or  extravasation  of 
blood  into  the  lungs,  the  circumscribed  and  the  diffused.  The  latter  con- 
dition is  more  properly  denominated  pneumorrhagia.  Circumscribed  pul- 
monary hemorrhage  is  called  JiemorrJiagic  nodular  infarction,  nodular  pul- 
monary apoplexy,  and,  recently,  Jiirgensen  has  given  it  the  name  of  embolic 
'pneumonitis,  names  that  are  certainly  misleading.  The  lung-tissue  is  not 
torn  or  rent  in  circumscribed  pulmonary  hemorrhage.  In  describing  this 
condition,  I  shall  adopt  the  term  ^^ pulmonary  infarction.''^ 

Morbid  Anatomy. — Lung-tissue,  which  is  the  seat  of  infarctions,  is  heav- 
ier than  normal  and  has  a  tough  feel ;  if  the  infarctions  are  near  the  sur- 
face of  the  lung,  they  can  readily  be  felt.  Their  more  frequent  seat  is  at 
the  centre  of  the  inferior  lobe,  near  the  root  of  the  lung  and  at  its  periph- 
ery, for  at  the  surface  the  anastomoses  are  fewer  and  the  circulation  feebler 
than  elsewhere  in  the  lung.  They  often  occupy  the  sharp  border  of  the 
lung.  The  pleura  over  these  spots  is  congested  or  covered  by  a  fibrinous 
exudation.  In  extensive  infarctions,  a  sero-fibrinous  or  a  sero-hemorrhagic 
effusion  takes  place  in  the  pleural  cavity  sufficient  to  somewhat  compress 
the  lung.  The  lung-tissue  immediately  surrounding  the  infarction  may  be 
normal,  congested,  oedematous  or  blood-stained. 

On  section  of  a  fresh  nodule  it  is  seen  to  be  wedge-shaped,  the  apex  of 
the  wedge  looking  toward  the  root,  and  the  base  toward  the  periphery  of 
the  lung.  The  nodules  vary  in  size  from  that  of  a  pin's  head  to  an  inch 
or  more  in  diameter.  There  are  usually  several  in  each  lung.  The  cut 
surface  of  a  fresh  infarction  is  firm,  maroon-colored,  moist,  and  airless ; 
and  from  it  flows  a  considerable  quantity  of  bright  blood.  Older  nodules 
cut  with  a  cheese-like  section  and  resemble  in  color  a  dark  blood  clot,  they 
are  distinctly  granular  and  quite  dry,  firm  pressure  causing  only  a  small 
quantity  of  blood  to  flow  from  their  cut  surfaces.  They  are  readily  broken 
down  into  small  masses.  The  brownish  colored  triangular  spots  have  a 
sharp  line  of  demarcation  which  distinguishes  them  from  the  normal  lung- 
tissue.  An  embolus  will  nearly  always  be  found  obstructing  the  artery 
leading  to  the  infarcted  portion  of  the  lung.'     These  nodules  may  undergo 

1  Virchow  and  Cohnheim  both  state  that  a  plug  does  not  necessarily  exist  in  all  cases  :  that  enfeebled 
capillaries  may  alone  be  the  cause. 


PULMONARY    INFAECTION". 


121 


a  variety  of  changes.  Eesolution  is  the  most  frequent,  and  takes  place  as 
follows  : — the  alveoli  and  terminal  bronchioles  fill  with  blood  and  become 
completely  airless  ;  the  blood  rapidly  coagulates,  and  its  color  changes 
from  the  maroon  of  a  recent  clot  to  a  chocolate,  yellow,  red,  or  gray  color. 
The  fibrin,  if  present,  becomes  granular  and 
fatty.  The  blood  globules  undergo  disorgan- 
ization, showing  well-marked  fatty  changes, 
and  all  that  remains  of  them  are  hsematoidin 
and  hgematin  crystals,  the  amount  of  which 
left  after  partial  absorption,  determines  the 
color  of  the  infarction.  The  infarction  is 
now  in  a  condition  to  be  gradually  and  com- 
pletely absorbed  or  expectorated.  The  re- 
stored lung  may  be  but  little  damaged,  a 
pigmented  stain  alone  remaining  to  mark  the 
site  of  the  infarction.  After  a  varying  length 
of  time  air  again  enters  the  air-cells  that 
were  formerly  filled  with  blood.' 

Microscopically  the  portion  of  the  lung 
which  is  the  seat  of  nodular  infarction  shows 
the  capillaries  distended  with  blood  ;  and  the 
arteries  and  veins  adjoining  are  obstructed  by 
coagula^  which  are  red  and  soft  in  recent,  and 
whitish  and  hard  in  old  infarctions.  Red, 
yellow,  or  brownish-black  pigment  granules 
are  mingled  with  the  granular  and  vesicular  elements  that  fill  the  air 
cells,  and  the  alveolar  septa  are  thinned  from  pressure,  and  contain  a  vary- 
ing number  of  red  blood  corpuscles  "  Coagulation-necrosis"  is  said  to 
diminish  the  number  of  nuclei  in  the  alveolar  walls. ^ 

When  resolution  does  not  occur,  a  cyst  may  form  whose  Avails  finally  con- 
tract and  form  a  dark  pigmented  cicatricial  spot,  in  whose  indurated  tis- 
sue are  found  cheesy  masses  or  calcareous  plates.  Again,  infarctions  may 
excite  adjacent  pneumonic  inflammation,  which  in  some  instances  may  be 
so  intense  as  to  cause  gangrene.  G-angrene  under  such  circumstances  is  rather 
a-  result  of  compression  of  the  nutrient  vessel  (the  bronchial  artery).  Usually 
gangrene  only  occurs  when  the  embolus  arrives  from  a  gangrenous  region. 

When  an  embolus  occurs  in  pymmia  or  some  allied  state,  and  is  stamped 
with  pygemic  infection,  the  infarction  will  suppurate  and  an  abscess  will 
be  formed  whose  anatomical  characteristics  do  not  differ  from  those  of  ordi- 
nary abscesses." 

»  Rokitansky  claims  that  "the  matters  extravasated  may  become  fluid  again,  and  become  partly  ab- 
sorbed and  partly  expelled  through  the  bronchi.  The  parenchyma  of  the  lung  then  gradually  returns  to  its 
normal  condition." 

*  Ktittner  states  that  "  emboli  do  not  always  cause  infarcts:  for,  although  the  pulTionary  vessels  are  of 
the  'terminal'  class,  yet  blood  may  reach  the  plugged  vessels  from  bronchial  vessels  that  enter  the  lung 
and  from  surrounding  capillaries." 

3  Cohnheim  and  Weigert. 

<  Cohnheim  states  that  "  when  we  find  in  the  lungs  infarcts  and  abscesses  an  embolus  has  lodged  on 
the  hither  side  of  the  point  of  obstruction  and  has  caused  the  abscess  :  while  infarction  depends  purely 


Diagram  showing  hemorrhagic  infarct. 

A.  Embolus  obliteratinfj  the  artery. 

B.  Centre  of  infarct,  distntegrating . 
CC.  Area  of  extravasation. 

B.  Vein  filled  with  secondary  throm- 
bus.   (After  Weber.) 


122  DISEASES   OF   THE   EESPIRATORY   ORGANS. 

Etiology. — Pulmonary  infarctions  are  either  the  result  of  rupture  of  the 
capillaries  or  small  veins  from  augmented  pressure  following  intense  (me- 
chanical) passive  hypersemia  (as  in  mitral  disease) ;  or  of  the  plugging  of 
a  branch  of  the  pulmonary  artery  by  an  embolus.  In  the  first  variety  the 
mechanism  is  simple  :  from  too  great  pressure  the  capillaries  are  distended, 
stasis  results,  and  an  infarction  is  formed.  In  the  second  variety  the  plug 
causes  arrest  of  the  current,  and  the  corresponding  vascular  area  becomes- 
filled  with  stagnant  blood  that  is  forced  back  into  it  from  the  adjoining- 
veins  and  capillaries — "venous  regurgitation."  The  arteries  do  not  anas- 
tomose. The  arrangement  of  the  vascular  distribution  determines  the  pyra- 
midal or  "  wedge-like  "  shape  of  the  infarct.  Specific  infectious  emboli 
induce  ijulmonary  (so-called  pysemic)  abscesses; — non-specific  emboli  produce 
hemorrhagic  infarction.  Cohnheim  states  that  a  specific  plug  can  never 
produce  doth  infarcts  and  abscesses.  This  view  is  not  taken  by  other  ob- 
servers. Disease  of  the  valves  of  the  right  heart  and  feeble  heart  power  are 
the  two  chief  causes  of  the  formation  of  coagulum  within  the  heart,  which, 
breaking  off,  plugs  a  branch  of  the  pulmonary  artery.  Any  foreign  body 
sufficiently  small  in  size,  or  a  clot  from  any  part  of  the  systemic  venous 
system,  may  find  its  way  to  the  right  heart  and  thus  cause  an  infarction.^ 
It  is  supposed  that  thrombi  may  form  in  the  pulmonary  artery  in  cases  of 
heart  disease,  i.  e,,  be  of  ''independent"  origin.  Blood  from  the  nasal  or 
buccal  cavities,  or  blood  from  the  bronchial  tubes,  may  make  its  way  into 
the  bronchioles  and  alveoli,  and  induce  an  appearance  difficult  to  distin- 
guish from  embolic  infarction.  It  is  admitted  as  possible  that  thrombi 
formed  in  the  left  heart  may  break  off,  go  the  round  of  the  circulation  and 
finally  lodge  in  some  branch  of  the  pulmonary  artery. 

Phthisis,  scurvy,  purpura  hemorrhagica,  gangrene  of  the  lung,  cholera, 
acute  yellow  atrophy,  typhoid  and  yellow  fever  are  not  infrequently  accom- 
panied by  pneumorrhagia  of  the  circumscribed  variety.  Sometimes  no 
cause  can  be  found  to  account  for  a  pulmonary  infarction.  Recent  experi- 
ments have  shown  that  infarction  does  not  talce  place  unless  arterial  blood 
from  some  source  is  still  sent  into  tJie  part  after  its  main  supply  is  cut  off.' 

on  the  mechanical  action  of  the  simple  embolus  in  the  terminal  arterj'."  Harvard  (in  Quain's  Diet.)  thus 
describes  the  pyaemic— the  metastatic  abscess  in  the  lungs:  "Embolic  passive  hyperremia  is  complicated  by 
suppuration  ;  but  this  suppuration  is  incomplete  and  consists  rather  in  a  rapid  breaking  down  of  the  tis- 
sues, than  in  the  formation  of  a  large  number  of  pus  cells  ;  while  the  cnaracteristic  deep  purple  congested 
zone  around  the  affected  spot  is  much  intensified.  Some  describe  this  as  a  true  sphacelus  of  the  part ;  but 
there  is  no  necrosis,  and  I'.o  foul  decomposition  of  the  patch  affected  in  the  suppurated  form  of  embolic 
inflammation."  When  abscesses  form,  disintegration  begins  at  the  centre  of  the  pyaemic  infarction,  and 
yellow  croupous  deposits  form  on  the  pleura  over  it,  causing  adhesions,  and  {Eokllansky) '■' a.vo\xn6.ed. 
nodular  prominence  like  a  boil  projects." 

'  Rokitansky  believes  that  an  embolus  always  exists  where  there  is  a  hemorrhagic  pulmonary  infarct. 
It  may  be  difficult  to  find  it,  but  it  exists.  But  Cohnheim  and  Virchow  state  that  emboli  are  not  alivays 
iweseid.  Simple  rupture  of  enfeebled  capillaries  may  be  the  sole  event.  Stagnant  venous  blood  is  inca- 
pable of  nourishing  the  walls  of  the  tubes  that  hold  it,  and  the  effused  corpuscles  speedily  fill  the  adjacent 
alveoli. 

2  Bed-sores,  ulcerations,  thrombosis  of  the  femoral  vein,  phlegmasia  alba  dolens,  wounds  and  maras- 
mic  thrombosis  are  common  peripheral  sources  of  emboli. 

3  Fat  Embolism  in  the  Lungs.— The  discovery  that  the  smaller  vessels  in  the  lungs  were  often  plugged 
with  fat  granules,  giving  rise  to  fat  embolism,  was  made  by  Wagner  and  Zenker.  Fat  emboli  have  been 
connected  with  the  origin  of  metastatic  abscesses  bj'  some  who  were  inclined  to  regard  fatal  pulmonary 
oedema  and  congestion  as  direct  results  thereof.  Of  this,  more  proof  is  wanted.  When  the  long  bones 
are  broken,  some  medullary  fat  gets  into  the  circulation ;    but  enough  may  enter  that,  when  passing 


PULMOlSrARY   INFAECTION".  123 

Symptoms. — The  subjective  symptoms  of  pnlmonary  infarction  are  few  and 
indefinite.  A  small  infarction  will  only  be  attended  by  the  expectoration 
of  small  blood  clots.  When  one  large  or  several  small  infarctions  occur  in 
the  lungs  of  one  who  has  had  chronic  heart  disease,  the  ''cardiac  "  dyspnoea 
will  be  increased  ;  there  will  be  a  sense  of  corfstriction  about  the  chest, 
attended  by  an  ill-defined  sense  of  the  occurrence  of  some  severe  pulmo- 
nary lesion  ;  irregular,  intermittent  and  disturbed  heart  action  nearly  always 
precedes  this  occurrence.  These  symptoms  are  more  apt  to  occur  during 
or  after  some  severe  physical  exertion  or  intense  mental  excitement,  and 
are  accompanied  by  the  expectoration  of  small  airless  blood-coagula  mixed 
with  tenacious  mucus.  During  the  first  three  days  the  temperature  some- 
times rises  to  101°  and  102°  F.  Cerebral  symptoms  are  frequently  present. 
Syncope  may  occur  in  patients  with  weak  hearts.  If  the  infarction  is 
large,  or  if  a  number  occur  at  the  same  time,  collapse,  intense  dyspncea  and 
convulsions  may  immediately  follow  its  occurrence.  If  the  infarction 
involves  the  surface  of  the  lung  and  gives  rise  to  local  pleurisy,  pain  will 
be  a  prominent  symptom.  Dark,  scanty  hcBmoptysis  is  t\\e  pathognomonic 
sign  of  pulmonary  infarction.  The  rational  symptoms  of  "  ijysmic  "  infarc- 
tions are  less  marked  than  those  of  hemorrhagic.  The  cough  and  expec- 
toration, the  increase  in  the  frequency  of  the  respiration  out  of  proportion 
to  any  rise  in  the  pre-existing  temperature,  the  constriction  across  the 
chest,  and  the  dyspncea  taken  in  connection  with  the  physical  signs  and  the 
history  will  generally  lead  to  the  diagnosis  of  what  some  now  call  ernboUc 
pneum.onia} 

Physical  Signs. — Inspection  and  palpation  give  negative  results,  but  there 
may  be  increased  vocal  fremitus  over  a  large  superficial  infarction. 

Percussion  may — in  the  case  of  superficial  and  large  infarctions — give 
localized  dulness  corresponding  to  the  site  of  the  infarction. 

Auscultation  may  give  bronchial  breathing  or  bronchial  expiration,  espe- 
cially in  the  mammary  and  mid-axillary  regions  ;  and  sub-crepitant  and 
crepitant  rales  may  be  heard  in  the  immediate  neighborhood  of  the  infarc- 
tions. Co-existent  peripheral  oedema  and  pre-existing  emphysema  may, 
and  frequently  do,  prevent  any  morbid  physical  phenomena  from  being  ap- 
preciated. 

Differential  Diagnosis. — The  etiology,  the  sputa,  and  the  spots  of  localized 
dulness  are  the  diagnostic  points  ;  of  these  the  etiology  is  the  most  impor- 
tant. The  sputa  of  cancer  and  of  schinococci  of  the  lung  may  be  similar  to 
that  of  infarction  ;  but  the  long  duration  and  the  attendant  signs  of  cancer, 
and  the  microscopical  examination  for  booklets,  in  the  case  of  hydatids, 
will  soon  decide  the  question. 

Prognosis. — In  the  slight  circumscribed  pulmonary  infarction  dependent 

through  the  lungs,  it  is  deposited  in  the  small  arteries  of  this  organ,  and  perhaps,  subsequently,  of  other 
organs.  This  is  all  the  more  liable  to  occur  when  the  heart  action  is  feeble.  The  fat  not  only  comes  from 
fracture  of  bones,  but  puriform  softening  of  right  cardiac  thrombi  may  cause  it.  Inflammation  of  bones, 
with  or  wifhout  operation,  may  induce  it,  and,  also,  os!teo-m)'elitis,  or  softening  of  the  marrow.  The 
acetonairaia  that  has  long  been  regarded  as  causing  death  in  diabetes,  is  by  many  supposed  to  be  inert, 
compared  with  fat  embolism  of  the  lungs,  in  hastening  death  in  diabetes.  Fat  embolism  may  be  the  direct 
result  of  general  lipajmia. 
1  Jiirgensen,  Ziem.  Encyc,  Vol.  i. 


124  DISEASES    OF    THE    KESPIRATORT    ORGANS. 

upon  or  accompanying  lieart  disease,  or  occurring  with  a  condition 
that  is  not  pyaemia,  the  prognosis  is  good.  Non-embolic  infarctions, 
and  even  small  non-specific  embolic  infarcts  may  be  absorbed.  The 
Targer  and  more  numerous  the  infarctions  the  worse  the  prognosis.  A 
large  infarction  may  quickly  terminate  fatally  by  collapse.^  In  all  pyaemic 
infarctions  and  in  those  occurring  with  cardiac  thrombosis,  the  prognosis  is 
bad. 

Treatment. — The  treatment  of  pulmonary  infarction  is,  for  the  most  part, 
expectant.  When  valvular  lesions  of  the  heart  exist,  the  main  thing  is  to 
regulate  the  heart's  action  and  increase  its  power.  Absolute  rest  in  bed, 
and  the  administration  of  stimulants  combined  with  small  doses  of  digitalis, ** 
are  indicated,  but  they  must  be  given  with  great  care  and  their  effects  care- 
fully watched.  Stimulation  may  be  made  to  the  extremities,  such  as  hot 
water  or  mustard  sinapisms,  and  dry  cups  are  to  be  freely  applied  over  th« 
chest.  Venesection  is  contraindicated.  But  collateral  hypersemia  and 
oedema,  attended  by  great  dyspnoea  and  lividity,  may  demand  wet  cups  and 
even  bleeding  from  the  arm.  Both  give  temporary  relief  and  they  avert 
danger.  The  constitutional  condition  of  the  patient  is  always  to  be  con- 
sidered. In  pyaemic  pulmonary  infarction  the  treatment  consists  in  sup- 
porting the  patient  by  free  administration  of  stimulants,  quinine  and  iron. 
Dry  cups  may  be  frequently  applied  over  the  chest.  If  pleurisy  and  pneu- 
monia occur  they  are  to  be  treated  as  complications. 


DIFFUSE    PULMONAEY   APOPLEXY. 

In  diffuse  pulmonary  hemorrhage  or  apoplexy  the  lung-tissue  becomes 
torn  and  infiltrated  with  blood,  which  may  be  either  fluid  or  coagulated. 
If  situated  near  the  surface  of  the  lung  the  pleura  may  be  lacerated.  Gen- 
erally the  cavity  made  in  the  lung-tissue  by  the  extravasation  is  of  consid- 
erable size,  and  the  coagulated  or  semi-coagulated  blood  in  this  cavity  has 
all  the  characteristics  of  a  blood  clot.  These  apoplectic  extravasations  are 
never  circumscribed,  are  usually  of  much  larger  size  than  infarctions, 
and  greatly  resemble  apoplectic  extravasations  in  the  brain,  being  a  mass 
of  blood  in  shreddy  oedematous  and  infiltrated  parenchyma.  They  may 
prove  immediately  fatal,  especially  when  the  pleura  is  perforated.  If  the 
patient  survives  the  shock  of  the  accident,  recovery  usually  takes  place 
either  by  adhesion  of  the  torn  surfaces  of  the  lung  after  absorption  of  the 
extravasated  blood,  or  by  the  formation  of  a  connective-tissue  capsule 
around  the  clot,  after  which  the  latter  undergoes  a  cheesy,  cre^.aceous,  or 
pigment  degeneration,  and  remains  permanently  imbedded  in  the  lung- 
tissue.     It   is  rarely  transformed  into   a  serous  cyst.     This  form  of  pul- 

'  Jiii'gensen  states  that  "embolic  abscesses  are  not  necessarily  fatal  to  life  ;  "  and  that  "the  pro^osis 
always  "  depends  more  upon  the  primary  disease  than  upon  the  accident  which  we  call  pneumonia  by  em- 
bolism. 

*  Gerhardt  states  that  digitalis  is  not  the  drug  for  cardiac  stimulation,  but  recommends  large  doses  of 
morphia,  hypodermatically,  for  the  dyspnoea,  and  musk  and  alcohol  to  excite  the  heart. 

3  This  use  of  the  word  apoplexy  is  unfortunate  both  for  etymological  reasons  and  because  of  its  asso- 
ciatioiu",  but  it  has  become  general. 


GANGRENE   OF  THE   LUNGS.  125 

monary  apoplexy  is  much  less  frequently  met  with  than  the  circumscribed 
form. 

Diffused  pulmonary  apoplexy  may  occur  from  a  very  large  infarction,  but 
this  is  comparatively  rare.  It  generally  occurs  as  a  result  of  changes  in 
the  walls  of  the  arteries.  A  branch  of  the  pulmonary  artery  may  be  t]ie 
seat  of  an  aneurism,  usually  of  small  size  ;  or  the  hemorrhage  may  occur  in 
connection  with  an  aneurism  of  some  other  vessel,  as  the  aorta,  which  has 
ruptured  into  the  lung  substance.  It  may  occur  as  the  result  of  a  fall  or 
shock ;  it  may  also  be  of  traumatic  origin,  resulting  from  fracture  of  the 
ribs,  gunshot  wounds,  etc.  Its  most  frequent  cause  is  the  rupture  of  tho- 
racic aneurisms.  Disease  of  the  pulmonary  artery  other  than  aneurismal, 
has  caused  it.  Erosions  from  cancer,  gangrene  or  abscesses,  may  induce  it. 
(Hertz.)  It  occurs  oftenest  in  males  (three  to  one),  and  after  the  twenty- 
first  year. 

Symptoms. — Profuse  haemoptysis,  dyspnoea,  lividity,  or  a  sense  of  oppres- 
sion, and  often  a  condition  bordering  on  collapse,  are  the  chief  symptoms 
of  ''diffuse  pneumorrhagia."  Convulsions  occur,  and  the  patient  may  suf- 
focate from  the  bronchi  becoming  filled  with  blood. 

Physical  Signs. — The  symptoms  which  mark  the  occurrence  of  diffuse 
pulmonary  apoplexy  are  usually  not  well  defined,  and  it  may  be  difficult 
to  positively  determine  its  existence.  There  may  be  a  profuse  hemorrhage 
with  the  development  of  extensive  pneumonic  consolidation,  but  this 
will  not  distinguish  it  from  other  diffuse  pulmonary  hemorrhages.  This 
form  of  apoplexy  often  goes  unrecognized  until  the  post-mortem  exami- 
nation. 

Prognosis. — This  is  always  grave.  Eecovery  is  only  possible  when  the 
extravasation  is  of  small  size  and  the  rent  in  the  lung  substance  slight. 

Treatment. — The  diffuse  variety  of  pulmonary  apoplexy  is  not  amenable 
to  treatment ;  in  most  cases  the  patient  dies  before  he  rallies  from  thy 
shock  of  the  hemorrhage.  Cold  internally  and  externally,  ergot  hypoder- 
matically,  and  a  solution  of  chloride  of  iron — all  may  be  given  if  he  rallies 
from  the  shock.  During  the  collapse  which  follows  the  shock,  alcohol  an<' 
diffusible  stimulants  must  be  freely  administered. 


GAIfGRENE    OF   THE    LUNGS. 

There  are  two  varieties  of  pulmonary  gangrene  :  the  circumscribed  and 
the  diffused.  Circumscribed  gangrene  of  the  lungs  is  of  much  more  fre- 
quent occurrence  than  the  diffused  variety.  It  usually  involves  the  periph- 
ery of  the  lower  lobes.  If  a  bronchus  opens  into  a  gangrenous  patch,  in- 
flammation of  the  bronchus  results. 

Morbid  Anatomy. — In  circumscribed  gangrene,  small  isolated  portions  of 
lung-tissue,  usually  of  a  single  lobe,  become  converted  into  bluish-green 
fetid  sloughs,  which  at  first  are  firm  and  surrounded  by  oedematous  lung- 
tissue,  but  soon  decompose  into  an  ichorous  fluid  containing  pus,  pigment, 
crystals    of    ammonio-magnesian     phosphate,  tyrosin,  margarin,   leucin. 


126  DISEASES   OF   THE    RESPIEATORY    OEGANS. 

vibriones,  and  bacteria,  which  may  be  discharged  through  a  bronchus  and 
leave  a  ragged,  sloughy  cavity  surrounded  by  inflamed  lung-tissue.  Com- 
monly, one  gangrenous  patch  is  solid,  while  another  is  becoming  diffluent 
at  its  centre.  A  zone  of  catarrhal  pneumonia  nearly  always  surrounds  a 
circumscribed  patch.  Vessels  may  traverse  this  cavity,  but,  as  coagula 
rapidly  form  in  them,  hemorrhage  rarely  occurs.  Sometimes,  by  the  gan- 
grenous process,  an  opening  is  formed  into  the  pleural  cavity  and  causes 
acute  pleurisy  or  pyo-pneiimothorax.  Sometimes  a  spot  of  circumscribed 
gangrene  becomes  the  centre  of  diffuse  gangrene.  In  exceptional  cases, 
the  disorganized  portion  is  expelled,  a  fibrous  capsule  forms,  and  healthy 
pus  is  produced.  In  such  cases,  the  cavity  may  ultimately  close  up  and 
cicatrize.  Sometimes  the  pulmonary,  but  oftener  the  bronchial,  arteries 
are  plugged. 

In  diffused  gangrene  of  the  lung,  an  entire  lobe  is  not  infrequently  involved, 
and  sometimes  an  entire  lung ;  unlike  the  preceding  form,  there  is  no  line 
of  demarcation ;  the  gangrenous  processes  are  not  abruptly  limited,  but 
gradually  merge  into  oedematous  or  hepatized  lung-tissue.  The  affected 
pulmonary  tissue  is  more  or  less  decomposed,  and  converted  into  a  putrid 
mass  within  an  anfractuous  cavity,  containing,  also,  swarms  of  bacteria, 
floating  in  a  grayish-black  fluid ;  as  the  gangrenous  process  reaches  the 
pleura  this  membrane  becomes  destroyed.  Eecovery  under  these  circum- 
stances rarely,  if  ever,  takes  place,  the  patient  dying  of  septicsemia  or  pyae- 
mia. Secondary  gangrenous  patches  may  be  found  in  the  same  or  opposite 
lung. 

Etiology. — The  conditions  under  which  gangrene  of  lung-tissue  may  oc- 
cur are  numerous.  Pulmonary  gangrene  has  resulted  from  inhalation  of 
noxious  gases.  In  children  it  has  followed  cancrum  oris.  It  may  occur  as 
the  result  of  certain  local  pulmonary  diseases,  such  as  acute  or  chronic 
pneumonia,  cancer,  hydatids,  bronchial  dilatation,  hemorrhagic  infarc- 
tions, obstruction  of  the  nutrient  vessels  leading  to  the  gangrenous  por- 
tions, or  from  the  entrance  of  foreign  particles,  e.g.,  bits  of  food  swallowed 
by  those  with  bulbar  paralysis.  It  may  result  from  erosive  processes,  e.  g., 
abscesses,  ulcers  or  cancer.  Putrefaction  in  bronchiectatic  or  phthisical 
cavities  may  lead  to  it.  Traumatism  not  infrequently  causes  it.  Pulmo- 
nary gangrene  may  occur  in  connection  with  blood-poisoning,  such  as  is 
met  with  in  low  fevers,  pygemia,  septicemia,  glanders,  etc.  Grangrene 
of  the  lungs  sometimes  occurs  in  certain  nervous  diseases,  as  dementia,  soft- 
ening of  the  brain,  epilepsy  and  chronic  alcoholismus.  It  is  difficult  to 
explain  the  occurrence  of  diffuse  pulmonary  gangrene  in  lunatics  and 
drunkards. 

Symptoms. — The  symptoms  of  pulmonary  gangrene,  at  its  commence- 
ment, are  often  very  obscure.  When  it  develops  from  hemorrhagic  infarc- 
tion, its  presence  cannot  generally  be  diagnosticated  until  the  gangrenous 
process  reaches  a  bronchial  tube  of  considerable  size.     There  may  be  dysp- 

J  Cornil  and  Ranvler  thus  explain  the  loss  of  substance  in  circumscribed  gangrene :  "  putrefaction  and 
molecular  destruction  commence  at  tlie  point  where  the  gangrened  inflammation  comes  in  contact  with  tha 
external  air." 


GANGEENE   OF  THE   LUKGS.  ►     127 

noea,  cough  and  pain.  The  two  symptoms  which  most  positively  indicate 
the  existence  of  pulmonary  gangrene,  are  an  extremely  fetid  breath,  and 
the.  expectoration  of  gangrenous  material ;  sometimes  the  fetid  breath  pre- 
cedes the  characteristic  expectoration.  The  expectoration  has  usually  a 
dirty  black  or  brown  color,  and  contains  small  black  masses,  and  in  rare 
instances  wavy  elastic  fibres  of  lung-tissue  are  to  be  found  in  it;  more 
or  less  blood  is  often  present,  and  death  may  occur  from  hemorrhage.  The 
sputa  are  yellow,  or  brown  :  i.  e.,  purulent  or  bloody  ;  alkaline  at  first,  but 
acid  on  standing ;  and  in  a  test  tube  they  form  three  layered  :  an  upper  of 
gray  froth  ;  a  middle,  clear  and  watery  ;  and  a  lower  containing  shreds  of 
lung-tissue.  In  some  cases  there  is  but  slight  constitutional  disturb- 
ance, and  the  gangrenous  process  goes  on  for  weeks  before  there  are  any 
general  symptoms  to  indicate  its  presence.  In  other  cases  the  greatest 
prostration  is  experienced  from  the  beginning,  the  pulse  becomes  small  and 
frequent,  and  the  vital  powers  rapidly  give  way  before  the  septic  fever. 
Dyspnoea  is  in  proportion  to  the  prostration.  Occasionally,  death  takes 
place  from  the  exhaustion  resulting  from  slow  hectic  fever.  When  diffuse 
gangrene  of  the  lung  occurs  in  connection  with  pneumonia,  its  occurrence 
is  marked  by  a  sudden  prostration,  accompanied  by  a  small  irregular  pulse, 
a  disturbed,  anxious  countenance,  a  fetid  breath,  and  a  black  liquid  expec- 
toration having  a  gangrenous  odor.  If  the  gangrenous  material  is  swal- 
lowed, as  sometimes  happens,  severe  diarrhoea  and  tympanitic  distention  of 
the  abdomen  occur.  G-astritis  sometimes  results  from  swallowing  putrid 
masses  of  sputa.  In  some  cases  of  gangrene  the  temperature  runs  very 
high. 

Physical  Signs. — The  physical  signs  of  pulmonary  gangrene  are  often  ob- 
scure, and  never  distinctive.  They  are  those  of  local  consolidation  followed 
by  the  evidences  of  breaking  down  of  lung-tissue,  and  the  formation  of  cavi- 
ties in  the  lung  substance.  Percussion  elicits  a  dull  or  tympanitic  note ; 
and  after  loose  crepitation,  gurgles  and  amphoric  breathing  are  heard. 
There  are  no  special  signs  indicating  the  nature  of  the  disorganizing  proc- 
ess ;  sometimes  it  is  preceded  by  the  signs  of  pneumonia,  generally  it  is 
accompanied  by  signs  of  bronchitis,  and  in  the  later  stages  of  the  disease 
there  are  physical  evidences  of  the  formation  of  cavities  in  the  lung-sub- 
stance. 

Differential  Diagnosis.— The  diagnosis  of  gangrene  of  the  lungs  rests 
almost  entirely  on  the  characteristic  odor  and  appearance  of  the  expectora- 
tion ;  prior  to  their  occurrence  the  existence  of  gangrene  cannot  be  deter- 
mined. Gangrenous  expectoration,  accompanied  by  the  physical  evidences 
of  softening  and  excavation  of  pulmonary  substance,  is  sufficient  for  its 
diagnosis.  Certain  conditions  may  arise  in  which  it  will  be  difficult 
to  make  a  differential  diagnosis ;  for  example,  in  some  cases  of  fetid  bron- 
chitis there  may  be  a  profuse,  greenish,  sero-purulent  expectoration,  at- 
tended by  an  extremely  fetid  odor,  not  distinguishable  from  that  of  gan- 
grene, and  yet  no  true  gangrene  of  the  lung  exists.  But  as  bronchiectasis 
is  neariy  always  present  with  fetid  bronchitis,  the  physical  signs  of  the  lat- 
ter would  be  very  different  from  those  of  a  gangrenous  focus.     ( Vide  p.  51.) 


128  DISEASES   OF  THE   EESPIEATORY  ORGANS. 

Again,  gangrene  of  the  lung  may  exist  without  any  perceptible  fetor  to  the 
breath  or  expectoration,  or  any  of  the  other  attendant  symptoms  of  gan- 
grene. Under  such  circumstances  the  gangrenous  portion  of  the  lung  does 
not  communicate  with  a  patent  bronchial  tube.  Again,  local  gangrene 
may  occur  in  a  phthisical  cavity  ;  when  it  does  it  is  very  difficult  to  distin- 
guish it  from  true  gangrene  of  tlie  lung,,  especially  if  the  patient  is  seen  for 
the  first  time  Just  as  the  gangrenous  process  is  established.  In  this  case 
the  previous  history  would  alone  enable  one  to  make  a  diagnosis.  A  fetid 
abscess  is  generally  distinguished  from  true  pulmonary  gangrene  not  by  the 
character  of  the  fetor,  but  by  the  fact  that  the  signs  of  excavation  precede 
the  occurrence  of  the  fetor,  while  in  true  gangrene  of  the  lung  the  signs  of 
excavation  follow  the  gangrenous  expectoration.  The  sputa  in  abscess  are 
decidedly  purulent,  and  fetor  does  not  usually  occur  until  some  time  after 
they  are  expectorated.  In  all  cases,  in  order  to  make  a  correct  diagnosis,  it 
is  necessary  to  have  found,  in  addition  to  the  fetid  breath  and  expectora- 
tion, decomposed  pulmonary  tissue  in  the  expectorated  matter. 

Prognosis. — The  prognosis  is  always  unfavorable,  although  the  circum- 
scribed form  is  not  regarded  as  absolutely  fatal.  Eecovery  can  only  take 
place  in  those  cases  where  the  gangrene  is  circumscribed  and  limited  to  a 
small  portion  of  the  lung-tissue.  Under  such  circumstances  it  is  possible 
for  the  slough  to  separate  and  be  discharged,  and  induration  and  final  cica- 
trization of  lung-tissue  to  take  place.  Circumscribed  gangrene  may  be 
latent,  and  it  often  progresses  slowly,  simulating  anaemia.  Diffuse  pulmo- 
nary gangrene  is  always  fatal.  Sometimes  death  is  the  result  of  profuse 
hemorrhage ;  at  other  times  it  is  due  to  perforation  of  the  pleura  ;  but 
more  frequently  the  patient  dies  from  the  exhaustion  which  attends  the 
septic  infection.  Gangrene  may  terminate  by  an  external  opening.  It 
may  be  complicated  by  emphysema  of  the  cellular-tissue,  hemorrhage, 
pneumothorax,  or  peritonitis.  Death  often  occurs  within  three  days  after 
the  first  gangrenous  expectoration. 

Treatment. — Under  no  circumstances  are  depressing  remedies  to  be  given. 
On  the  contrary,  the  vital  powers  of  the  patient  must  be  sustained  in  every 
possible  way  by  the  administration  of  stimulants,  tonics,  and  a  most  nutri- 
tious diet.  Opium  may  be  given  in  moderate  doses  to  alleviate  pain,  allay 
the  cough,  and  overcome  constitutional  irritation.  Quinine  is  to  be  given 
for  any  fever  that  may  exist.  I  have  never  found  antiseptic  inhalations  to 
produce  the  beneficial  effects  claimed  for  them  by  some  authorities,  nor  have 
I  been  able,  by  the  internal  administration  of  chloride  of  potash,  to  obtain 
satisfactory  results.  If  antiseptic  sprays  are  used,  thymol  and  salicylic  acid 
are  the  best.  Traube  gives  acetate  of  lead  and  tannin  preparations  with 
opium.  Charcoal,  carbolic  acid,  creosote  and  chloride  of  sodium  are  recom- 
mended as  deodorizers  and  internal  disinfectants.  Bromine,  chlorine,  oxy- 
gen, and  permanganate  of  potash  are  similarly  given.  My  own  experience 
leads  me  to  believe  that  all  remedies  of  this  class  are  powerless  either  to 
arrest  the  gangrenous  processor  even  mitigate  its  unpleasant  effects.  It  has 
been  suggested  that  the  lung-cavities  should  be  tapped  and  washed  out. 


ATELECTASIS.  139 


PULMONAEY   ANEMIA. 

Angemia  of  the  lungs  may  be  due  to  local  or  general  causes.  In  general 
anseujia  from  any  cause,  the  lungs  are  paler  and  lighter  than  normal.  In- 
dependent of  senile  atrophy,  it  is  never  met  with  except  in  conditions  of 
extreme  general  anaemia.  Local  pulmonary  anaemia  may  be  caused  by 
the  compression  of  local  emphysema  ;  and  by  obstruction  of  the  pulmonary- 
artery  or  its  branches. 

Symptoms. — Dyspnoea  and  palpitation  are  its  only  signs. 


ATELECTASIS. 

{Pulmonary  Collapse.) 

Pulmonary  atelectasis  is  a  condition  of  the  lungs  where  there  is  partial 
or  total  absence  of  air  in  the  alveoli.  When  acquired,  it  is  denominated 
pulmonary  collapse  or  compression  of  the  lung.  Atelectasis  is  physiolog- 
ical in  foetal  life,  and  may  be  described  as  absolute  absence  of  air  from  the 
alveoli. 

Morbid  Anatomy. — In  the  new-born,  atelectasis  is  usually  lobular ;  rarely 
is  more  than  one-half  of  a  lobe  involved.  The  lower  lobes  are  oftenest  the 
seat  of  atelectasis,  then  the  tongue-like  prolongations  of  the  upper  left  lobe 
and  the  middle  lobe  of  the  right  lung.  The  affected  portions  appear  as 
sunken  masses  of  violet  or  blue-red  color ;  they  do  not  crepitate,  have  a  soft 
feel,  but  are  tough,  and  resistant,  and  sink  in  water.  In  the  atelectatic 
spots  little  yellow  tubercle-like  masses  are  found,— so-called  "  hronchial 
abscesses,''^  vesicular  bronchitis,  and  granulations  purulentes. 

On  section,  the  atelectatic  part  is  brownish-red,  smooth  [not  granular), 
airless,  and  in  the  earlier  stages  dilatable  ;  later  on,  not.  The  walls  of  the 
alveoli  are  approximated,  touch,  and,  according  to  some,  grow  together. 
Fatty  degeneration  and  cell  proliferation  occur  in  the  collapsed  spots.  A 
whole  lung  may  be  involved,  but  usually  only  a  lobe  or  a  portion  of  a  lobe. 
The  collapsed  portions  contrast  strongly  with  the  surrounding  parts.  Its  seat 
is  most  often  in  the  periphery  and  the  lower  lobes  of  the  lung.  The  affected 
portion  has  the  same  tough,  "liver-like"  characteristics  as  in  congenital 
atelectasis,  the  difference  being  that  in  acquired  collapse  the  lobular  points 
are  disseminated.  The  collapsed  portion  may  be  engorged  and  oedematous, 
a  condition  sometimes  called  ''splenization."  The  bronchi  leading  to 
the  collapsed  lobules  are  usually  congested  and  plugged.  When  collapse 
occurs  from  pressure — compression  of  the  lung — the  part  involved  and 
its  extent  depend  on  the  site  and  extent  of  the  pressure.  The  air  cells  in 
the  collapsed  portion  may  or  may  not  be  wholly  void  of  air.  It  is  flesh- 
like ;  and  for  a  time  can  be  inflated  and  caused  to  return  to  its  normal  size 
and  condition.  If  the  inspiration  is  insufficient  and  the  expiratory  efforts 
normal  in  force,  after  a  time  ail  air  will  be  expelled,  and  the  dry,  tough 
9 


130  DISEASES    OF   THE    RESPIRATOEY    ORGAlfS. 

gray-red  mass  assumes  a  condition  known  as  ''  carnification  "  ;  and  in  time 
only  a  fibroua  or  connective-tissue  cicatrix  remains.  Small  blood-clots  may 
be  found  in  the  affected  lobes,  that  are  frequently  decolorized  and  perhaps 
adherent  to  the  walls  of  the  vessels,  whose  calibres  are  impervious  or  oblit- 
erated. ' 

Etiology. — Congenital  atelectasis  occurs  in  feeble  infants,  in  those  born 
prematurely,  and  in  those  whose  bronchi,  nares  or  other  parts  accessory  to 
respiration  are  plugged  with  mucus.  Pulmonary  collapse  is  rarer  in  adults 
than  in  young  children.  Any  disease  or  condition  that  weakens  or  ob- 
structs the  power  of  inspiration  may  induce  it.  Brain  diseases  are  some- 
times accompanied  by  it.  Too  tight  clothing  about  the  chest  of  feeble 
children  may  lead  to  it.  Paralysis  of  the  vagus  is  said  to  cause  it,  and 
muscular  paralysis  from  disease  of  the  cord  may  lead  to  it.  The  most 
frequent  cause  is  some  catarrhal  condition  of  the  respiratory  tract  that 
induces  the  formation  of  a  plug  in  a  small  bronchus;  e.g.,  capil- 
lary bronchitis,  catarrhal  pneumonia  and  bronchitis  with  tenacious  secre- 
tion. Twenty-five  per  cent,  of  the  total  mortality  of  very  young  in- 
fants may  be  safely  set  down  to  pulmonary  collapse,  following  bronchitis. 
Collapse  from  compression  of  the  lung  results  from  fluid,  pus,  air  or  blood 
in  the  pleural  cavity  ;  from  mediastinal  tumors,  from  rachitic  and  spinal 
deformities,  and,  rarely,  from  abdominal  tumors. 

Symptoms. — In  the  new-born,  atelectasis  is  shown  by  feeble  breathing, 
slight  motion  of  the  chest,  a  low,  almost  inaudible,  "  whining  "  cry,  lividity 
and  coldness  of  extremities,  constant  sleepiness,  and  often  muscular  twitch- 
ings  and  convulsions.  The  child  cannot  nurse.  Since  the  foramen  ovale 
and  ductus  arteriosus  so  often  remain  opeii  in  congenital  atelectasis, 
anomalies  of  the  circulation  may  cause  asphyxia,  convulsions,  suffoca- 
tion and  death.  Blood  clots  may  form  in  the  cerebral  sinuses.^  In 
collapse  there  is  labored  breathing,  dyspnoea,  frequent  respirations  (70 
to  100  per  minute),  and  a  cough  with  muco-purulent  expectoration.  Chil- 
dren utter  the  low,  whining  cry.  Passive  hypersemia  and  oedema  of  the  ex- 
tremities and  central  organs  are  common  results  of  pulmonary  collapse. 
The  pulse  is  small  and  feeble,  the  skin  cool,  the  urine  scanty.  There  is 
an  interval  between  inspiration  and  expiration,  instead  of  after  expiration. 
The  whole  act  is  "shallow." 

Physical  Signs. — Inspection  shows  compensatory  retraction  of  the  most 
yielding  portions  of  the  thorax  during  the  act  of  inspiration,  and  the  inter- 
costal spaces  retract.  On  percussion  precordial  dulness  is  increased  ;  there 
may  be  dulness  when  there  is  much  condensation,  but  if  emphysematous 
patches  develop  about  the  collapsed  lobules  the  dulness  may  have  a  tym- 
panitic quality.  On  auscultation  respiratory  sounds  may  be  feeble  or  ab- 
isent.  Later  there  may  be  bronchial  breathing  and  bronchophony.  Eales 
may  be  due  to  associated  bronchitis  ;  they  are  coarse  and  sonorous.      The 

*  Lichtheim's  recent  experiments  go  to  prove  Virchow's  assertion  that  air,  shut  in  by  closure  of  a  bron- 
chus,  is  absorbed  by  the  blond-vessels,  and  also  that  elasticity  of  the  lung  acts  until  the  air  is  completelj 
absorbed.— ^Irc/?./.  exper.  Palhologie  u.  Pharni.,  vol.  x.,  p.  54. 

*  Virchow's  Archiv.,  Bd.  xi.,  p.  240. 


PULMONARY    EMPHYSEMA.  131 

physical  signs  of  compression  are  merely  those  of  the  causative  condition, 
e.  g.,  hydrothorax,  pleurisy  with  effusion,  etc.,  etc. 

DUfferential  Diagnosis. — Pneumonia  is  distinguished  by  the  fever,  flushed 
face,  fine  rdles,  lobar  instead  of  lobular  outline  of  dulness,  pain,  and  ab- 
sence of  "inspiratory  retraction."  Miliary  tuberculosis  is  distinguished 
by  the  fever,  cough,  and  wasting,  all  of  which  will  precede  the  physical 
signs.  The  history  of  the  parents  will  here  aid  us.  In  pleurisy  with 
ejfusion  the  flatness  and  change  in  line  of  flatness  with  a  change  in  the 
patient's  position  will  establish  the  diagnosis. 

Prognosis. — Extreme  atelectasis  is  rarely  recovered  from.  Occurring 
with  whooping-cough  it  is  especially  fatal.  Emphysema,  bronchitis,  lobu- 
lar pneumonia,  tuberculosis  and  pleurisy  may  complicate  it.  Asphyxia  or 
complications  cause  death.  When  compressioji  occurs  from  tumors, 
hydro-  or  pneumo-thorax  the  prognosis  is  more  unfavorable  than  with 
other  causes.  Cheesy  pneumonia  or  jjhthisis  may  follow  atelectasis  or 
collapse. 

Treatment. — In  the  new-born  the  treatment  should  be  that  described  in 
works  on  diseases  of  children  and  obstetrics.  Efforts  at  full  inspira- 
tion should  be  encouraged.  Cold  water  may  be  poured  over  the  neck  and 
chest.  A  stream  of  water  thrown  on  the  nuchal  region  is  said  to  excite 
violent  and  strong  inspiratory  impulses.  Counter-irritation  and  stimulating 
embrocations  are  recommended.  The  catarrh  that  induces  collapse  must 
be  treated  with  stimulating  expectorants,  or,  in  children,  with  emetics. 
Arsenic,  belladonna,  and  salts  of  potash  and  ammonia  are  recommended. 
In  compression  remove  the  cause  when  possible,  e.g.,  the  emphysema  and 
hydrothorax.  In  all  cases  tonics  and  stimulants  with  good  nourishment 
are  demanded  ;  the  "  depletory "  plan  is  never  indicated.  Inhalation  of 
compressed  air  may  do  good.  Never  let  the  diaphragm's  action  be  im- 
peded by  clothing  or  a  distended  abdomen. 


PULMONAEY   EMPHYSEMA. 

Pulmonary  emphysema  is  seldom  met  with  unless  associated  with  more 
or  less  bronchitis  ;  and  emphysematous  persons  are  especially  liable  to  at- 
tacks of  spasmodic  asthma.  Emphysema  is  essentially  a  chronic  affection  ; 
it  comes  on  slowly,  and  when  once  developed  is  permanent. 

By  the  term  is  understood  either  an  abnormal  accumulation  of  air 
within  the  air-cells  or  an  infiltration  of  air  into  the  sub-pleural  and  inter- 
stitial connective-tissue.  There  are  two  recognized  varieties,  termed, 
first,  vesicular  emphysema  ;  second,  interlobular  emphysema.  The  first 
is  by  far  the  more  frequent  and  more  important  affection.  There  are 
no  definite  rules  for  the  diagnosis  of  interlobular  emphysema,  and  it  rarely 
occurs  except  in  connection  with  advanced  vesicular  emphysema.  When 
the  unqualified  term  emphysema  is  used,  reference  is  always  had  to  the 
vesicular  variety. 

Morbid  Anatomy. — In  emphysema,  there  may  be  simple  dilatation  of  the 


133 


DISEASES    OF    THE    RESPIRATOKY    OEGANS. 


air-cells  without  rupture  of  their  walls  ;  or  there  may  be  dilatation  of  the 
air-cells  with  rupture  of  their  walls.  The  rupture  of  the  air-cells  leads  to 
the  formation  of  what  may  be  called  air-sacs,  which  vary  in  size  from  that 
of  a  pin's  head  to  that  of  a  pigeon's  egg,  and  even  larger.  Both  forms  of 
the  affectioD,  the  vesicular  and  the  interlobular,  are  generally  present  in 
cases  in  which  these  larger  air-sacs  have  formed.  The  changes  which  take 
place  in  the  anatomical  structure  of  the  lung  in  this  affection  are  as  fol- 
lows :  in  slight  cases  there  is  dilatation  of  the  infundibula,  and  a  dimin- 
ished prominence  of  the  alveolar  walls,  followed,  later,  by  their  rupture  and 
partial  disappearance  ;  as  a  result,  a  small  air-sac  is  formed,  in  which  lit- 
tle ledges  and  filaments  of  tissue  alone  mark  the  site  of  the  alveolar  septa. 
At  this  time  there  is  no  well-marked  line  of  demarcation  between  the 
infundibulum  and  the  alveoli.  As  the  disease  advances  rupture  of  the 
walls  of  these  little  air-sacs  occurs  and  establishes  a  communication  between 
their  cavities.  The  openings  thus  made  between  the  air-sacs  are  at  the 
very  central  portion  of  the  sac,  where  the  wall  is  thinnest.  By  this  grad- 
ual enlargement  and  the  union  of  many  small  sacs,  a  large  air  cavity  is 
formed,  across  and  along  the  walls  of  which  exist  remains  of  the  original 
tissue.     These  larger  air-sacs  communicate  with  the   bronchi,  which  are 

sometimes  enlarged.  The  result  of 
this  destruction  of  the  alveolar  septa 
is  the  abolition  of  the  capillary 
plexus  which  is  normally  spread  over 
the  walls  of  the  air-cells.  At  times 
ovoid  collections  of  fat  granules  are 
seen  in  the  thinned  septa.  Whether 
these  fat  cells  are  in  the  nuclei  of 
the  capillaries,  or  in  the  inter-capil- 
lary cells  is  undetermined  ; — prob- 
ably they  are  in  both.  This  fatty 
metamorphosis  as  a  rule  precedes  the 
dilatation,  and  is  not  constant.  Fatty 
granules  are  found  in  the  protoplasm 
about  the  nuclei  of  the  epithelial 
cells  taken  from  an  emphysematous 
vesicle.  The  small  branches  of  the 
pulmonary  artery  are  the  longest  retained  ;  they  become  dilated  and  looped, 
and  communicate  by  anastomosis  with  the  pulmonary  vein,  and  thus  the 
circuit  of  the  pulmonary  circulation  is  kept  up,  but  it  is  not  nearly  so  free 
or  abundant  as  that  which  exists  normally.  The  pulmonary  circulation 
is  therefore  materially  interfered  with  by  this  structural  change. 

Well-marked  emphysema  generally  affects  both  lungs  ;  it  is  most 
marked  in  the  upper  lobes,  especially  along  their  anterior  borders. 
Emphysematous  degeneration  throughout  both  lungs  is  rare.  If  the 
emphysema  is  compensatory  its  site  will  vary  with  that  of  the  produc- 
ing cause.  When  it  is  the  result  of  strong  pleuritic  adhesions,  it  most  fre- 
quently affects  the  anterior  border  of  the  lung.     In  partial  collapse  of  the 


Fig.  29. 


Section  of  Emphysematous  Lung  sbowing  dilatation 
of  the  alveola  with  and  without  rupture  of  the  walls. 

A.  Portion  of  an  air-sac  formed  by  dilatation  of  the 

vifundibvlvm. 

B.  Air-sac  formed  by  rupture  of  the  alveolar  walls. 

C.  Wall  of  alveolus,     x  200.     After  Thierf elder. 


PULMONARY   EMPHYSEMA.  133 

lung  following  obstruction  of  the  bronchi,  or  in  inexpansibility  from 
disease  of  its  structure,  emphysema  will  usually  be  limited  to  the  vicinity  of 
the  bronchial  obstructions  or  the  structural  disease.  When  emphysema  is 
the  result  of  forced  inspiration  with  closure  of  the  glottis,  as  occurs  in  vio- 
lent spasmodic  croup,  etc.,  the  apex  and  anterior  borders  of  the  lungs  are 
mainly  involved. 

Emphysematous  lungs  do  not  collapse  when  the  thoracic  cavity  is 
opened.  In  well-marked  cases,  the  lungs  meet  and  overlap  each  other 
in  the  median  line.  The  left  overlaps  the  superficial  cardiac  region, 
both  extend  lower  than  normal,  and  the  heart  is  pushed  downwards  and 
nearer  to  the  median  line  than  normal.  The  diaphragm  may  also  be 
pushed  below  its  normal  position,  and  all  of  the  abdominal  viscera  crowded 
out  of  their  normal  situations  in  consequence.  In  some  cases  the  liver  has 
been  so  displaced  as  to  lie  entirely  below  the  free  border  of  the  ribs.  The 
lungs  removed  from  the  thoracic  cavity  bear  the  impress  of  the  ribs  as 
furrows  on  their  surface.  Indentations  made  by  pressure  of  the  fingers  on 
the  surface  of  the  lung  are  permanent,  showing  a  loss  of  elasticity.  The 
dilated  alveoli  may  at  times  be  seen  on  the  surface  of  the  lung  through  the 
pleura,  or  on  section  maybe  found  distributed  through  its  substance  ;  they 
are,  however,  much  more  apparent  after  the  lung  has  been  blown  up  and 
dried.  They  appear  as  whitish  or  gray  prominences,  or  as  spherical  vesic- 
ular appendages  filled  with  air.  When  the  air-sacs  are  large  they  protrude 
beyond  the  surface  of  the  lung,  and  generally  have  a  globular  form  ;  in 
some  cases  they  seem  to  be  separated  by  a  neck  from  the  rest  of  the  lung, 
looking  like  appendages  to  it.  In  well-marked  examples  of  emphysema, 
the  whole  anterior  surface  of  the  lungs  may  be  covered  over  with  air-sacs, 
sometimes  resembling  the  lungs  of  reptiles.  The  color  of  an  emphy- 
sematous lung  is  usually  abnormally  pale  ;  it  is  soft  and  cushion-like  to 
the  touch  ;  it  crepitates  but  little  when  pressed  between  the  thumb  and 
finger  ;  it  sinks  in  water  less  readily  than  healthy  lung-tissue,  for  though 
its  volume  is  increased,  its  weight  is  diminished.  By  pressure  the  air  can 
be  forced  out  of  the  larger  and  smaller  sacs  into  the  bronchi.  The  evi- 
dences of  bronchitis  are  usually  present  in  the  bronchial  tubes.  The  pa- 
renchyma of  the  lung  may  present  lesions  which  may  be  either  a  cause  or 
a  complication  of  emphysema.  Phthisis  and  pneumonia,  although  of  rare 
occurrence,  are  not  as  infrequent  as  many  writers  would  have  us  suijpose. 
As  a  rule  in  advanced  cases  of  emphysema,  the  right  heart  will  be  found 
hypertrophied  and  dilated  ;  as  soon  as  the  systemic  circulation  is  inter- 
fered with,  the  left  ventricle  becomes  hypertrophied,  and  this  hypertrophy 
will  for  a  time  compensate  for  the  obstruction  to  the  return  circulation,  but 
as  a  result  of  this  interference  when  it  is  long-continued,  anatomical  changes 
take  place  in  the  liver,  kidneys  and  spleen,  which  are  similar  in  character 
to  those  which  occur  in  connection  with  valvular  heart  lesions,  and  give 
rise  to  general  dropsy  ;  changes  of  this  class,  however,  belong  to  the  remoter 
lesions  of  emphysema. 

Senile  emphysema  differs  from  the  variety  which  has  just  been  described 
in  the  following  respects  :  the  lungs  are  not  only  diminished  in  weight  but 


134  ,         DISEASES    OF    THE    RESPIEATOKY    ORGAifS. 

very  markedly  in  size  ;  the  lobes  are  usually  united,  and  their  fissures  di- 
rected vertically  instead  of  horizontally ;  the  lower  lobes  having  lost  the 
most  in  bulk,  their  surface  is  irregular,  and  their  structure  is  composed  of 
enlarged  air  vesicles  and  sacs  which  are  the  result  of  the  natural  atrophy 
of  the  lung-tissue  which  takes  place  in  old  age.  In  the  aged  the  walls  of 
the  emphysematous  cavities  are  usually  deeply  pigmented.  The  lung  often 
consists  merely  of  a  number  of  large  cavities. 

In  interlobubar  emphysema  an  air-vesicle  or  sac  ruptures,  so  that  the 
air  escapes  into  the  interlobular  cellular-tissue,  forming  sacs  of  large  or 
small  size.  These  sacs,  or  rather  these  collections  of  air,  may  form  be- 
neath the  pleura,  or,  extending  between  the  lobules  of  the  lung  and  along 
its  vessels,  reach  its  root,  spread  into  the  mediastinal  cellular- tissue,  and  be 
distributed  over  the  neck  and  subcutaneous  cellular-tissue  of  the  body.  The 
size  of  the  air-sacs  beneath  the  pleura  may  be  only  that  of  small  vesicles, 
and  these  limited  to  the  circumference  of  a  lobule,  or  they  may  reach  the 
size  of  the  stomach.  "They  look  like  a  membrane  uplifted  by  foam." 
They  may  be  distinguished  from  the  vesicular  dilatations  by  being 
freely  movable  beneath  the  pleura.  Perforation  of  the  pleura,  produc- 
ing pneumothorax,  is  a  rare  resulb  of  interlobular  emphysema.  More 
or  less  interlobular  emphysema  is  always  present  in  advanced  vesicular 
emphysema. 

Etiology. — The  causes  of  emphysema  may  be  divided  into  primary  and 
secondary,  or  compensatory.  Primary  emphysema  may  exist  independently 
of,  or  be  associated  with  bronchitis.  Among  its  causes  are  forced  expiratory 
efEorts,  the  glottis  being  closed  or  narrowed  as  in  violent  coughing,  strain- 
ing at  stool,  etc.  .  In  a  few  rare  instances  the  emphysematous  distention  is 
produced  during  strong  inspiratory  efforts.  In  both  instances  the  disease  is 
developed  in  the  upper  lobes  of  the  lung.  Another  cause  of  this  variety  of 
emphysema  is,  that  there  exists  in  many  persons  either  an  hereditary  or  an 
acquired  impairment  of  the  elasticity  of  the  lungs  which  renders  them  more 
readily  dilatable  and  more  easily  torn.  There  are  three  prominent  theories 
which  have  been  advanced  to  account  for  this  :  first,  that  it  is  due  to  fatty 
degeneration  of  the  alveolar  walls.  The  constancy  of  this  change  has  not 
as  yet  been  demonstrated.  It  is  true  that  molecules  of  fat  are  sometimes 
seen  in  the  alveolar  septa,  but  they  may  be  the  result  rather  than  the  cause 
of  the  emphysema.  Secondly,  there  is  a  theory  that  the  weakness  of  the 
alveolar  walls  is  due  to  the  growth  of  the  inter-capillary  nuclei.  Thirdly, 
that  it  is  due  to  the  fibroid  degeneration  of  the  alveolar  septa.  No  one  of 
these  theories  has  as  yet  received  full  confirmation  ;  a  co-operation  of  all  of 
them,  more  particularly  of  the  last  two,  is  necessary  in  many  cases  to  satis- 
factorily explain  the  production  of  the  disease.  Recently  another  cause  for 
the  development  of  this  form  of  emphysema  has  been  advanced,  viz. :  an 
abnormal  increase  in  the  capacity  of  the  chest,  due  to  excessive  growth  of 
its  walls.     This  theory  as  yet  lacks  proof. 

The  causes  of  secondary  emphysema  are  conveniently  considered  under 
three  subdivisions,  in  all  of  which  the  emphysema  is  best  denominated  com- 
pensatory.    The  first  of  these  subdivisions  comprises  all  cases  in  which  the 


PULMONARY    EMPHYSEMA.  135 

emphysema  is  developed  around  small  portions  of  lung  rendered  inexpansible 
by  disease  of  its  tissue,  as,  for  example,  lobular  collapse  from  obstruction  of  a 
small  bronchus,  a  lobular  pneumonia,  a  pulmonary  infarction,  etc.  ;  the  lob- 
ules adjacent  to  those  that  are  thus  rendered  inexpansible  become  over-dis- 
tended by  a  forced  inspiration  or  a  forced  expiration  during  a  violent  fit  of 
coughing.  Some  would  make  these  obstructions,  operating  in  different  parts 
of  the  lung,  a  primary  cause.  A  second  subdivision  comprises  those  cases 
where  a  large  portion  of  lung,  either  from  some  internal  cause,  as  pneumo- 
nia, hypostasis,  atelectasis,  etc.,  or,  from  some  external  cause,  as  pleurisy, 
etc.,  is  rendered  inexpansible,  and  emphysema  is  developed  in  healthy  por- 
tions. In  both  of  these  subdivisions  the  capacity  and  mobility  of  the  chest 
remaining  normal,  the  usual,  and  especially  forced,  inspiratory  efforts 
require  extra  distention  of  the  alveoli  to  compensate  for  those  rendered 
more  or  less  useless.  A  third  subdivision  includes  those  cases  secondary  to 
croup,  lobular  pneumonia,  whooping-cough,  pressure  on  the  trachea  or 
main  bronchi.  The  emphysematous  distention  in  this  class  of  patients  is  pro- 
duced during  inspiration.  It  is  questionable,  however,  whether  compensatory 
emphysema  is  ever  developed  when  the  walls  of  the  air-cells  have  not  been 
enfeebled.  Interlobular  emphysema  is  produced  by  forced  expiration  with 
narrowed  glottis,  as  during  severe  cough,  parturition,  straining  at  stool, 
etc.  It  is  usually  preceded  by  vesicular  emphysema.  It  may  also  occur 
from  perforation  of  the  lung  from  without,  as  in  fracture  of  the  ribs. 
Senile  emphysema  is  mainly  an  atrophy  of  the  alveolar  septa,  which  become 
obliterated,  so  that  vesicles  coalesce.  It  is  due  to  impaired  nutrition,  which 
affects  the  lungs  as  well  as  other  organs  in  old  age. 

Symptoms. — The  prominent  and  most  constant  subjective  symptom  of 
emphysema  is  dyspnoea.  It  is  a  dyspnoea  which  is  increased  by  physical 
exercise,  by  the  occurrence  of  fresh  attacks  of  bronchitis,  and  by  spasm  of 
the  bronchi,  such  as  occurs  in  spasmodic  asthma.  When  the  emphysema 
is  well  marked,  very  slight  exertion  will  give  rise  to  dyspnoea  ;  when  the 
emphysema  is  slight,  only  violent  exertion  will  be  followed  by  it.  It  is 
mitigated  by  a  warm  atmosphere,  and  returns  with  increased  severity  during 
the  cold  of  winter.  There  is  often  a  "smothering"  sensation  in  the  chest, 
and  when  present  it  is  constant.  In  congenital  cases  the  only  symptom 
during  childhood  and  early  adult  life  is  a  moderate  degree  of  dyspnoea.  In 
advanced  cases  of  the  disease  the  dyspnoea  is  liable  to  be  paroxysmal,  the 
paroxysms  depending  upon  a  tendency  to  spasm  which  emphysema  in  its 
development  seems  to  impart  to  the  bronchi.  A  cough  is  usually  present, 
but  it  is  due  to  bronchial  irritation,  and  unless  bronchitis  exists  the  cough 
may  be  wanting.  The  expectoration  varies  with  the  extent  and  character 
of  the  accompanying  bronchitis,  and  it  is  not  uncommonly  a  part  of  the  his- 
tory of  the  emphysema ;  if  it  occurs  independently  of  bronchitis  it  will 
have  nothing  characteristic  about  it.  Usually  there  is  no  pain  in  the  chest 
dependent  upon  the  emphysema.  In  advanced  cases  the  countenance  is 
peculiar  and  somewhat  characteristic  ;  it  is  of  a  dusky  hue  and  has  a  puffy 
appearance  which  contrasts  remarkably  with  the  wasted  appearance  of  the 
rest  of  the  body.     The  nostrils  are  distended,  thickened,  and  vascular,  and 


136  DISEASES    OF   THE   KESPIRATOKY   ORGANS. 

expand  with  each  inspiration ;  the  angles  of  the  mouth  are  drawn  down- 
ward,  the  voice  is  feeble,  the  patient  stoops  in  the  act  of  walking,  and  his 
whole  body  has  a  cachectic  appearance  ;  the  capillary  circulation  of  the 
extremities  is  markedly  imperfect,  as  shown  upon  the  slightest  exertion. 
There  is  a  gradual,  though  steady  loss  of  flesh  and  strength.  Usually,  the 
disease  is  not  attended  by  febrile  excitement ;  the  pulse  is  not  accelerated, 
but  is  markedly  feeble,  and  the  temperature  of  the  body  sub-normal. 

The  other  symptoms  observed  in  connection  with  emphysema  are  indirect, 
and  due  to  interference  with  the  circulation.  JSTot  only  is  there  always  dis- 
turbance of  the  capillary  circulation  in  the  extremities,  but  the  face  and 
neck  present  a  fulness  or  even  a  turgidity  of  the  blood-vessels  altogether  ab- 
normal. The  distention  of  the  Jugular  veins,  and  the  lividity  of  the  face 
and  hands,  are  unquestionably  due  to  the  interference  with  the  circulation 
through  the  right  heart,  but  do  not  occur  until  that  stage  is  reached 
in  which  there  is  more  or  less  hypertrophy  and  dilatation  of  the  right  ven- 
tricle. Patients  who  have  reached  this  stage  become  very  purple  in  the 
face  after  and  during  fits  of  coughing,  often  presenting  the  appearance  of 
impending  suifocation.  The  paroxysms  are  perfectly  characteristic  ;  an 
attack  of  coughing  comes  on,  grows  more  and  more  severe,  gathers  more 
or  less  of  the  spasmodic  element,  and  when  it  has  reached  its  climax  the 
face  and  hands  become  livid,  and  the  patient  is  completely  exhausted. 
Vertigo  is  a  common  symptom  in  advanced  emphysema  ;  it  is  most  apt  to 
be  developed  during  a  fit  of  coughing,  and  depends  upon  the  interference 
with  the  return  circulation  from  the  head.  Slight  haemoptysis  may  occur. 
Emphysema  of  itself  does  not  give  rise  to  dropsy,  although  in  advanced 
cases  the  feet  and  ankles  are  almost  always  oedematous.  The  oedema  is  the 
result  of  cardiac  or  renal  complications.  Ordinarily,  there  is  more  or  less 
disturbance  of  the  digestive  organs  in  these  advanced  cases  ;  the  disturbance 
is  due  to  catarrh  of  the  stomach,  the  result  of  passive  hyperemia  of  the  mu- 
cous membrane  of  the  stomach  from  failure  of  the  right  heart.  For  a  like 
reason  other  functions  are  more  or  less  disturbed.  Emphysematous  patients 
are  especially  liable  to  hemorrhoids,  and  very  often  have  profuse  bleeding 
from  the  rectum.  As  has  been  already  stated,  the  development  of  emphy- 
sema is  almost  always  slow;  in  rare  instances  it  advances  rapidly,  and  it  is 
then  called  acute.  If,  from  the  rational  symptoms,  there  is  any  doubt  as 
to  the  diagnosis  of  emphysema,  the  doubt  will  disappear  after  a  physical 
exploration  of  the  chest,  for  the  physical  signs  in  a  well-marked  case  are 
characteristic. 

Physical  Signs. — On  inspection,  it  will  be  noticed  that  there  are  alterations 
in  the  shape  and  movements  of  the  chest.  There  is  an  unnatural  elevation 
and  arching  of  the  sternum  (as  if  from  congenital  deformity),  and  an  un- 
natural bulging  of  the  infra-clavicular  and  mammary  region,  which  gives 
to  the  chest  a  more  rounded  appearance  than  in  health  :  this  has  been 
termed  "barrel-shaped."  The  scapulae  are  brought  forward,  and  there  may 
be  antero-posterior  curvature  of  the  spine,  which  gives  to  this  class  of  pa- 
tients a  stooping  posture  which  is  habitual.  The  muscles  of  the  neck  are 
unnaturally  prominent.     The  lower  portion  of  the  chest  seems  contracted. 


PULMONARY   EMPHYSEMA.  137 

and  the  intercostal  spaces  are  depressed  and  wider  than  above.  If  the  em- 
physema is  extensive,  the  apex  of  the  heart  will  be  found  beating  lower 
down  than  normal  and  more  toward  the  median  line  ;  if  the  right  side  of 

the  heart  is  extensively  dilated  there  will  be  an  epigastric  impulse this 

impulse  is  due  to  an  increase  in  the  size  of  the  heart,  and  to  its  being 
crowded  to  the  right,  and  lower  down  in  the  thoracic  cavity.  In  some  in- 
stances, when  the  general  symptoms  of  emphysema  are  well  marked,  the 
lungs  are  atrophied  instead  of  abnormally  dilated,  and  no  bulging  of  the 
chest  (either  general  or  local)  occurs.  The  movements  of  the  chest  walls 
are  also  altered  and  peculiar.  At  the  upper  portion  expansion  on  inspira- 
tion is  diminished  or  entirely  wanting  ;  the  whole  chest  moves  vertically 
up  and  down  with  inspiration  and  expiration,  as  if  it  were  passively  lifted 
from  the  shoulders,  and  composed  of  one  solid  piece ;  while  below,  the  chest, 
instead  of  being  dilated  with  inspiration,  is  contracted.  The  respiratory 
efforts  are  labored,  and  the  breathing  is  chiefly  abdominal.  The  diaphragm 
seems  to  be  more  actively  engaged  than  the  chest  walls  in  the  process  of 
respiration.  In  cases  far  advanced,  the  existence  of  emphysema  can  be 
made  out  by  inspection  alone. 

On  2Mlpation  the  vocal  fremitus  varies  :  it  may  fall  below,  or  equal,  or  it 
may  exceed  that  in  health.  In  senile  emphysema,  the  vocal  fremitus  is 
usually  increased. 

The  intensity  of  the  percussion  sound  is  increased,  the  pitch  is  lowered, 
the  pulmonary  quality  of  the  sound  is  greatly  diminished,  and  it  becomes 
vesiculo-tympanitic — that  is,  there  is  added  to  the  vesicular  element  a  tym- 
panitic quality  which  is  the  characteristic  percussion  sound  of  emphysema, 
and  is  not  met  in  connection  with  any  other  pulmonary  disease.  The  per- 
cussion note  is  not  materially  affected,  either  by  forced  inspiration  or  by 
forced  expiration.  The  precordial  region  is  usually  resonant,  owing  to  the 
distended  lungs  coming  between  the  heart  and  the  wall  of  the  chest. 

On  auscultation,  the  inspiratory  sound  is  either  short  or  feeble,  or  act- 
ually suppressed,  while  the  expiratory  is  greatly  prolonged,  the  ratio  of  the 
two  being  as  one  to  four  instead  of  four  to  one.  As  a  rule,  the  pitch  of 
both  the  inspiratory  and  expiratory  sound  is  lower  than  in  health.  In  some 
extreme  cases  of  emphysema,  the  respiratory  sounds  are  of  equal  length, 
greatly  exaggerated  in  intensity,  and  of  a  harsh,  sibilant  or  sonorous  quality, 
the  harsh  quality  undoubtedly  being  due  to  diminution  in  the  calibre  of  the 
minute  bronchial  tubes.  In  some  cases,  when  interlobular  and  vesicular 
emphysema  are  combined,  a  crumpling  sound  is  heard,  which  has  been  des- 
ignated as  the  "crumpling  sound  of  emphysema."  This  sound  has  been 
said  to  resemble  the  crepitant  rale,  but  it  more  nearly  resembles  the  sound 
of  crumpling  parchment,  than  the  crackling  sound  of  the  crepitant  rdle; 
but  "  Laenneds  rdW' — a  modification  of  the  sub-crepitant  idle — is  very 
often  heard.  The  vocal  sounds  vary  greatly  ;  they  may  be  diminished,  or 
altogether  absent,  or  their  intensity  may  be  greatly  increased.  The  heart 
sounds  are  feeble.     The  sphygmograph  may  afford  valuable  information. 

Differential  Diagnosis. — Slight  empliysema  cannot  be  diagnosticated  with 
certainty ;  but  those  advanced  emphysematous  cases  which  give  rise  to  se- 


138  DISEASES    OF   THE   KESPIRATORY   OEGAJS'S. 

vere  dyspnoea  and  cyanosis  are  readily  distinguished,  by  a  physical  exami- 
nation of  the  thorax,  from  other  diseases  which  manifest  similar  symptoms. 
The  disease  with  which  emphysema  is  especially  liable  to  be  confounded  is 
pneumothorax.  If  the  physical  signs  of  the  two  diseases  are  properly  ap- 
preciated, it  is  not  difficult  to  distinguish  between  them.  In  emphysema 
the  percussion  sound,  althcugh  somewhat  tympanitic  in  character,  still  re- 
tains a  pulmonary  quality,  and  there  is  a  vesicular  element  to  the  respira- 
tory sound,  while  in  pneumothorax  the  percussion  sound  has  a  well-marked 
purely  tympanitic  character,  and  the  respiratory  sound,  if  audible,  is  am- 
phoric in  character  with  no  vesicular  element.  Emphysema  affects  both 
sides,  pneumothorax  only  one  side.  The  symptoms  of  pneumothorax  come 
on  suddenly,  while  those  of  emphysema  are  slowly  developed,  and  are  never 
so  urgent  as  those  of  pneumothorax.  A  diagnosis  of  compensatory  em- 
physema may  not  be  made  out  during  life,  but  the  fact  being  well  estab- 
lished that  it  does  almost  invariably  exist  in  certain  conditions,  the  proba- 
bility of  its  existence  should  always  be  borne  in  mind  in  the  study,  exam- 
ination, and  treatment  of  those  pulmonary  diseases  in  which  it  is  liable  to 
occur. 

Prognosis. — Emphysema  rarely  if  ever  destroys  life  ;  but,  when  once  de- 
veloped, is  never  recovered  from,  and  incapacitates  the  person  to  a  greater 
or  less  degree  for  active  exercise,  rendering  life  at  least  uncomfortable.  It 
strongly  predisposes  to  bronchitis  and  renders  existing  bronchitis  severe. 
Acute  bronchitis  of  the  smaller  tubes  is  an  extremely  grave  affection  when 
it  occurs  in  an  emphysematous  person.  Again,  emphysema  develops  heart 
disease.  The  impediment  to  the  pulmonary  circulation,  which  exists  as 
the  result  of  emphysematous  changes  in  the  lung  substance,  gives  rise  to 
an  overloaded  state  of  the  right  cardiac  cavities,  which  in  time  leads  to 
their  permanent  dilatation  and  to  hypertrophy  of  their  walls  ;  insufficiency 
of  the  tricuspid  valves  follows,  and  the  resulting  regurgitation  through  the 
tricuspid  orifice  into  the  right  ventricle  causes  obstruction  to  the  systemic 
venous  circulation,  and  as  a  result  there  is  congestion  and  a  permanent  dis- 
turbance of  the  function  of  the  kidneys,  liver,  etc.  In  giving  a  prognosis 
in  any  case  of  emphysema,  the  liability  to  this  complication  should  be  con- 
sidered. Emphysema  also  predisposes  to  fatty  degeneration  of  the  different 
organs  and  tissues  of  the  body,  the  result  of  an  impoverished  state  of  the 
blood.  The  occurrence  of  these  secondary  affections  renders  emphysema  a 
serious  disease.  It  is  undoubtedly  a  more  serious  affection  when  it  occurs 
in  childhood  or  adult  life,  than  in  old  age.  Pleurisy,  asthma,  bronchitis 
and  anaemia  are  the  most  frequent  complications. 

Treatment. — The  treatment  of  this  affection  will  be  briefly  considered  un- 
der two  heads  :  first,  the  treatment  of  the  disease  itself ;  secondly,  the 
treatment  of  secondary  changes  in  other  organs,  which  changes  are  more  or 
less  directly  induced  by  the  emphysema.  Accepting  the  view  that  the 
lesions  in  this  disease  in  the  lung-tissue  are  the  result  of  imperfect  or  dis- 
ordered nutrition,  we  may  reasonably  expect  that,  by  improving  the  nutri- 
tion, the  progress  of  the  degeneration  may  be  checked  or  arrested,  and  per- 
haps even  the  elasticity  of  the  unaffected  portion  of  the  lung  may  be  re- 


PULMONART   EMPHYSEMA.  '      139 

stored.  The  most  rational  method  of  treatment  is  that  by  which  we  aim 
to  remedy  faulty  nutrition  in  other  organs  and  tissues.  With  this  object 
in  view,  the  drug  which  is  of  the  greatest  service  is  iron.  This  remedy, 
should  be  taken  daily  with  meals,  for  a  long  period,  by  persons  who  have 
emphysema  or  in  whom  it  is  developing.  In  this  class  of  cases,  the  prepa- 
ration which  I  prefer  is  the  ethereal  tinctare  of  the  acetate  of  iron ;  sul- 
phate of  quinine  in  small  doses  may  be  given  with  the  iron  in  most  cases 
with  benefit.  Strychnia,  which  has  some  reputation  in  the  treatment  of 
\;his  disease,  I  am  confident  has  no  power  in  arresting  its  development,  and 
it  has  seemed  to  me  to  increase  the  frequency  and  violence  of  the  parox- 
ysms of  dyspnoea,  and  thus  hasten  rather  than  retard  the  emphysematous 
development.  If  an  emphysematous  patient  has  dyspeptic  symptoms  the 
mineral  acids  in  combination  with  bitter  vegetable  infusions  will  be  found 
of  service.  When  there  is  a  tendency  to  great  emaciation,  I  have  found 
cod-liver  jOil  of  service.  Stimulants,  vinous  and  spirituous,  when  taken 
in  small  quantities  after  or  during  meals,  often  give  beneficial  results,  and 
when  their  use  is  followed  by  marked  improvement  in  the  general  condition 
of  the  patient,  they  should  be  used  in  the  treatment  of  the  disease. 

The  regulation  of  the  diet,  and  the  general  management  of  the  emphy- 
sematous patient  is,  however,  of  much  greater  importance  than  the  medical 
treatment.  The  diet  should  be  of  the  most  nutritious  character,  and  com- 
posed largely  of  animal  food  ;  overloading  the  stomach  should  be  especiallj 
avoided,  as  well  as  everything  which  has  a  tendency  to  produce  flatulence. 
The  food  should  not  be  bulky  or  watery  in  character,  and  should  be  as  di- 
gestible as  possible  ;  the  quantity  of  liquids  taken  into  the  stomach  should 
always  be  small.  Exercise  in  the  open  air  should  be  taken  systematically, 
but  fatigue  should  be  avoided.  All  sudden,  violent  exercise,  or  great  physi- 
cal exertion  must  be  strictly  prohibited.  The  condition  of  the  skin  should 
be  carefully  considered.  Emphysematous  patients  should  not  expose  them- 
selves to  cold.  All  localities  where  attacks  of  spasmodic  asthma  are  liable 
to  be  developed  should  be  carefully  avoided,  as  also  everything  which  may 
develop)  dyspnoea  or  predispose  the  patient  to  asthmatic  attacks.  The  in- 
halation of  compressed  air  is  highly  esteemed  by  the  Germans.  The  patient 
should  live  in  the  open  air  as  much  as  possible,  and  in  such  conditions  as 
will  make  the  minimum  of  effort  sufficient  for  respiration.  The  rule  for 
all  emphysematous  persons  is  to  change  their  residence  to  that  locality 
where  they  suffer  the  least  and  are  not  troubled  with  dyspnoea.  The  treat- 
ment of  those  complications  which  accompany,  or  are  induced  by,  the  em- 
physema is  also  of  importance  in  arresting  the  progress  of  the  disease.  Of 
these  accompaniments,  bronchitis  (generally  chronic)  stands  first.  The 
dyspncea  may  be  so  urgent  as  to  demand  treatment  of  itself  ;  the  quebracho 
bark  has  recently  received  much  attention  as  the  drug  for  emphysematous 
dyspncea.  In  addition  to  all  that  can  be  accomplished  by  change  of  cli- 
mate and  other  hygienic  measures  in  the  management  of  that  form  of  bron- 
chitis which  is  so  constant  an  accompaniment  of  emphysema,  there  is  one 
drug  which  I  have  found  especially  serviceable,  viz.,  iodide  of  potassium. 
It  should  be  given  in  doses  varying  from  five  to  twenty  grains,  three  times 


140 


DISEASES    OF    THE    RESPIKATOEY    0EGA2TS. 


during  the  day,  and  its  administration  should  be  continued  at  intervals  over 
a  long  period.  The  treatment  of  diseases  of  the  heart,  liver  and  kidneys, 
which  occur  as  complications  or  accompaniments  of  emphysema,  will  be 
considered  in  connection  with  the  history  of  cardiac,  renal  and  hepatic 
diseases. 

CANCEK    OF   THE    LUJSTGS. 


There  is  no  variety  of  cancer  which  has  not  been  found  in  the  lungs.  Can- 
cer here  is  usually  secondary  to  cancerous  development  in  other  parts  of 
the  body.  It  may  extend  to  the  lungs  by  direct  peripheral  extension  of  a 
cancer  of  the  mediastinum  or  other  adjacent  parts,  or  by  metastasis  from 
distant  cancer ;  and  in  either  case  it  begins  in  the  connective-tissue  either 
of  the  walls  of  the  air-cells,  the  interlobular  tissue,  the  bronchial  tubes,  or 
the  pleural  or  subpleural  tissues. 
Morbid  Anatomy. — Medullary  or  enccihaloid  cancer  is  the  mosji  frequent 

variety  met  with  in  the 
lungs ;  next  is  scirrhus, 
then  epithelioma,  and 
melanotic  cancer.  Me- 
dullary cancer  of  the  lungs 
occurs  in  the  form  of  nod- 
ules of  various  sizes  scat- 
tered through  the  lung- 
substance,  or  a  large 
portion  of  lung  may  be- 
come the^  seat  of  medul- 
lary infiltration.  Discrete 
nodules  of  medullary 
cancer  cause  great  de- 
struction of  tissue  and 
hemorrhage.  Primary 
cancer  usually  involves 
only  one  lung,  and  is  often 
infiltrated  or  disseminated 
in  nodules  the  size  of 
peas,  while  secondary  can^ 
cer  affects  both  lungs  and 
is  generally  nodular,  the 
nodules  varying  m  size. 
By  the  union  of  the  nod- 

E  E.  Lvng- alveoli  filled  with  cells  "of  same  character  as  those  filling    ulcs   an  entire  luUfif  SOmC- 
the  alveoli  of  the  cancer-     x  250.  ° 

times  becomes  involved. 
After  a  time  the  cancerous  tissue  may  undergo  fatty  degeneration  and 
softening,  and  the  pulmonary  vessels  and  bronchi  are  either  involved  in  the 
cancerous  development  or  are  obliterated  by  its  pressure.  Scirrhus  develops 
most  frequently  in  the  bronchi. 

The  unaffected  portion  of  lung-tissue  may  be  normal,  oedematous  or  pneu- 


Cancer  of  the  Lung. 

Section  of  Lvng  through  a  small  cancerous  nodule.  Tlie  illustration 
shows  only  apart  of  the  nodule  with  the  air-vesicles  bounding  the 
upper  and  left  hand  sides. 

A.  Fibrous  stroma  Qf  the  cancer. 
B  B.  Empty  alveoli  of  the  cancer. 

C  0.  Cancer  alveoli  filled  with  larr/e  nucleated  cells  of  various  forms. 
J)  D.   Walls  of  air-vesicles  'bordering  the  nodule 


CANCER   OF   THE   LUNGS.  141 

monic ;  extensive  pleuritic  thickenings  and  adhesions  are  present  in  most 
cases.  Authorities  differ  as  to  which  lung  is  oftener  involved,  and  there 
are  not  sufficient  statistics  to  decide  the  question.  The  lymphatics  of  the 
lungs  are  the  channels  along  which  the  process  extends.  Hemorrhagic  pleu- 
risy, cancer  of  the  pleura  and  bronchial  glands,  and  hydrothorax,  usually 
co-exist.  The  infundibula  are  filled  with  cancerous  elements,  about  which 
is  extensive  pigmentation.  The  alveolar  walls  may  be  intact,  but  their  ves- 
sels are  engorged.  There  is  no  newly  formed  stroma  in  pulmonary  cancer  ; 
the  alveolar  septa  take  the  place  of  a  stroma. 

Etiology.— The  etiology  of  pulmonary  cancer  is  the  same  as  the  etiology 
of  cancer  in  general.  Hereditary  predisposition  may  be  regarded  as  an  ele- 
ment in  its  production.  It  is  most  frequently  met  with  between  the  ages  of 
twenty  and  sixty,  and  is  more  common  in  males  than  females.  As  has 
already  been  stated,  it  is  generally  secondary  to  cancerous  developments  in 
other  organs  of  the  body.  In  the  female,  cancer  of  the  breast  usually  pre- 
cedes the  development  of  cancer  o£  the  lungs.  It  may  be  secondary  to  car- 
cinoma of  the  bones,  testicles,  uterus,  stomach,  liver,  or  oesophagus. 

Symptoms. — Cancer  of  the  lung  usually  comes  on  very  insidiously,  with 
few  subjective  symptoms.  There  is  usually  pain  in  the  chest  and  a  cough 
accompanied  by  a  muco-hemorrhagic  expectoration  resembling  currant-jelly, 
which  occasionally  contains  cancerous  elements.  More  or  less  dyspnoea  is 
present,  especially  if  mediastinal  tumors  co-exist.  The  cancerous  cachexia 
may  or  may  not  be  present.  As  the  disease  advances,  emaciation,  fever, 
night-sweats,  with  failure  of  strength,  become  more  and  more  marked,  and 
this  steadily  increasing  weakness  and  emaciation  is  one  of  the  most  constant 
rational  symptoms.  The  ''^ pressure  effects  "  producing  lividity,  oedema,  dys- 
phagia, and  laryngeal  symptoms,  are  like  those  of  a  thoracic  aneurism.  The 
glands  in  the  axilla  and  above  the  clavicle  are  nearly  always  enlarged.  If 
dyspnoea,  cough,  haemoptysis,  pain  in  the  chest,  rapid  emaciation,  and 
cachexia  should  come  on  in  one  from  whom  a  carcinomatous  breast  had 
been  extirpated,  there  would  be  reason  to  suspect  the  development  of  cancer 
of  the  lung.  Signs  of  pleurisy,  bronchitis,  emphysema,  or  catarrhal  pneu- 
monia, may  mask  the  signs  of  pulmonary  cancer. 

Physical  Signs. — These  will  vary  according  to  the  seat  and  extent  of  the 
cancerous  development.  If  the  lung  is  extensively  involved  with  nodular 
cancer,  inspection  will  show  enlargement  of  the  affected  side  with  widening 
of  the  intercostal  spaces  and  deficiency  or  entire  absence  of  respiratory 
motion.  Yocal  fremitus  may  be  diminished  or  absent.  On  percussion 
there  will  be  complete  dulness  attended  by  friction  over  the  space  corre- 
sponding to  the  cancer.  The  signs  of  a  cavity  are  sometimes  present. 
On  auscultation  the  respiratory  sounds  may  be  feeble  or  absent,  or,  if  a 
large  open  bronchus  is  intimately  connected  with  the  cancerous  mass, 
bronchial  respiration  may  be  heard.  Disseminated  cancer  of  the  lungs 
cannot  be  distinguished,  by  physical  examination,  from  general  bronchitis. 
In  the  infiltrated  form  the  lung  is  often  contracted,  and,  as  a  consequence, 
there  is  retraction  of  the  ohefst-walls  on  the  affected  side. 

Differential  Diagnosis. — Pulmonary  cancer  is  liable  to  be  confounded  with 


143  DISEASES    OF   THE    EESPIEATOEY   ORGAJSTS. 

pleurisy  with  effusion.  In  cancer,  the  percussion  dulness  usually  begins  at 
the  upper  portion  of  the  chesty  while  in  pleurisy  it  begins  at  the  lower 
portion.  In  cancer  the  dulness  is  most  marked  in  front,  in  pleurisy  it  is 
most  marked  behind.  In  cancer  there  are  isolated  spots  of  resonance  in 
the  area  of  dulness,  while  in  pleurisy  the  dulness  is  uniform  over  all  the 
space  occupied  by  the  fluid.  In  pleurisy  the  line  of  dulness  changes  with 
the  position  of  the  patient ;  this  never  varies  in  cancer. 

It  may  also  be  mistaken  for  tJioracic  aneurism  and  iov  phthisis.  The  his- 
tory, the  long  duration  and  the  physical  signs  of  the  latter  will  soon  enable 
a  diagnosis  to  be  made.  It  may  also  be  mistaken  for  fibroid  induration  of 
the  lung,  but  its  secondary  character,  more  rapid  course,  greater  marasmus 
and  emaciation,  and  the  absence  of  wooden  dulness  over  an  extensive  tract, 
with  retraction  of  the  chest-walls,  will  suffice  to  make  a  diagnosis. 

Prognosis. — The  prognosis  is  always  unfavorable,  death  occurs  either 
from  local  or  general  causes  in  from  six  months  to  two  years. 

Treatment. — This  is  altogether  palliative,  and  is  restricted  to  the  relief  of 
symptoms. 

NOlS'-MALIGIfANT    GROWTHS    IN   THE    LUNGS. 

Non-malignant  growths  in  the  lungs  are  of  little  pathological  or  clinical 
interest. 

Sarcomatous  growths  starting  in  the  alveoli  or  in  the  inter- alveolar  septa 
are  always  secondary  ;  primary  sarcoma  of  the  bones  is  very  apt  to  be  fol- 
lowed by  secondary  pulmonary  sarcoma.  Melanotic  sarcoma  occurs  with 
extensive  pigmentation. 

Fibromata  occur  as  small  hard  masses  varying  in  size  from  that  of  a  pea 
to  that  of  a  hazel  nut.     They  rarely  occur  singly. 

Lipomata  are  usually  situated  beneath  the  pleura  in  the  form  of  slightly 
flattened  spherules. 

Enchondromata — usually  secondary  to  enchondromata  of  bones — are  met 
with  as  discrete,  irregularly  roundish  masses  sometimes  reaching  the  size  of 
an  egg  and  partly  or  wholly  calcified — at  times  densely  ossified. 

Osteomata  occur  in  lungs  which  are  the  seat  of  fibroid  pneumonia.  Vir- 
chow  describes  one  the  size  of  a  man's  fist.  They  are  usually  small  and 
multiple.  They  may  be  branched,  following  the  line  of  new  connective- 
tissue  developments. 

Simple  melanotic  tumors  in  the  lungs  are  similar  in  constitution,  both  to 
the  naked  eye  and  microscopically,  to  the  interstitial  pneumonia  of  miners, 
except  that  the  black  granules  are  small  and  round  instead  of  angular.  A 
melanotic  tumor  of  the  lung  may  invade  the  vertebral  column  in  such  a 
manner  as  to  destroy  the  bodies  of  one  or  more  of  the  vertebrae,  thus  giving 
rise  to  one  variety  of  Pott's  disease. 

Dermoid  cysts,  myxoma,  and  hematoma  are  very  rarely  met  with  in  the 
lungs ;  any  of  these  tumors  may  displace,  compress,  or  cause  atrophy  and 
absorption  of  lung-tissue  ;  they  may  cause  an  excess  of  air  in  one  part  of 
the  lung  and  a  deficiency  in  another ;  they  may  cause  congestion  or  anae- 


SYPHILITIC    DISEASE    OF   THE   LUNG.  143 

mia ;  may  ulcerate  and  form  cavities  ;  may  induce  acute  local  catarrhal 
pneumonia  or  fibroid  induration.  They  may  lead  to  bronchial  irritation, 
induce  pleurisy,  or  erode  adjacent  organs  or  bones.  The  general  symptoms 
of  non-malignant  tumors  within  the  lung  are  dyspnoea,  which  may  depend 
upon  pressure  on  the  heart  or  trachea  ;  aphonia  from  pressure  on  the  re- 
current laryngeal  nerve  ;  pain  from  pleurisy  or  pressure  ;  cyanosis  and 
dropsy  of  the  head,  neck  and  upper  extremity,  the  result  of  pressure  on  the 
veins  ;  and  changes  in  the  pulse  from  pressure  on  the  pneumogastric.  There 
may  be  dysphagia.  Cough  and  expectoration  come  from  pulmonary  hyper- 
semia  and  oedema. 

On  inspection  there  may  be  local  bulging  or  general  enlargejjient  of  the 
affected  side  with  diminished  respiratory  movements.  Vocal  fremitus  may 
be  increased,  or,  if  the  tumor  is  large  and  presses  on  a  large  bronchus,  it 
may  be  diminished  or  absent.  There  is  an  irregular  outline  of  dulness  over 
the  seat  of  the  tumor.  On  auscultation  there  may  be  bronchophony  and 
bronchial  breathing,  or  feeble  respiration  and  feeble  voice  sounds  over  the 
seat  of  the  tumor. 

Differential  Diagnosis. — Pleurisy,  phthisis  and  pneumonia  are  excluded 
very  readily  by  their  febrile  phenomena,  constitutional  symptoms  and  phys- 
ical signs.  The  prognosis  is  always  unfavorable,  and  the  treatment  is  wholly 
symptomatic. 

SYPHILITIC    DISEASE    OF   THE   LUJSTG. 

The  most  common  and  certain  changes  in  the  lungs  which  can  be  ascribed 
to  syphilis  are  gummata. 

Morbid  Anatomy. — They  vary  in  size  from  a  pea  to  an  egg,  and  are  single 
or  multiple  ;  they  appear  in  the  lungs  as  well-defined  rounded  tumors,  often 
surrounded  by  a  fibrous  capsule,  and  are  usually  situated  in  the  deeper  pul- 
monary structures.  Syphilitic  fibroid  infiltration  originating  about  the 
interlobular  blood-vessels,  about  gummata,  or  from  an  ulcerating  peri- 
bronchitis does  not  become  caseous,  but  may  ulcerate  or  become  gangre- 
nous. "  Syphilitic  pneumonia  of  the  neio-horn,''''  white  hepatization,  or 
''  epithelioma,''^  as  it  is  variously  called,  is  a  diffuse  infiltration  of  one  or  both 
lungs.  The  organ  is  heavy,  enlarged,  dense,  resistant  and  indented  by  the 
ribs.  White  dry  spots  are  seen  on  section.  There  is  thickening  of  the  alve- 
olar walls  and  minute  bronchi,  and  thickening  and  obliteration  of  the  pul- 
monary vessels.  Syphilitic  affection  of  the  bronchial  tubes  is,  in  such  cases, 
extensive.  Gummata  may  be  developed  in  the  nodules  of  syphilitic  pneu- 
monia. The  bronchial  glands  are  enlarged  and  often  cheesy.  Abscesses 
may  form  from  suppuration  in  gummatous  patches.  The  pleurae  may  show 
fibroid  thickening.  Senile  syphilitic  gummata  bear  a  close  resemblance  to 
caseous  tubercle,  but  are  much  less  friable — syphilitic  patients  often  become 
phthisical,  and  there  are  good  grounds  for  the  belief  that  the  phthisical 
developments  commence  in  a  proliferation  of  the  pulmonary  connective- 
tissue  which  terminates  in  the  formation  of  gummata,  and  thav,  these  gum- 
mata have  a  course  and  results  similar  to  those  of  tubercle. 

Symptoms. — The  symptoms  are  either  the  physical  signs  of  a  iumor^  or  of 


144  DISEASES    OF   THE    KESPIRATORY    ORGANS. 

interstitial  pneumonia.     The  diagnosis  is  reached  by  exclusion.     The  treaU 
ment  is  antisyphilitic. 

ATEOPHT    OF   THE   IMSiQ. 

This  may  be  general  or  partial. 

Morbid  Anatomy. — An  atrophied  lung  is  small,  dry,  anaemic,  and  some- 
what pigmented  ;  it  pits  readily  and  can  be  compressed  into  a  very  small 
space.  In  extreme  old  age  the  lungs  atrophy,  they  crepitate  less,  the  pleura 
over  them  is  less  moist  than  normal,  and  they  cannot  be  inflated  as  normal 
lungs  can.  They  lie  close  to  the  vertebral  column,  and  their  surface  is  un- 
even and  "crumpled  ;"  the  fissures  change  their  position  ;  the  lobes  may 
be  attached  to  one  another  by  pedicles  ;  the  alveoli  have  no  definite  form; 
and  the  cells  are  enlarged.  The  change  in  the  lobes  may  bring  the  apex 
down  to  the  base  of  the  thoracic  cavity.  Atrophied  lungs  are  "  marbled  " 
by  lines  and  dots.  The  pulmonary  artery  and  its  branches  are  diminished 
in  size,  and  the  bronchial  tubes  are  thinned.  The  first  step  toward  atrophy 
is  a  general  disappearance  of  the  capillaries  in  the  alveolar  septa.  Some 
fatty  degeneration  is  always  present.  "When  it  is  the  result  of  pressure  by 
tumors,  or  liquid  in  the  pleural  cavity,  the  atrophy  is  generally  limited  to 
one  lobe,  and  the  atrophied  part  presents  the  lesions  of  interstitial  pneu- 
monia. Pigmentation  and  atrophy,  whether  local  or  general,  are  usually 
associated.  It  is  commonly  best  marked  in  the  superior  lobes.  Sometimes 
the  lobes  appear  to  be  adherent  to  one  another.  The  right  heart  is  gen- 
erally found  in  a  condition  known  as  "brown  atrophy."  Bronchitis  nearly 
always  complicates  it.     The  diaphragm  is  thin,  flabby,  and  pale. 

Etiology. — Old  age,  pulmonary  emphysema,  and  general  marasmus  are 
frequent  causes  of  pulmonary  atrophy.  Pressure  of  a  tumor  or  fluid  ac- 
cumulation within  the  thoracic  cavity  may  induce  local  atrophy.' 

Symptoms. — Dyspnoea,  cyanosis,  and  oedema  and  coldness  of  the  extrem- 
ities are  its  only  constant  rational  signs. 

Inspection  reveals  a  small  thorax  ;  the  lower  ribs  are  approximated,  giv- 
ing a  "pigeon-breasted"  appearance.  The  whole  thorax  moves  as  if  it 
were  one  piece,  as  in  emphysema,  and  the  chest  movements  are  restricted. 

Percussion. — The  percussion  note  is  particularly  loud,  clear,  and  resonant ; 
but  the  pulmonary  area  is  less  than  normal.  The  extent  of  the  precordial 
dulness  is  increased. 

Auscultation. — The  respiratory  sounds  lose  their  vesicular  character  and 
are  feeble. 

Atrophy  of  the  lung  admits  of  no  treatment. 

HYDATIDS    OF    THE    LTJlSra. 

In  this  country  hydatids  of  the  lung  is  a  rare  disease.  There  is  usually 
one  tumor,  and  its  most  common  seat  is  the  lower  portion  of  the  right  lung. 

1  Buhl  (in  Virchow's  Archiv.,  Bd.  XI.,  p.  275)  describe?  an  atrophy  observed  by  him  in  three  cases  of 
typhus  fever  analogous  to  acute  yellow  atrophy  of  the  liver.  He  thinks  it  is  due  to  a  high  grade  of 
desauamative  pneumonia,  which  latter  disease  will  then  come  in  the  list  of  causes. 


HYDATIDS    OF   THE   LUISTG.  145 

Jlorbid  Anatomy. — The  cysts  vary  in  size  from  that  of  an  egg  to  that  of  a 
cocoa-nut.  They  are  usually  single,  but  may  be  multiple.  They  may  be 
situated  wholly  within  the  lung  or  be  an  outgrowth  from  the  liver  into  the 
pleural  cavity.  The  walls  of  the  cysts  vary  in  thickness  and  density.  They 
develop  in  the  interstitial  tissue  to  which  the  parent  sac  is  firmly  adherent. 
These  cysts  may  cause  serious  pulmonary  complications  by  their  pressure. 
They  may  suppurate  and  be  discharged  into  the  bronchi,  and  then  a  cavity 
may  remain.  In  many  cases  a  pulmonary  hydatid  cyst  is  the  result  of  an 
hydatid  of  the  liver  which  has  ruptured  through  the  diaphragm.  Some 
authorities  state  that  primary  hydatids  of  the  lung  is  a  condition  yet  to  be 
met  with.  General  pleurisy  is  of  rare  occurrence  ;  for  the  slow  growth  of 
the  tumor  excites  local  adhesions  rather  than  a  general  pleurisy.  In  some 
instances  an  hydatid  cyst  ruptures  into  the  pleural  cavity  and  causes 
empyema.  Bronchitis,  pneumonia,  and  gangrene  may  be  excited  in  the 
surrounding  tissue  by  the  pressure  of  the  hydatid  tumor. 

Etiology. — Hydatids  of  the  lung  are  nearly  always  secondary  to  hydatids 
of  the  liver.  The  affection  is  met  with  most  in  the  Norse  countries  of 
Europe,  where  men  and  animals  live  together. 

Symptoms. — Hydatids  of  the  lung,  when  small,  give  rise  to  no  symptoms 
by  which  they  can  be  detected  ;  but  as  they  enlarge 
they   excite   bronchitis,    attended   by   cough,   with        ^^^    «>      ►.    3) 
mnco-purulent  expectoration,  pain  in  the   chest,  a     J^^/      -^  f  0/1 
sense  of  suffocation,  haemoptysis,  night  sweats,  pallor     \/  */^ps^V ^^,*3^ 
and  emaciation.     When  blood  is  expectorated  goose-       l||»®<.  ^j^p^'^o^^J;? 
berry-like  skins  (the  sacs  of  echinococci)    or   hook-      -gJ^B.^.  1     a  ^  99^ 
lets  may  be  found  in  the  expectorated  matter.  Unless 
the  daughter-cysts,  or  booklets,  are  expectorated  the 
diagnosis  can  never  be  positive.      When  an  hydatid        ^_ 
attains  any  considerable  size  it  may  cause  bulging  Pi^  3L 

of  the  chest  wall  and  displace  the  mediastinum  and       Hydatids  of  the  Lung. 

diaphragm.      The    circumscribed    dulneSS   on  perCUS-    Microscopical   appearance  of 
.    ^        1-1  n   ,      ji  -11  1    p,       J.      1  elements  fofund  in  the  spiitum. 

sion,  which  may  extend  to  the  right  or  left  of  the  ^  EooicsfromneaaofTcBrAa 
median  line,  with  absence  of  respiratory  sound  and        EcMnococcus. 
vocal  fremitus  over  the  area  of  dulness,  is  a  strong  ^\EedZmTdis%.    x  250. 
evidence  of  pulmonary  hydatids. 

Differential  Diagnosis. — The  rupture  of  the  cyst  and  the  escape  of  its  con- 
tents into  a  bronchial  tube  are  its  only  diagnostic  features  and  will  prevent 
it  from  being  confounded  with  any  other  condition.  If  an  hydatid  is  super- 
ficial a  portion  of  the  fluid  may  be  withdrawn  by  aspiration,  and  a  micro- 
scopical examination  will  establish  the  diagnosis.  It  is  impossible  to  dis- 
tinguish between  hydatid  tumors  at  the  base  of  the  right  lung  and  those  in 
the  right  lobe  of  the  liver. 

Prognosis. — These  tumors  sometimes  disappear  by  spontaneous  retrogres- 
sion, or  by  discharge  into  a  bronchial  tube  ;  or  suppuration  may  be  estab- 
lished in  the  cysts  which  afterward  undergo  calcification.  Recovery  occurs. 
in  fifty  per  cent,  of  cases.  Earely  do  patients  die  from  emaciation  or  ma- 
rasmus. They  may  die  from  suffocation,  when  the  cysts  rupture  into  the 
10 


Oo^V 


146  DISEASES    OF   THE    EESPIRATORY    ORGANS. 

bronchi,  from  long-continued  suppuration,  or  from  an  empyema  established 
by  the  rupture  of  a  cyst  into  the  pleural  cavity.  Inilammation  of  any  of 
the  three  adjacent  serous  membranes  may  cause  death,  or  this  may  result 
from  extensive  hemorrhage  and  from  gangrene. 

Treatment. — They  should  be  treated  as  hydatids  of  the  liver.  It  is  a 
question  if  they  should  be  injected  with  iodine. 

PLEUKISY. 

Pleurisy  is  either  a  partial  or  general  inflammation  of  one  or  both  pleuraB. 
It  may  run  an  acute,  sub-acute,  or  chronic  course,  and  have  for  its  pro- 
ducts fibrin,  serum  and  fibrin,  serum,  fibrin  and  pus,  or  new  connective- 
tissue.  I  shall  describe  four  varieties  of  pleurisy : — (1)  Acute  or  Dry 
Pleurisy ;  (2)  Sul-acute  Pleurisy,  or  Pleurisy  luitli  Effusion ;  (3)  Sup- 
'pur alive   Pleurisy    or  Empyema;  and,  (4)  Adhesive  Pleurisy. 

ACUTE    PLEURISY. 

In  this  variety  the  symptoms  are  well  defined,  the  course  rapid,  and  the 
exudation  principally  fibrinous. 

Morbid  Anatomy. — The  first  stage  of  the  inflammatory  process  is  marked 
by  a  reddening  of  some  part  of  the  pleural  membrane  from  hypermaeia  of 
the  capillaries  of  the  serous  and  sub-serous  tissue  with  degeneration  of  the 
endothelial  cells.  The  pleura  loses  its  natural  glistening  appearance  on 
account  of  a  slight  fibrinous  exudation  and  the  swelling  and  increase  in 
number  of  its  fixed  connective-tissue  cells.  These  changes  take  place  dur- 
ing the  first  forty-eight  hours.  Following  this,  the  fibrinous  exudation 
increases  and  \\\q  free  surface  of  the  pleura  assumes  a  rough,  shaggy  ap- 
pearance. If  any  serum  exudes  it  gravitates  to  the  most  dependent  por- 
tions of  the  pleural  sac.  In  the  substance  of  the  pleura  and  in  the  fibrinous 
exudation  new  cells  are  now  found  which  are  young  connective-tissue  or 
pus  cells.  These  cells  are  at  first  more  numerous  on  the  inner  surface  of 
the  pleura.  As  the  inflammation  progresses  they  increase  in  number 
and  collect  on  the  free  surface  of  the  pleura  under  the  fibrinous  exudation. 
By  the  fifth  day  of  the  pleurisy  new  blood-vessels  are  formed  in  the  fibri- 
nous exudation  and  become  connected  with  the  original  vessels  of  the  pleura. 

The  nature  of  the  subsequent  changes  will  depend  upon  the  intensity  of 
-the  inflammatory  process  ;  in  the  milder  types  the  fibrin  gradually  dimin- 
ishes and  disappears,  some  of  the  cells  become  fatty  and  are  absorbed,  and 
the  remainder  enter  into  the  formation  of  a  basement  substance  which  grad- 
ually increases  and  finally  a  permanent  new  connective-tissue  forms  upon 
the  inner  surface  of  the  pleura.  If  the  inflammatory  process  subsides  with- 
lout  much  serous  effusion,  the  opposing  surfaces  of  the  pulmonary  and  costal 
-j)leur8e  come  into  contact  and  adhesions  are  formed  between  them  composed 
of  permanent  connective-tissue  containing  long,  slender  vessels.  These 
adhesions  follow  the  general  law  that  governs  all  new  connective-tissue  : 
they  may  be  permanent,  or — ^their  blood  supply  becoming  insufficient — 


ACUTE   PLEURISY. 


147 


they  may  undergo  fatty  degeneration  and  be  absorbed,  the  thickened  pleura 
alone  remaining  to  tell  of  the  past  inflammation.  When  an  individual  has 
once  had  this  form  of  pleurisy  he  will  always  have  a  permanent  lesion. 
This  pathological  process  may  be  completed  in  two  weeks,  or  the  sero-fibri- 
nous  effusion  may  not  be  absorbed  for  months,  and  then  the  pleuritic  thick- 
ening becomes  very  extensive. 

Etiology. — The  etiology  of  acute  pleurisy  is  sometimes  very  obscure.  Ex- 
posure to  wet  and  cold  has  been  regarded  as  one  of  its  most  frequent  causes, 
but  it  is  very  doubtful  if  it  ever  occurs  as  the  result  of  simple  exposure  to  wet 
and  cold.  In  all  cases  that  have  come  under  my  observation  where  it  has  fol- 
lowed such  exposure,  I  have  been  able  to  find  some  previously  existing  predis- 
posing cause.  It  may  be  the  result  of  a  penetrating  wound,  or  blows  upon 
the  chest  walls.  Fracture  of  the  ribs,  if  the  broken  ends  of  the  ribs  pene- 
trate the  pleura,  may  cause  it.  It  is  often  a  complication  of  other  diseases, 
such  as  pyaemia,  the  exanthematous  fevers,  acute  and  chronic  alcoholismus, 
acute  rheumatism,  Bright's  disease,  pneumonia,  etc.  Sometimes  it  is  the 
result  of  extension  of  inflammation  from  adjacent  organs  and  tissues.  There 
is  a  strong  predisposition  to  it  in  some  individuals,  and  one  attack  predis- 
poses to  another.  It  may  occur  at  any  age.  Although  it  has  been  claimed 
that  it  never  occurs  in  young  children,  my  experience  leads  me  to  believe 
that  it  is  of  quite  frequent  occurrence  in  children  of  two  or  three  years  of 
age,  and  pus  is  usually  formed  in  the  pleurisies  of  children  which  occur 
as  complications  or  sequelae  of  the  exanthematous  fevers.  Whenever  acute 
pleurisy  occurs  on  the  right  side  it  is  important  to  determine  if  it  is,  or  is 
not,  the  result  of  an  extension  of  inflammation  from  the  liver. 

Symptoms, — Acute  pleurisy  may  be  mild  or  severe ;  in  either  case  it  is 
ushered  in  by  well-marked  symptoms.  The  most  prominent  and  constant 
at  its  onset  is  a  sharp  stitch-like  pain  in  some  portion  of  the  chest ;  it  usu- 
ally is  referred  to  the  nipple  of 
the  affected  side.  Each  inspira- 
tion increases  its  severity.  The 
patient,  to  prevent  motion  of 
the  affected  side,  assumes  a  pe- 
culiar position,  leaning  forward 
and  toward  that  side.  At  first 
the  countenance  is  pale  and 
anxious ;  after  a  few  hours  it 
becomes  flushed.  The  pulse  is 
accelerated,  beating  from  90  to 
120  per  minute ;  it  is  firm, 
small  and  tense  in  character — 
in  this  respect  differing  from 
the  pulse  of  all  other  pulmonary 
diseases.  The  respiration  is 
hurried  and  difficult ;  each  in- 
spiration is  jerking  in  character;  as  soon  as  the  general  symptoms  of 
pyrexia  are  present,  the  pain,  in  most  cases,  diminishes — in  a  small  pro- 


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Fig.  32. 

Temperature  in  a  case  of  Acute  Pleurisy.  Patient  set.  24. 
Recovery. 


148 


DISEASES   OF   THE   KESPIEATORY   ORGAN'S. 


portion  of  cases  it  maintains  its  intensity  throughout  the  attack.  The 
temperature  follows  no  regular  course  and  has  no  fixed  relation  to  the  pulse 
or  respiration  ;  in  ordinary  cases  it  rarely  rises  above  100°  F. ;  in  very  severe 
cases  it  may  reach  104°  F.  There  is  a  short,  dry,  tearing  cough,  which 
is  very  distressing  ;  the  patient  restrains  it  as  much  as  possible  on  account 
of  the  intense  pain  which  it  produces.  In  very  severe  cases  of  acute  pleurisy, 
where  the  fibrinous  exudation  is  very  abundant  and  takes  place  rapidly, 
causing  compression  of  the  lung,  the  primary  symptoms  are  very  violent, 
resembling  those  of  pneumonia.  A  distinct  chill  is  followed  by  high 
fever,  the  temperature  often  reaching  105°  F.  The  countenance  assumes 
an  anxious  expression,  the  pulse  beats  120  per  minute  and  is  feeble,  but  the 
pain  in  the  side  is  not  so  severe  as  in  the  milder  cases.  Under  these  circum- 
stances, at  the  onset  of  tiie  attack  it  is  difficult  to  distinguish  it  from  croup- 
ous pneumonia.  Such  severe  cases  are  rare  ;  when  they  do  occur  they  are  apt 
to  prove  fatal.  There  are  occasionally  very  mild  cases  of  acute  pleurisy  which 
are  attended  by  few  of  the  subjective  symptoms  of  pleurisy  :  the  febrile  move- 
ment is  slight,  the  pain  in  the  side  is  not  severe,  and  cough  and  dyspnoea  may 
be  entirely  absent.  These  patients  continue  their  ordinary  occupations,  com- 
plaining only  of  an  uneasy  sensation  in  the  side,  and  the  disease  would 
pass  unrecognized  but  for  the  physical  signs.  Although  the  rational  symp- 
toms of  acute  pleurisy  may  vary  in  different  cases  and  in  some  be  very 
obscure,  the  physical  signs  at  once  dispel  all  doubts. 

Physical  Signs. — During  the  first  twenty-four  hours  of  acute  pleurisy, 
inspection  will  show  the  movements  of  the  chest  wall  on  the  affected  side 
to  be  more  or  less  restricted.  Palpation,  percussion,  and  mensuration  will 
give  negative  results.  On  auscultation  the  respiratory  murmur  will  be 
found  feeble  over  the  affected  side,  and  jerking  in  character  both  on  in- 
spiration and  expiration,  and  a  grazing  friction  sound  will  be  heard  ;  this 

friction  sound  will  be  most  intense 
at  the  end  of  inspiration. 

As  the  plastic  exudation  takes  place 
inspection  will  show  a  greater  loss  of 
expansive  motion  on  the  affected 
side ;  and  on  palpation  there  will  be  a 
diminution  of  the  vocal  fremitus  over 
its  seat.  On  percussion  there  will 
be  slight  dulness  over  the  seat  of  the 
pleurisy.  The  amount  and  extent  of 
the  dulness  will  correspond  to  the 
amount  of  the  plastic  exudation. 
Upon  auscultation  the  respiratory 
murmur  will  be  distant  and  feeble 
or  entirely  absent,  and  a  crepitating 
Fig.  33.  frictiou  souud  will  be  heard  both  with 

Diagram  illustrating  Physical  Signs  in  Acute  Pleu-  :„„„,-„„4-,-p.^     ^f.A     pxr>irfltion  *       it     is 
risy  with  a  small  amount  of  EfEusion.    Alter  Da  ^^^P^^^*^^""     '''""      t;.spUciLiuu  ,       iu     lo 

tJosta.  usually  most  intense  with  inspiration  ; 

this  sound  sometimes  very  closely  resembles  the  so-called  crepitant  rale  and 


Normal  respiratory  soundi 


Crepitating  friction 
sounds 

Eespiratory  mnr- 
7iiur  feeble  or 
absent 

Flatness  on  percus- 
sion   

Absent  vocal  fre- 
mitus   

Absent  voice 


ACUTE  PLEURISY.  149 

may  be  mistalien  for  it.  At  times  this  sound  loses  its  crepitant  character 
and  becomes  rubbing  and  sticky ;  it  is  always  due  to  the  rubbing  together 
of  the  two  roughened  pleural  surfaces.  Often  it  will  not  be  heard  unless 
the  patient  cough  or  take  a  deep  inspiration.  If  the  pleurisy  is  confined 
to  the  diaphragmatic  or  mediastinal  pleura  the  friction  sound  will  not 
be  heard. 

If  a  considerable  fluid  effusion  accompany  the  plastic  exudation,  the 
expansive  movements  on  the  affected  side  will  be  more  restricted,  and 
the  vocal  fremitus  at  the  bottom  of  the  pleural  cavity  will  be  markedly 
diminished.  Upon  'percussion  there  will  be  flatness  over  the  region  occu- 
pied by  the  fluid.  It  is  difficult,  however,  to  recognize  the  presence  of 
a  small  amount  of  fluid  effusion,  for  the  level  of  the  fluid  is  not  appre- 
ciably changed  by  changing  the  position  of  the  patient.  On  auscultation 
the  respiratory  sounds  will  be  absent  below  the  level  of  the  fluid,  and 
feeble  above  it ;  and  both  respiratory  acts  will  be  accompanied  by  the 
friction  sound. 

During  the  period  of  absorption  of  the  fluid  and  plastic  exudation  there 
will  be  a  gradual  return  of  the  pulmonary  resonance  and  of  the  normal, 
vocal,  and  respiratory  sounds,  and  as  the  roughened  pleural  surfaces  play 
upon  each  other,  the  friction  sound  will  assume  more  of  a  rubbing  char- 
acter. In  some  instances  the  friction  sounds  remain  audible  for  a  long 
time  after  the  disappearance  of  all  the  other  signs  of  pleurisy.  Retraction 
of  the  affected  side  does  not  follow  acute  pleurisy  except  in  rare  instances, 
when  the  inflammation  has  been  very  severe  and  a  large  plastic  effusion 
has  taken  place.  In  those  having  extensive  plastic  exudations  in  acute 
pleurisy  which  compress  the  lung,  the  respiratory  sound  may  assume  a 
bronchial  character  and  be  mistaken  for  that  of  a  pneumonic  condition. 

Differential  Diagnosis. — In  the  majority  of  cases  the  diagnosis  of  acute 
pleurisy  is  easily  made.  Acute  ^pneumonia  is  the  only  disease  with  which 
it  is  liable  to  be  confounded.  In  both  affections  there  are  dyspnoea,  fever, 
and  cough ;  but  in  pleurisy  the  temperature  rarely  rises  above  100°  F., 
while  in  pneumonia  it  usually  reaches  103°  F.  within  the  first  twenty-four 
hours.  The  cough  of  pleurisy  is  short  and  hacking,  and  is  attended  by 
little  or  no  expectoration,  whereas  in  nearly  every  case  of  pneumonia  expec- 
toration is  present,  and  the  substance  expectorated  is  characteristic  of  the 
pneumonia.  The  countenance  at  the  onset  of  pleurisy  is  pale  and  anxious  ; 
in  pneumonia  it  is  flushed  and  the  cheeks  have  a  purple  hue.  There  is  also 
a  very  marked  difference  in  the  physical  signs  of  the  two  diseases.  In  pleu- 
risy the  vocal  fremitus  over  the  affected  portion  of  the  pleura  is  somewhat 
diminished ;  in  pneumonia  it  is  more  or  less  increased.  In  pleurisy  the 
respiration  is  feeble  ;  in  pneumonia  it  is  rude  or  bronchial.  In  pleurisy  a 
grazing,  rubbing,  or  crepitating  friction  sound  is  heard  with  both  respira- 
tory acts.  In  pneumonia  the  crepitant  rale  is  heard  at  the  end  of  inspira- 
tion. Sometimes  it  is  difficult  to  distinguish  a  crepitating  friction  sound 
from  a  sub-crepitant  rale,  but,  as  the  sub-crepitant  rale  is  not  present  until 
the  last  stage  of  pneumonia,  the  question  will  not  arise  if  the  patient  is  seen 
before  that  period  has  arrived. 


150  DISEASES   OF   THE    RESPIEATOEY   ORGANS. 

Occasionally  it  is  difficult  to  make  a  differential  diagnosis  between  inter- 
costal neuralgia  or  pleurodynia,  and  acute  pleurisy.  Intercostal  neuralgia 
or  pleurodynia  may  be  attended  by  many  of  the  ushering-in  symptoms  of 
acute  pleurisy.  They  may  come  on  after  exposure,  be  attended  by  violent 
pain  in  the  side,  jerking  respirations,  anxious  countenance,  and  often  by 
considerable  fever.  On  physical  examination  the  respiration  may  be  as 
feeble  as  in  the  first  stage  of  pleurisy.  The  presence  or  absence  of  a  pleuritic 
friction  sound,  and  the  painful  points  on  pressure,  are  the  principal  points 
of  difference. 

Prognosis. — The  prognosis  in  acute  pleurisy  is  generally  good.  Its  natu- 
ral termination  is  in  recovery  within  two  or  three  weeks  after  its  commence- 
ment. But  it  is  to  be  remembered  that  patients  even  with  the  milder  form 
of  the  disease  are  liable  to  have  frequent  pleuritic  thickenings  and  adhesions 
between  the  pulmonary  and  costal  pleurae.  These  thickenings  predispose 
to  other  attacks  of  pleurisy,  and  each  new  attack  interferes  more  and  more 
with  the  expansion  of  the  lungs  and  leads  to  the  development  of  intersti- 
tial pneumonia  or  bronchitis,  and  finally  to  fibrous  phthisis.  If  this  form 
of  pleurisy  complicates  any  grave  form  of  disease,  as  septicaemia,  pyaemia, 
Bright's  disease,  etc.,  there  is  a  liability  to  acute  empyema.  In  some  very 
acute  cases,  where  there  is  a  large  plastic  exudation,  death  may  result  in  a 
few  days. 

Treatment. — The  only  remedial  agent  which  has  seemed  to  me  to  have  a 
controlling  power  over  acute  pleurisy  is  opium.  The  best  method  of  admin- 
istering it  is  by  the  hypodermic  injection  of  morphine.  It  has  been  claimed 
that  free  blood-letting  at  the  commencement  of  an  acute  pleurisy  will  arrest 
its  progress.  But  the  facts  deduced  from  recorded  cases  are  strongly  against 
this  statement.  A  free  general  bleeding  will  undoubtedly  relieve  the  pleu- 
ritic pain  with  great  promptitude,  but  no  more  so  than  a  hypodermic  of 
morphine,  and  the  morphine  does  not  increase  the  liability  to  a  large  seroua 
effusion,  as  does  general  bleeding.  For  the  successful  management  of 
ordinary  acute  pleurisy  all  that  I  have  found  necessary  is  to  place  the 
patient  in  bed.  This  is  important,  however  mild  the  attack  may  be.  The 
sick  room  should  be  well  ventilated  and  kept  at  an  even  temperature  of  about 
65°  F.  The  patient  should  be  allowed  to  assume  that  position  in  bed  which 
he  finds  most  comfortable.  He  should  be  forbidden  to  talk,  and  should  be 
prevented  from  making  any  unnecessary  movements,  and  a  nutritious  diet 
without  stimulants  should  be  given  him.  If  he  is  robust,  three  or  four 
leeches  may  be  applied  over  the  seat  of  pain,  and  followed  by  an  anodyne 
poultice.  Hypodermics  of  morphine  must  be  given  in  sufficient  quantities 
to  relieve  all  pain.  After  the  first  week  the  morphine  can  usually  be  dis- 
continued and  the  patient  will  be  able  to  sit  up,  and,  at  the  end  of  three 
weeks,  to  resume  his  ordinary  occupation  unless  it  requires  great  physical 
exertion.  If  there  is  an  abundant  plastic  or  serous  exudation  the  convales- 
cence will  be  reached  more  slowly  and  the  recovery  will  be  less  complete. 
In  such  cases  there  will  be  some  crippling  of  the  lung,  and  pain  and  uneasi- 
ness in  the  affected  side  will  continue  for  months.  After  recovery  it  is  well 
to  inform  the  patient  that  he  may  expect  pain  after  active  physical  exer- 
cise.    If  the  patient  presents  the  signs  of  anasmia,  the  syrup  of  the  iodide 


SUB-ACUTE    PLEURISY.  151 

of  iron  should  be  given  in  teaspoonful  doses  three  or  four  times  each  day. 
Stimulants  should  rarely  be  allowed  before  the  third  week.  Counter-irri- 
tants by  means  of  cups  and  blisters,  are  rarely  of  service  in  the  treatment  of 
this  form  of  pleurisy.  I  have  found  in  some  cases,  when  the  pain  in  the 
side  continued  after  the  friction  sound  had  disappeared,  that  the  use  of  the 
constant  current  over  the  affected  side  for  twenty  minutes  at  a  time,  gives 
almost  instantaneous  relief. 

SUB-ACUTE    PLEURISY. 

{Pleurisy  with  Effusion.) 

This  is  the  most  common  form  of  pleurisy,  and  the  inflammatory  proc- 
ess usually  invades  the  whole  of  the  pleura  on  the  side  affected.  It  may 
commence  at  any  point  on  the  pleural  surface,  but  it  most  frequently  com- 
mences on  the  costal  portion. 

Morbid  Anatomy. — The  anatomical  changes  in  this  form  are  similar 
to  those  which  take  place  in  acute  pleurisy,  except  that  the  new  tissue 
formations  are  more  extensive,  the  pleural  membrane  more  uniformly 
thickened,  and  there  is  more  abundant  serous  effusion  containing  flocculi  of 
lymph.  The  pleural  cavity  may  be  partly  or  completely  filled  with  fluid. 
The  entire  pleura  becomes  coated  with  a  layer  of  fibrin  varying  in  thick- 
ness, usually  most  abundant  on  its  costal  portion.  New  connective-tissue 
cells  and  basement  substance  are  mingled  with  the  exudation.  Sometimes 
the  serous  effusion  contains  blood  globules  from  the  rupture  of  the  thin- 
walled  vessels  in  the  new  connective-tissue.  It  is  the  large  amount  of 
serous  effusion,  containing  more  or  less  cellular  elements,  that  distinguishes 
sub-acute  from  acute  pleurisy.  This  indicates  a  difference  in  the  grade 
rather  than  in  the  nature  of  the  inflammatory  process.  When  the  cell  ele- 
ments are  abundant  it  is  characterized  as  a  sero-purulent  effusion.  If  the 
pleural  cavity  is  not  filled  with  fluid,  the  effusion  will  occupy  the  most 
dependent  portion  of  the  pleural  cavity.  It  may  be  confined  to  circum- 
scribed portions  of  the  pleural  cavity  by  adhesions.  If  it  occupy  the  most 
depending  portion  of  the  cavity  the  adjacent  lung-tissue  will  be  compressed 
and  pushed  upward.  When  the  pleural  cavity  is  filled  with  fluid  the  in- 
tercostal spaces  will  be  more  or  less  bulging,  the  diaphragm  will  be  pushed 
downward,  and  the  abdominal  viscera  upon  either  side  may  be  displaced 
downward  ;  the  heart  will  be  displaced  either  to  the  right  or  left,  accord- 
ing as  the  fluid  occupies  the  left  or  right  pleural  cavity.  The  lung  on  the 
affected  side  is  compressed  either  toward  the  vertebral  column  or  upward 
and  inward  against  the  mediastinum.  Occasionally  the  lung  occupies 
the  anterior  portion  of  the  pleural  cavity  and  the  fluid  the  posterior 
portion ;  the  direction  of  the  compression  is  influenced  by  the  location 
and  extent  of  previous  pleuritic  adhesions.  If  no  adhesions  exist  the 
lung  may  be  compressed  to  one-eighth  of  its  normal  size,  and  assume  a 
pale-red  or  greenish  color,  have  a  tough,  leathery  feel,  and  be  entirely 
void  of  air.  With  the  compression  of  the  lung  there  may  be  compression 
of  the  bronchi,  but  the  larger  bronchial  tubes  usually  remain  pervious. 

If  recovery  takes  place  the  fluid  disappears  by  absorption,   the  fibrin 


152  DISEASES   OF   THE   RESPIRATORY    ORGANS. 

undergoes  fatty  metamorphosis,  liquefies,  and  slowly  disappears.  As  the 
fluid  disappears  the  thickened  pleural  surfaces  come  in  contact,  and  more 
or  less  extensive  adhesions  form  between  the  two  surfaces.  On  account  of 
the  changes  which  take  place  in  the  pulmonary  pleura  the  lung-tissue  does 
not  expand  to  its  normal  dimensions,  but  more  or  less  retraction  of  the 
chest  walls  on  the  affected  side  takes  place.  The  longer  the  fluid  remams 
in  the  pleural  cavity  the  more  extensive  will  be  the  retraction.  As  the 
fluid  disappears,  the  orgafls  which  have  been  displaced  by  its  pressure  re- 
turn to  their  normal  positions.  If  the  retraction  is  considerable  they  will 
be  displaced  upward,  and  the  heart  may  be  drawn  from  its  normal  position 
to  the  right  or  left. 

Etiology. — The  causes  of  this  form  of  pleurisy  may  be  the  same  as  those 
of  acute  pleurisy.  In  a  large  proportion  of  cases  it  is  secondary  to  some 
form  of  organic  disease,  as  chronic  Bright's  disease  of  the  kidneys,  pulmo- 
nary phthisis,  etc.  Occasionally  it  seems  to  occur  idiopathically,  or  at  least 
from  causes  not  well  understood.  It  is  a  clinical  fact  familiar  to  every 
careful  observer  that  sub-acute  pleurisy  is  not  infrequently  the  first  step 
to  the  development  of  phthisis.  The  pathological  relations  between  these 
two  diseases  are  exceedingly  interesting,  but  not  at  all  times  ajiparent.  The 
weak  and  enfeebled,  rather  than  the  strong  and  robust,  are  liable  to  attacks 
of  sub-acute  pleurisy. 

Symptoms. — This  form  of  pleurisy  may  come  on  suddenly  with  active 
symptoms,  or  insidiously  with  very  mild  symptoms.  In  the  majority  of 
cases  the  symptoms  are  mild.  There  is  no  chill  of  invasion  ;  it  comes  on 
insidiously  after  exposure  to  wet,  cold,  and  fatigue,  in  the  enfeebled  or  in 
those  who  are  suffering  from  some  chronic  disease.  It  is  rarely  attended 
by  any  noticeable  pain  in  the  side,  or  at  least  not  by  the  severe  pain  which 
attends  acute  pleurisy.  On  close  questioning  the  patient  will  state  that 
some  time  before  exposure  an  uneasy  sensation  in  the  affected  side,  attended 
occasionally  by  a  sharp  pain  of  short  duration,  was  experienced.  This 
form  of  pleurisy  is  often  so  insidious  in  its  approach  that  the  patient  will 
be  unable  to  tell  when  he  commenced  to  be  sick  ;  for  a  period  of  several 
weeks  he  will  have  gradually  lost  flesh  and  strength,  yet  will  have  been 
able  to  attend  to  his  ordinary  avocations  if  they  required  but  little  physi- 
cal exertion.  There  will  be  slight  dyspnoea  on  exertion,  with  slight  febrile 
excitement  at  night.  Sometimes  there  is  an  almost  continual  cough  with 
a  scanty  muco-purulent  expectoration  ;  at  other  times  the  cough  will  be 
entirely  absent.  Usually  when  this  class  of  patients  consult  a  physician 
the  only  subjective  symptoms  will  be  a  frequent,  small,  feeble  pulse,  and 
slight  heat  and  dryness  of  the  skin,  the  temperature  rarely  rising  above 
101°  F.  The  countenance  will  be  pale  and  anxious,  and  the  breathing  short 
and  catching  in  character.  On  speaking,  especially  after  exercise,  the  sen- 
tences are  uttered  in  a  broken,  interrupted  manner.  The  patient  will  be  un- 
able to  lie  comfortably  except  on  his  back,  or  on  the  affected  side  with  his 
head  slightly  elevated.  The  pulse,  usually  small  and  feeble,  will  vary  from 
110  to  120  beats  in  the  minute  ;  in  fact,  there  will  be  no  subjective  symptom 
which  will  enable  one  to  reach  a  positive  diagnosis. 

In  those  cases  which  are  ushered  in  by  active  symptoms  the  invasion  wiU 


SUB-ACUTE    PLEURISY.  153 

resemble  that  of  acute  pleurisy.  There  will  be  rigors  followed  by  a  tem- 
perature of  102°  or  103°  F. ;  the  joulse  will  be  full  and  frequent,  the  pain 
on  the  affected  side  well  marked  and  the  breathing  rapid  and  shallow. 
Patients  will  sometimes  ascribe  the  pain  to  the  lumbar  I'egion,  as  in  ne- 
phritic colic,  for  which  it  is  sometimes  mistaken.  After  a  few  days  the  fe- 
brile symptoms  abate,  but  do  not  entirely  subside,  and  the  serous  effusion, 
which  is  much  larger  than  that  in  acute  pleurisy,  for  a  time  steadily  in- 
creases, then  remains  stationary  for  a  number  of  days  or  even  weeks,  and 
then  there  is  a  sudden  renewal  of  the  febrile  symptoms,  the  dyspnoea  is 
greatly  increased,  the  cough  becomes  more  constant  and  harassing,  the  pa- 
tient is  unable  to  lie  down,  and  the  fluid  rapidly  increases  ;  in  twenty-four 
hours  the  pleural  cavity, — which  previously  has  been  only  half  full  of 
fluid, — becomes  entirely  filled,  and  the  dyspnoea  becomes  so  urgent,  and 
the  danger  from  collateral  congestion  and  oedema  of  the  opposite  lung  so 
imminent,  that  immediate  relief  is  demanded  by  paracentesis.  With  the 
rapid  increase  of  the  effusion  the  pain  in  the  side  subsides.  However  ill- 
defined  the  rational  symptoms  may  be  in  acute  pleurisy,  its  physical  signs 
are  more  distinctive  than  in  any  other  thoracic  disease. 

Physical  Signs. — The  physical  signs  of  pleurisy  with  effusion  will  vary  with 
the  amount  of  the  fluid  effusion.  At  its  onset,  before  there  is  much  fluid 
effusion,  a  friction  sound  will  be  heard  over  the -affected  side  with  more  or 
less  feebleness  of  the  respiratory  sound.  After  the  pleural  cavity  partly  fills 
with  fluid,  the  vocal  fremitus  will  be  diminished  cr  absent  at  the  bottom 
of  the  pleural  sac  below  the  level  of  the  fluid  ;  there  will  be  flatness  on  per- 
cussion, and  an  absence  of  vocal  and  respiratory  sounds.  A  change  in  the 
position  of  the  patient  will  change  the  level  of  the  fluid  and  the  line  of 
flatness.  Above  the  level  of  the  fluid  the  percussion  resonance  will  be  nor- 
mal or  exaggerated,  and  in  some  cases  tympanitic  in  quality.  The  respira- 
tory murmur  will  be  exaggerated,  and  at  the  level  of  the  fluid  it  may  as- 
sume a  bronchial  character.  The  vocal  sounds  may  be  intensified,  or  a 
distinct  bronchial  voice  may  be  heard.  All  of  these  physical  signs  are 
most  marked  posteriorly. 

When  the  pleural  cavity  is  completely  filled  with  fluid,  and  the  lung  is 
compressed  backward  against  the  spinal  column,  important  modifications 
in  the  physical  signs  take  place. 

Inspection  will  show  an  enlargement  of  the  affected  side,  and  a  bulging 
of  the  intercostal  spaces.  The  respiratory  movements  on  the  affected  side 
will  be  changed  from  an  up-and-out  movement  to  a  direct  up-and-down 
motion,  while  on  the  unaffected  side  the  expansive  respiratory  movements 
are  increased.  If  the  effusion  is  in  the  left  pleural  cavity  the  heart  will  be 
displaced  to  the  right,  and  the  apex  beat  may  be  noticed  under  the  right 
nipple  ;  if  it  occupies  the  right  pleural  cavity  the  apex  beat  will  be  carried 
to  the  left,  beyond  its  normal  position. 

The  circumference  of  the  affected  side  at  the  end  of  expiration,  will  be 
one  or  two  inches  greater  than  that  of  the  healthy  side  ;  but  at  the  end  of 
inspiration  the  difference  will  be  but  slight.  The  expansive  motion  in  in- 
spiration on  the  healthy  side  may  be  two  or  three  inches  greater  than  on 
the  affected  side. 


154 


DISEASES   OF   THE    RESPIRATORY    ORGANS. 


On  palpation  there  is  usually  complete  absence  of  vocal  fremitus  over  the 
affected  side.  There  are  a  few  cases,  however,  in  which  the  vocal  fremitus 
persists  even  when  the  cavity  is  filled  with  fluid. 

Upon  percussion  there  will  be  flatness  over  the  whole  of  the  affected  side, 
and  the  flatness  will  extend  below  the  normal  limits  of  the  lung. 

On  auscultation  there  is  usually  entire  absence  of  the  respiratory  sounds 
over  the  affected  side,  and  the  vocal  sounds  will  be  distant  and  indistinct. 
Not  infrequently,  however,  at  the  upper  and  posterior  portion  of  the 
pleural  cavity  distant  bronchial  respiration  and  bronchophony  will  be  heard. 
The  bronchial  respiration  and  the  bronchial  voice  are  sometimes  diffused 
and  heard  over  the  whole  of  the  posterior  portion  of  the  affected  side. 

As  the  fluid  subsides  in  the  pleural  cavity,  inspection  shows  that  the  en- 
largement of  the  affected  side  is  decreasing,  that  the  intercostal  spaces 
are  regaining  their  normal  condition,  and  that  the  respiratory  movements 
are  returning.  Mensuration  shows  a  gradual  diminution  in  the  size  of  the 
affected  side  until  it  becomes  smaller  than  the  other.  On  percussion  the 
pulmonary  resonance  will  gradually  return,  first  at  the  upper  portion  of  the 
pleural  cavity ;  but  it  is  not  completely  restored  until  some  time  aftei* 
the  fluid  has  disappeared,  especially  over  the  lower  portions  of  the  pleural 
cavity. 

On  auscultation,  as  the  fluid  disappears,  the  vocal  and  respiratory  sounds 
will  gradually  return.  At  first,  the  respiratory  sounds  are  feeble  and  dis- 
tant ;  gradually  they  become  more  and  more  distinct.  As  the  two  rough- 
ened pleural  surfaces  come  in  contact  and  move  on  each  other,  a  creaking. 


Absent  respiratory  motion 


Diminished  or  absent  vocal  fremitus 


Flatness  on  percussion. 


Absence  of  respiratory  murmur  in 
front,  bronchial  breathing  behind. 


Vocal  sounds  distant  or  absent 


Fig.  34. 
Diagram  showing  Physical  Signs  in  Pleurisy  with  EfEusion  ;  pleural  cavity  filled  with  fluid. 

rubbing,  friction  sound  is  heard.  These  rubbing  friction  sounds  are  often 
audible  for  months  after  the  fluid  has  disappeared.  If,  as  sometimes  hap- 
pens, the  lower  portion  of  the  affected  lung  remains  permanently  imper- 
vious to  air,  the  upper  portion  of  the  lung  becomes  emphysematous.  Un- 
der such  circumstances  the  emphysema  is  compensatory,  and  the  percussion 


SUB-ACUTE    PLEURISY.  155 

note  in  the  infra-clavicular  space  on  that  side  will  have  a  tympanitic 
quality,  and  the  expiration  in  this  space  will  become  prolonged,  harsh,  and 
blowing  in  character. 

Differential  Diagnosis. — The  diagnosis  in  uncomplicated  cases  of  sub- 
acute pleurisy  is  usually  very  readily  made.  The  diseases  with  which  it  is 
most  likely  to  be  confounded  are  pneumonic  or  phtldsical  consolidation  of 
the  lung,  enlargement  of  the  liver  or  spleen,  cancer  of  the  lung  and  i^leura, 
and  intra-thoracic  tumors.  It  is  hardly  possible  for  a  thoracic  aneurism 
to  be  developed  in  such  a  manner  as  to  be  mistaken  for  sub-acute  pleurisv. 
Pleurisy  with  effusion  may  be  distinguished  from  phthisical  and  pneu- 
monic consolidation  by  the  history  of  the  case,  by  the  absence  of  the  charac- 
teristic expectoration,  and  by  the  lower  range  of  temperature.  Upon  phys- 
ical examination  it  may  be  distinguished  by  the  enlargement  or  retraction 
of  the  affected  side,  by  the  diminution  or  absence  of  vocal  fremitus,  and  by 
the  flat  note  of  the  percussion  sound.  If  the  cavity  is  partly  filled,  by 
the  change  in  the  line  of  flatness  on  change  in  the  position  of  the  patient, 
and  by  the  feeble  or  absent  respiratory  sounds  over  the  fluid.  The  bron- 
chial respiration  which  is  sometimes  heard  over  a  pleural  cavity  filled  with 
fluid  differs  from  the  bronchial  respiration  of  pneumonic  or  phthisical  con- 
solidation, in  that  it  is  more  diffused  and  less  tubular  in  quality.  In 
phthisical  consolidation  the  progress  of  the  physical  signs  is  usually  from 
above  downward ;  in  pleuritic  effusion  they  advance  from  below  upward. 
Phthisis  of  an  entire  lung  rarely  exists  without  the  other  lung  being  in- 
volved, while  any  amount  of  pleuritic  effusion  may  exist  in  one  cavity,  and 
the  other  remain  unaffected.  If  doubt  exists  after  considering  all  these 
points  of  difference,  it  may  be  removed  by  the  use  of  an  exploring 
trochar. 

Serous  effusion  into  the  right  pleural  cavity  is  distinguished  from  an 
enlargement  of  the  liver  upward,  by  the  fact  that  when  percussion  is  made, 
the  patient  being  in  a  sitting  posture,  the  line  of  flatness  in  liver  enlarge- 
ments is  higher  in  front  than  behind.  The  liver  does  not  enlarge  in  such 
a  manner  as  to  fill  the  pleural  cavity  posteriorly  and  anteriorly  to  the  same 
level. 

Sub-acute  pleurisy  of  the  left  side  will  rarely  be  mistaken  for  enlarge- 
ment of  the  spleen,  for  when  the  spleen  is  sufficiently  enlarged  to  encroach 
upon  the  left  pleural  cavity  the  enlargement  will  be  downward  as  well  as 
upward,  the  splenic  tumor  will  be  readily  felt  in  the  abdominal  cavity,  and 
the  flatness  on  percussion  at  the  lower  portion  of  the  pleural  cavity  will 
be  continuous  with  the  tumor  in  the  abdomen. 

The  diagnosis  between  pleurisy  with  effusion  and  cancer  of  the  lung  or 
pleura  is  often  very  difficult,  and  in  some  instances,  if  one  relies  only  upon 
the  rational  symptoms  and  physical  signs,  it  will  be  impossible.  All  such 
doubtful  cases  can  only  be  decided  by  the  use  of  the  exploring  trochar. 
The  needle  of  the  exploring  trochar  can  be  introduced  into  the  thoracic 
cavity  without  the  least  danger,  whether  the  needle  enter  a  pleuritic  effusion, 
a  hepatized  lung,  a  cancer  of  the  pleura  or  lung,  or  an  aneurism. 

Prognosis. — The  prognosis  in  sub-acute  pleurisy  varies  greatly  in  different 
cases.    While  the  majority  will  terminate  in  recovery,  sudden  death  occurs 


156  DISEASES   OE   THE   KESPIRATORY    ORGANS. 

in  a  limited  number  without  lesions  to  account  for  it.  A  large  serous  effu- 
sion may  take  place  suddenly,  and  cause  death  by  its  interference  with  res- 
piration and  circulation.  Cases  may  be  protracted  over  a  period  of  months, 
and  finally  a  sero-fibrinous  effusion  may  change  into  a  sero-purulent  one, 
and  a  sub-acute  pleurisy  may  thus  become  an  empyema  ;  in  giving  a  prog- 
nosis it  is  to  be  remembered  that  in  most  cases  that  recover,  more  or  less 
extensive  adhesions  result,  which  cause  permanent  crippling  of  the  lung, 
and  lead  to  the  development  of  more  or  less  extensive  compensatory  emphy- 
sema, chronic  bronchitis,  and  fibroid  induration  of  lung-tissue.  When 
the  new  tissue  formations  are  extensive,  and  the  general  health  much  im- 
paired, in  those  who  have  a  strong  hereditary  or  acquired  tendency  to  pul- 
monary phthisis,  there  is  always  danger  that  the  new  tissue  may  become  the 
seat  of  tubercular  developments.  One  of  the  greatest  dangers  after  recovery 
from  sub-acute  pleui'isy  is  a  relapse. 

Treatment. — The  main  thing  to  be  accomplished  in  the  treatment  of  sub- 
acute pleurisy  is  to  remove  the  fluid  effusion  as  rapidly  as  possible,  at  the 
same  time  taking  care  to  sustain  the  patient.  The  principal  means  which 
have  been  employed  for  the  accomplishment  of  this  object  are  hydragogue 
cathartics,  diuretics,  diaphoretics,  and  blisters  applied  in  succession  over 
different  parts  of  the  affected  side.  On  account  of  the  anemic  condition 
of  the  majority  of  these  patients,  general  or  local  bleeding,  as  well 
as  the  use  of  mercury,  is  now  very  rarely  employed  ;  for  a  like  reason  I 
very  much  question  the  beneficial  effects  claimed  for  cathartics,  diuretics 
and  blisters  ;  it  is  very  questionable  if  the  condition  which  favors  the  ab- 
sorption of  the  fluid  in  the  pleural  cavity  can  be  reached  by  the  employ- 
ment of  any  of  the  so-called  depurative  remedial  agents.  It  is  claimed  that 
the  use  of  hydragogue  cathartics  and  diuretics  quickly  removes  large  quan- 
tities of  fluid  from  the  body,  and  consequently  the  fluid  portion  of  the 
blood  is  greatly  diminished,  and  that  whenever  a  cavity  contains  fluid,  the 
absorbents  and  blood-vessels  of  the  part  take  it  up  to  replace  that  lost  by 
the  blood,  and  thus  fluid  in  the  pleural  cavity  is  absorbed.  There  is  little 
doubt  but  that  hydragogue  cathartics  and  diuretics  will  hasten  the  absorp- 
tion of  non-inflammatory  serous  effusion  in  simple  hydrothorax,  but  there  is 
no  evidence  that  they  have  power  to  promote  the  absorption  of  inflammatory 
products  from  the  pleural  cavity  in  sub-acute  pleurisy.  It  is  certain  that 
by  the  action  of  these  depurative  means  the  vital  powers  of  the  patient  are 
greatly  enfeebled  and  the  processes  of  digestion  and  nutrition  seriously  in- 
terfered with.  It  is  also  well  established  that  when  the  nutritive  processes 
are  going  on  most  rapidly  absorption  takes  place  most  rapidly.  Conse- 
quently anything  that  interferes  with  these  processes  is  contra-indicated  in 
the  treatment  of  this  form  of  pleurisy.  There  are  also  other  conditions 
which  greatly  impede  the  absorption  of  the  fluid  effusion  in  pleurisy. 
When  the  pleural  cavity  is  distended  with  fluid,  its  absorption  is  impeded 
or  prevented  by  the  obstruction  offered  to  the  flow  of  blood  throngh  the 
pleural  and  sub-pleural  vessels  by  the  pressure.  Under  such  circumstances  it 
is  useless  to  resort  to  diuretics  and  hydragogue  cathartics.  The  mechanical 
withdrawal  of  a  sufficient  amount  of  liquid  to  relieve  the  tension  of  the  cavity 
and  remove  the  pressure  from  the  lung  and  the  sub-pleural  veins  is  an  abso- 


SUB-ACUTE    PLEUEISY.  157- 

lute  necessity  before  the  processes  of  absorption  can  commence.  If  the  surface 
of  the  pleura  is  covered  by  a  thick  layer  of  exudative  material,  this  layer  is 
interposed  between  the  sub-pleural  vessels  and  the  fluid  effusion,  and  must 
greatly  interfere  with  the  absorption  of  the  liquid  ;  as  it  becomes  thicker 
and  thicker  by  successive  deposits  of  fibrin,  it  is  obvious  that  the  longer  the 
liquid  remains  in  the  pleural  cavity  the  thicker  the  fibrinous  deposit  be- 
comes, and  the  less  is  the  probability  that  the  liquid  will  be  absorbed. 
Against  these  conditions  cathartics  and  diuretics  are  powerless. 

For  many  years  I  have  rarely  employed  any  depurative  agents  in  the  treat- 
ment of  sub-acute  pleurisy.  The  remedial  agent  which  seems  to  me  to  have 
the  greatest  power  in  promoting  the  absorption  of  an  effusion  is  the  syrup 
of  the  iodide  of  iron.  In  connection  with  the  administration  of  iron  the 
patient  should  take  the  largest  amount  of  the  most  nutritious  food,  with 
wine  or  some  form  of  alcoholic  stimulant.  The  principle  of  treatment 
is  to  employ  all  those  remedial  and  hygienic  measures  which  improve 
nutrition. 

As  so  little  can  be  done  by  medication  to  excite  or  hasten  the  absorption 
of  pleuritic  effusion,  the  question  of  the  employment  of  mechanical  means 
for  its  removal  presents  itself.  There  is  some  difference  of  opinion  in  the 
profession  upon  this  point.  One  class  of  observers  claim  that  a  single  re- 
moval of  the  fluid  is  of  little  service,  and  that  the  danger  of  admitting  air 
into  the  pleural  cavity  is  so  great  that  if  the  operation  is  frequently  per- 
formed a  serous  effusion  is  very  apt  to  be  changed  into  a  purulent  one,  thus 
jeopardizing  life.  On  the  other  hand,  the  advocates  of  the  operation  main- 
tain that  if  the  fluid  is  permitted  to  remain  in  the  pleural  cavity  it  becomes 
purulent.  The  causes  which  impede  or  render  impossible  the  absorj^tion  of 
the  fluid  seem  to  me  reasons  in  favor  of  its  early  mechanical  removal,  es- 
pecially as  the  practice  of  aspiration  has  inaugurated  a  new  era  in  the 
management  of  these  cases,  and  has  removed  all  objections  to  such  early 
removal.  When  a  perfect  instrument  is  used  and  a  small  needle  intro- 
duced into  the  pleural  cavity,  the  entrance  of  air  is  impossible.  In  any 
case  of  pleurisy,  when  the  accumulated  fluid  remains  stationary  for  one 
week,  or  is  increasing  after  the  cavity  has  become  half  filled,  and  especially 
when  the  cavity  is  completely  full,  there  should  be  no  delay  in  aspirating. 
With  every  day  that  the  lung  remains  compressed,  and  with  every  addition 
to  the  plastic  deposit  upon  the  pleural  surfaces,  the  chances  of  its  absorp- 
tion are  diminished,  and  the  danger  that  the  lung  will  be  permanently 
crippled  is  increased. 

The  following  rules  should  be  observed  in  the  performance  of  aspira- 
tion of  the  chest.  Place  the  body  of  the  patient  in  the  erect  posture,  lean- 
ing somewhat  forward,  with  the  arm  of  the  affected  side  thrown  partly 
across  the  chest.  This  position  of  the  arm  is  preferable  to  any  other  for 
the  reason  that  the  integument  is  not  made  unnaturally  tense  over  the  inter- 
costal spaces.  Select  a  needle  of  small  size  for  the  first  tapping,  and  in- 
troduce it  to  the  depth  of  at  least  one  inch  into  the  fifth  or  sixth  inter- 
costal space,  at  the  junction  of  the  axillary  and  infra-scapular  regions. 
After  the  needle  has  been  introduced  the  fluid  may  be  permitted  to  flow 
through  the  instrument  until  the  patient  complains  of  a  sense  of  con- 


158  DISEASES   OF  THE   EESPIEATOKY   OEGANS. 

striction  about  the  chest,  when  the  withdrawal  of  the  fluid  must  b8 
stopped.  The  amount  of  fluid  that  can  be  withdrawn  at  the  first  aspiration, 
if  the  cavity  is  distended,  will  depend  upon  the  length  of  time  which  the 
fluid  has  remained  in  the  pleural  cavity.  If  it  has  accumulated  rapidly, 
the  cavity  may  frequently  be  emptied  without  giving  rise  to  any  un- 
pleasant symptoms ;  if,  however,  it  has  been  slow  in  its  accumulation 
and  the  pleural  cavity  has  contained  a  large  quantity  of  fluid  for  a  consid- 
erable time,  only  a  small  amount  can  be  withdrawn  without  producing  a 
severe  attack  of  dyspnoea.  When  this  is  the  case  the  patient  may  be  per- 
mitted to  remain  quiet  for  a  few  days,  and  then  the  operation  should  be 
repeated  as  often  as  it  can  be  without  producing  unpleasant  symptoms. 
The  sense  of  constriction  about  the  chest  always  indicates  that  no  more 
fluid  should  be  withdrawn  at  that  time.  It  is  claimed  by  some  that  aspira- 
tion of  the  chest  in  pleurisy  may  cause  death  suddenly  or  within  twenty-four 
hours  after  the  aspiration,  and  that  the  cause  of  death  under  such  circum- 
stances cannot  be  accounted  for,  as  there  are  no  lesions  found  after  death 
which  are  sufficient  to  produce  it.  I  cannot  understand  how  this  is  pos- 
sible if  the  aspiration  is  performed  with  sufficient  care ;  it  certainly  has 
never  happened  in  any  of  my  cases.  I  can  conceive  how  the  sudden  with- 
drawal of  a  large  quantity  of  fluid  from  the  left  chest  might  cause  a  severe 
attack  of  syncope  from  which  a  crippled  heart  might  not  rally.  I  have  no 
hesitation  in  recommending  this  operation  in  all  cases,  provided  it  be  done 
according  to  the  rules  just  given,  and  I  am  not  disposed  to  delay  aspiration 
long  after  the  pleural  cavity  has  once  become  filled  with  fluid,  for  I  am 
convinced  that  its  early  removal  tends  to  promote  a  more  rapid  recovery, 
and  prevents  those  changes  in  the  pleura  which  lead  not  only  to  a  tedious 
convalescence,  but  also  to  an  incomplete  ultimate  recovery. 

EMPYEMA. 

{Plev/risy  with  a  Sero-fibrinous  and  Purulent  Effusion.) 

This  is  a  suppurative  inflammation  of  the  whole  pleura,  usually  confined 
to  one  side  of  the  chest.  It  may  be  primary  or  secondary.  When  it  is 
primary  it  usually  commences  as  an  acute  affection  ;  when  secondary,  it  is 
sub-acute  or  chronic  from  its  commencement. 

Morbid  Anatomy. — The  pathological  changes  in  this  form  of  pleurisy  are 
most  extensive  and  best  marked  on  the  costal,  diaphragmatic,  and  medias- 
tinal portions  of  the  pleural  membrane.  In  primary  suppurative  pleurisy 
there  is  poured  out  a  large  amount  of  plastic  material  which  undergoes 
histological  transformation  into  pus,  and  thus  a  large  amount  of  thick  pus 
is  rapidly  formed  in  the  pleural  cavity.  In  the  secondary  variety  of  sup- 
purative pleurisy  a  sero-purulent  effusion  will  slowly  accumulate  in  the 
pleural  cavity,  varying  in  consistency  in  different  cases,  sometimes  being 
quite  thin  and  mainly  composed  of  serum,  at  others  extremely  thick  and 
containing  comparatively  little  serum.  This  purulent  fluid  usually  occu- 
pies the  most  dependent  portion  of  the  pleural  cavity  ;  it  may,  however,  be 
confined  either  to  the  posterior  or  anterior  half  of  the  chest  by  old  adhesions. 

The  manner  in  which  large  purulent  accumulations  are  formed  in  the 


EMPYEMA.  159 

pleural  cavity  is  as  folloy>^s  : — in  acute  suppurative  pleurisy  with  sero-fibri- 
nous  exudation,  a  large  number  of  pus  cells  form  in  the  connective-tissue  of 
the  pleura  and  also  on  its  surface,  from  which  they  are  waslied  into  the 
cavity,  along  with  the  fibrinous  exudation,  by  the  serous  effusion.  Some- 
times the  accumulation  is  very  large  and  takes  place  very  rapidly.  This  is 
characteristic  of  the  pleurisies  which  occur  in  connection  with  pyaemia.  A 
sero-fibrinous  exudation  may  become  purulent  when  a  fresh  cause  of  in- 
flammatory irritation  gives  rise  to  an  active  cell-exudation  ;  the  new  irrita- 
tion may  come  from  the  admission  of  a>r  into  the  pleural  cavity,  or  from 
some  change  in  the  fluid  which  has  previously  occupied  the  cavity,  or,  per- 
haps, from  suddenly  developed  sepsis.  Under  these  circumstances  a  variety 
of  cell-formative  processes  are  established.  Some  are  produced  in  the  plas- 
tic exudation,  and  some  in  the  pleura  itself.  The  clear  serum  becomes  tur- 
bid, shreds  of  false  membrane  are  loosened  from  their  connection  with  the 
underlying  tissue  and  undergo  liquefaction,  and  the  whole,  or  a  large  por- 
tion of  the  pleural  membrane  becomes  a  suppurating  surface,  and  thus  a 
large  amount  of  pus  is  formed  in  the  pleural  cavity.  If  the  pleural  cavity 
is  aspirated  at  the  commencement  of  the  purulent  process  in  such  cases,  the 
first  fluid  removed  will  be  found  to  contain  a  moderate  number  of  cells  ;  at 
a  second  operation,  a  week  or  two  later,  a  large  number  of  cells  may  be 
found,  and  it  is  usual  under  such  circumstances  to  attribute  the  increased 
number  of  cells  to  the  effects  of  the  first  aspiration.  This  is  not,  however, 
a  legitimate  inference,  for  the  increase  in  the  cell  develoj)ment  is  the 
natural  result  of  the  morbid  process  which  was  in  operation  at  the  first 
aspiration. 

Purulent  accumulations  in  the  pleural  cavity  may  become  so  large  that 
death  may  ensue  in  consequence  of  the  depression  caused  by  their  pro- 
duction. The  tendency  of  sujopurative  pleurisy  is  never  toward  convales- 
cence, unless  by  spontaneous  openings.  The  inflammatory  process  is  not 
limited  to  the  pleura ;  it  may  extend  from  the  costal  pleura  to  the  connec- 
tive-tissue underneath,  to  the  periosteum  of  the  ribs,  causing  necrosis, 
or  it  may  perforate  the  walls  of  the  chest  and  be  discharged  externally.  In 
some  instances  the  lung  may  be  perforated  and  the  discharge  take  place 
through  a  bronchial  tube,  or  the  diaphragm  may  be  perforated  and  the  pus 
find  its  way  into  the  abdominal  cavity.  If  the  patient  survives  the  empty- 
ing of  the  pleural  cavity,  repair  is  accomplished  by  the  rapid  and  abundant 
formation  of  cicatricial  tissue  ;  the  pleural  cavity  is  contracted  in  every  di- 
rection like  a  huge  cicatrix,  the  chest  walls  on  the  affected  side  retract  to 
their  fullest  extent,  and  the  thoracic  and  abdominal  viscera  are  dragged  out 
of  their  normal  positions  to  help  fill  the  space  formerly  occupied  by  lung- 
tissue.  In  some  cases  of  circumscribed  empyema  the  fluid  portion  of  the 
pus  is  absorbed  and  the  solid  constituents  undergo  cheesy  transformation, 
the  salts  of  lime  are  deposited  and  the  thickened  pleura  becomes  calcified. 
The  bony  or  calcareous  plates  which  are  occasionally  found  in  the  pleural 
cavity  at  post  mortem  examinations  usually  have  their  origin  in  an 
empyema. 

Etiology. — The  cause  of  suppurative  pleurisy  is  not  always  readily  de- 
termined.    It  may  be  of  traumatic  origin.     When  it  occurs  spontaneously 


160  DISEASES   OP   THE   KESPIEATORY   ORGAKS. 

it  is  always  associated  with  some  vice  of  constitution,  such  as  results  from 
some  exhausting  disease,  or  the  debility  which  attends  chronic  alcoholismus. 
It  often  complicates  acute  and  chronic  infectious  diseases.  In  the  en- 
feebled it  is  frequently  developed  from  a  sero-fibrinous  pleurisy  which  has 
continued  for  a  long  time,  but  in  most  instances,  under  such  circumstances^, 
the  occurrence  of  the  suppurative  process  is  due  to  some  new  infection, 
or  to  some  new  local  excitement  of  pleuritic  inflammation.  Pleurisies 
that  are  developed  in  advanced  phthisis  are  very  apt  to  be  suppurative  in 
character.  It  may  be  secondary  to  abscess  of  the  liver,  or  to  the  opening 
into  the  pleural  cavity  of  a  vomica  in  the  lung  in  chronic  phthisis.  An 
abscess  in  the  abdominal  cavity  or  in  the  chest  walls  may  open  into  the 
pleura,  and  establish  a  suppurative  pleurisy. 

Symptoms. — The  rational  symptoms  of  empyema  will  vary  with  its  char- 
acter. Those  cases  in  which  the  inflammatory  processes  are  acute  at  the 
onset,  accompanied  by  the  rapid  production  of  fibrin  and  pus,  will  be 
ushered  in  by  chills,  followed  by  a  rapid  rise  in  temperature,  and  a  rapid, 
full  pulse.  There  will  be  severe  pain  in  the  affected  side,  with  the  signs  of 
great  prostration.  The  prostration  is  greater  than  in  acute  fibrinous  pleu- 
risy, and  the  countenance  early  assumes  an  anxious  expression  ;  if  the  in- 
flammatory products  become  gangrenous  the  prostration  is  extreme,  and  the 
patient  presents  the  appearance  of  one  suffering  from  peritonitis ;  typhoid 
symptoms  manifest  themselves  very  early  ;  and  these  cases  usually  termi- 
nate fatally  within  two  or  three  weeks.  In  other  cases  the  active  symptoms 
subside  after  a  week  or  ten  days,  and  symptoms  of  the  more  chronic  form 
of  empyema  are  developed.  The  symptoms  of  chronic  empyema  are  often 
very  obscure  ;  the  presence  of  pus  in  the  pleural  cavity  in  these  cases  can- 
not be  determined  either  by  the  rational  symptoms  or  by  physical  signs. 
The  patient  rarely  suffers  from  local  pain — there  is  simply  a  sense  of  un- 
easiness, or  weight  in  the  affected  side  ;  there  is  a  gradual  loss  of  flesh  and 
strength  ;  the  countenance  assumes  a  pale,  anxious  expression  ;  and  there 
is  an  irregular  diurnal  chill  followed  by  profuse  sweats.  Ordinarily  the 
patient  has  a  cough  with  a  scanty  muco-purulent  expectoration,  the  voice 
becomes  weak  and  there  is  more  or  less  dyspnoea,  and  the  patient  gradually 
assumes  the  appearance  of  one  in  the  last  stages  of  pulmonary  phthisis.  If 
empyema  occurs  as  a  complication  of  septicaemia  or  pyaemia,  its  commence- 
ment is  also,  at  times,  very  insidious.  In  these  conditions  patients  some- 
times pass  into  a  semi-comatose  state.  Not  infrequently  pysemic  patients 
make  no  complaints  which  would  direct  attention  to  the  pleura,  and  the 
pleural  cavity  may  be  found  two-thirds  full  of  pus,  without  having  given 
a  single  symptom  of  its  presence. 

If  an  empyema  is  about  to  open  externally,  it  will  usually  make  itself 
manifest  by  a  protrusion  between  the  ribs,  which  gives  a  sense  of  fluct- 
uation, and  after  a  time  grows  red,  and  finally  a  valvular  opening  is 
formed  and  pus  is  discharged.  If  the  opening  takes  place  through  the 
lung  into  a  bronchial  tube,  the  discharge  of  pus  is  ordinarily  preceded 
by  symptoms  of  pneumonia ;  the  patient  will  have  a  chill,  followed  by 
a  cough  and  a  more  or  less  profuse  expectoration  containing  blood,  which 
will  be  followed  by  a  profuse  purulent  expectoration,  which  will  afford 


EMPYEMA.  161 

marked  relief.  The  profuse  purulent  expectoration  will  occur  two  or 
three  times  a  day ;  the  chest  walls  gradually  retract,  and  finally  the  ex- 
pectoration will  cease  altogether  and  the  pleural  cavity  become  obliterated. 
If  the  opening  takes  place  into  the  peritoneal  cavity,  its  occurrence  is 
usually  followed  by  a  rapidly  fatal  peritonitis.  If  the  communication 
is  established  with  the  intestinal  canal,  pus  will  appear  in  the  discharges 
from  the  bowels.  If  the  patient  survives  the  establishment  of  either 
an  external  or  internal  oi^ening,  spontaneous  or  artificial,  a  connec- 
tive-tissue development  takes  place  in  the  pleural  cavity,  and  as  the  con- 
tents of  the  cavity  are  being  discharged  retraction  of  the  chest  and  dis- 
placement of  the  abdominal  and  thoracic  viscera  take  place  ;  this  process  is 
necessarily  slow,  and  years  may  elapse  before  it  is  completed. 

Physical  Signs. — The  physical  signs  of  empyema  are  essentially  the  same 
as  those  of  pleurisy  with  elfusion,  except  that  the  level  of  the  fluid  is  not  so 
readily  changed  by  a  change  in  the  position  of  the  patient ;  if,  however, 
the  physical  signs  indicate  the  existence  of  fluid  in  the  pleural  cavity  in 
one  who  is  very  much  debilitated,  who  has  a  constant  cough  with  muco- 
purulent expectoration,  hectic  fever  with  profuse  sweats,  and  whose  history 
indicates  tliat  the  fluid  has  existed  for  a  long  time,  one  may  be  almost  cer- 
tain that  the  fluid  is  purulent. 

Diiferential  Diagnosis. — Unless  a  fistulous  opening  exist,  a  positive  diag- 
nosis of  empyema  is  impossible,  except  by  an  explorative  puncture. 
When  such  a  puncture  has  been  made,  and  some  of  the  contents  of  the 
pleural  cavity  have  been  drawn  ofl  and  subjected  to  microscopical  ex- 
amination, it  is  not  possible  to  confound  an  empyema  with  any  other 
thoracic  disease. 

Prognosis. — The  prognosis  in  empyema  is  unfavorable.  In  acute  sup- 
purative pleurisy  death  may  occur  at  the  end  of  one  or  two  weeks.  In  the 
more  chronic  cases  it  may  take  place  from  gangrene  produced  by  decompo- 
sition of  the  inflammatory  products  in  the  pleural  cavity.  Statistics  show 
that  in  empyema  of  slow  development,  where  spontaneous  openings  occur, 
about  one  in  five  recover,  while  in  those  in  whom  artificial  openings  are 
established  the  rate  of  mortality  is  greater.  This  class  of  patients  die 
from  the  exhaustion  produced  by  the  accumulation  of  large  quantities  of 
pus,  and  from  the  exhaustion  which  attends  a  prolonged  and  abundant 
purulent  discharge.  A  large  number  of  these  patients  live  for  a  year  or 
more.  The  judicious  use  of  the  aspirator  will  tend  to  render  the  prog- 
nosis more  favorable  in  the  acute  cases.  I  am  confident  that  the  early  in- 
troduction of  a  drainage  tube  into  the  pleural  cavity  in  chronic  cases  will 
save  many  lives.  In  estimating  the  prognosis  in  this  disease,  the  treatment 
to  which  the  patient  is  to  be  subjected  must  always  be  considered. 

'Che  majority  of  empyemic  children  recover,  while  in  adults,  although 
for  a  time  recovery  seems  almost  certain,  phthisis  is  sooner  or  later 
developed. 

Treatment. — In  the  treatment  of  this  afi'ection  it  is  useless  to  attempt  to 
produce  absorption  of  the  purulent  accumulation  by  remedial  agents.  Its 
removal  can  only  be  accomplished  by  mechanical  means — either  by  aspira- 
tion or  by  making  a  permanent  opening  in  the  chest  walls.  If  aspiration  is 
11 


162  DISEASES   OF  THE   EESPIEATORT   ORGAN'S. 

resorted  to  a  large-sized  needle  should  be  used,  and  no  attempt  should  be 
made  to  empty  the  cavity  at  the  first  operation.  Eemove  only  a  small  por- 
tion of  the  accumulation,  being  governed  by  the  same  rules  which  have  been 
given  for  the  removal  of  serous  effusions,  and  allow  from  three  to  six  days 
to  elapse  between  successive  aspirations.  At  each  aspiration  something  in 
excess  of  the  amount  which  was  taken  at  the  previous  seance  should  be 
removed.  Never  continue  the  removal  of  pus  in  empyema  after  the  patient 
complains  of  constriction  in  breathing,  even  though  only  three  or  four 
ounces  have  been  removed.  If  the  aspiration  is  to  be  successful  the  fluid 
will  become  thinner  at  each  aspiration,  and  retraction  of  the  chest  wall  will 
be  noticed.  If  the  fluid  becomes  thicker  and  emits  an  unpleasant  odor,  a 
permanent  opening  should  immediately  be  made.  In  empj^ema  occurring 
with  septicaemia  and  pysemia  the  accumulation  will  exceed  in  quantity  that 
removed,  unless  the  aspirator  is  used  daily.  Under  such  circumstances  a 
free  opening  should  be  made.  If  a  permanent  opening  is  to  be  made,  let  it  be 
made  in  the  axillary  line  in  the  seventh  or  eighth  intercostal  space.  After 
a  free  opening  has  been  made  into  the  chest  cavity,  a  quarter-inch  rubber 
drainage  tube  should  be  introduced,  and  so  fastened  that  it  will  remain. 
Oft-^en  when  there  is  little  space  between  the  ribs  a  portion  of  bone  should 
be  removed,  that  the  tube  may  not  be  compressed  during  respiration.  A 
double  drainage,  by  making  two  openings  in  the  chest  cavity,  is  rarely 
advisable.  As  regards  the  washing  out  of  the  pleural  cavity  after  the  intro- 
duction of  the  drainage  tube,  although  it  is  strongly  advocated  by  some,  my 
recent  experience  is  very  positively  against  it,  even  when  the  purulent  dis- 
charge has  an  offensive  odor.  Thrice  have  I  had  reason  to  believe  that  my 
patients  have  died  from  the  direct  effects  of  washing  out  the  pleural  cavity 
with  a  weak  solution  of  carbolic  acid.  From  the  commencement  empyemic 
patients  must  receive  a  most  nutritious  diet  with  moderate  stimulation. 
Tonics,  such  as  quinine  and  iron,  are  always  indicated  ;  cod-liver  oil  will  be 
of  service  if  it  does  not  interfere  with  stomach  digestion.  The  patient 
must  be  kept  in  the  open  air  as  much  as  possible,  and  a  change  of  climate  is 
often  attended  by  very  marked  improvement.  The  majority  of  cases  of  em- 
pyemic children  will  recover  if  aspiration  is  performed  early  and  repeated 
at  short  intervals.  In  most  adults  it  will  be  necessary  to  make  a  permanent 
opening  in  the  chest  wall. 

ADHESIVE    PLEURISY. 

Adhesive  pleurisy  may  commence  as  a  primary  disease,  or  be  the  sequela 
of  an  acute,  plastic,  or  a  sub-acute  effusive  pleurisy.  In  any  case  there  is 
more  or  less  extensive  new  connective-tissue  formations  over  a  greater  or 
Jess  extent  of  the  pleural  surface. 

Morbid  Anatomy. — The  essential  lesion  in  this  form  of  pleurisy  is  the  for- 
Tuation  of  new  connective-tissue  over  the  pleural  surfaces.  This  hyperpla- 
sia may  or  may  not  have  its  origin  in  a  pleurisy  which  gives  fibrin,  serum, 
or  pus  as  its  product.  As  a  result  the  pleura  becomes  thickened  sometimes 
to  the  extent  of  half  an  inch  ;  but  the  most  important  and  constant  lesion  is 
adhesion  between  the  costal  and  pulmonary  pleurae.      These  adhesions. 


ADHESIVE    PLEURISY.  163 

however  they  originate,  are  progressive,  and,  after  a  time,  become  very 
extensive.  In  some  cases  the  two  surfaces  may  become  closely  agglutinated 
to  each  other  throughout  their  Avhole  extent,  and  then  the  entire  space  be- 
tween them  may  be  obliterated.  As  a  result  of  these  adhesions  the  expan- 
sive motion  of  the  lungs  is  interfered  with,  and  sometimes  to  such  an  extent 
as  to  cause  constant  dyspnoea.  The  heart  may  be  displaced  to  the  right  and 
backward.  In  one  case  where  the  adhesions  were  extensive  over  both  lungs, 
the  heart  cavities  were  much  dilated,  and,  a  loud  ventricular  murmur  always 
being  heard,  valvular  disease  of  the  heart  was  diagnosticated  by  good  ob- 
servers who  saw  the  case  during  life.  This  form  of  pleurisy  often  leads  to 
the  development  of  fibrous  phthisis. 

Etiology. — It  occurs  most  frequently  in  rheumatic  and  gouty  subjects.  It 
is  often  associated  with  general  fibroid  degeneration.  When  it  occurs  as 
a  sequela  of  sero-plastic  pleurisy  it  begins  with  the  disappearance  of  the 
sero-plastic  effusion. 

Symptoms.— Its  development  is  always  slow  and  often  intermittent.  Its 
most  constant  early  symptom  is  a  dull  pain  over  the  affected  part,  accom- 
panied by  a  sense  of  constriction.  An  early  symptom  is  dyspnoea  on  exer- 
tion, which  steadily  increases  with  the  advance  of  the  disease,  and  becomes 
so  severe  that  even  slight  exertion,  such  as  going  up  stairs,  will  give  rise 
to  such  severe  paroxysms  that  signs  of  collapse  sometimes  follow.  There 
is  usually  a  dry,  hacking  cough,  frequently  attended  by  free  bronchial 
hemorrhages.  I  have  frequently  found  these  pleuritic  adhesions  the  only 
apparent  cause  of  quite  profuse  bronchial  hemorrhage.  As  the  adhesion 
becomes  extensive,  the  patient  loses  flesh  and  strength,  and  in  some  cases 
the  ordinary  symptoms  of  chronic  phthisis  are  present.  If  there  is  much 
displacement  of  the  heart  the  patient  will  be  troubled  with  cardiac  palpita- 
tion on  slight  excitement  or  physical  exertion,  so  that  his  dyspnoea  and 
cough  are  often  supposed  to  be  due  to  some  obscure  cardiac  lesion. 
Often  after  this  class  of  patients  have  suffered  much  and  seem  to  be  stead- 
ily getting  worse,  periods  of  remission  occur,  during  which  for  months  and 
perhaps  years  they  will  seem  to  be  recovering.  The  appetite  returns,  they 
gain  flesh  and  strength,  the  dyspnoea  becomes  less,  and  then,  while  they  are 
apparently  recovering,  they  suddenly  get  worse,  all  their  aggravating  symp- 
toms return  greatly  exacerbated,  and  they  rapidly  pass  into  a  decline. 

Physical  Signs. — Inspection  shows  diminished  expansive  motion  of  the 
affected  side,  or  of  the  entire  chest  if  both  pleurae  are  affected. 

Palpation  shows  diminished  vocal  fremitus  over  the  seat  of  the  adhesions. 

Careful  mensuration  of  the  chest  will  often  establish  the  diagnosis  when 
doubt  exists  as  to  the  exact  character  of  the  changes. 

On  percussion  there  will  be  slight  dulness,  which  will  be  most  marked 
at  the  part  where  the  adhesions  are  most  extensive. 

On  auscultation  the  respiratory  sound  will  be  feeble,  sometimes  scarcely 
audible  even  during  a  full  inspiration  ;  friction  sounds  will  be  heard.  These 
friction  sounds  are  creaking  or  crepitating  in  character,  very  loud,  and 
often  resemble  mucous  r41es  and  gurgles,  for  which  they  are  sometimes  mis- 
taken, but  the  loss  of  chest  expansion  and  the  feebleness  of  the  respiratory 
sounds  will  readily  correct  the  mistake. 


164  DISEASES    OF   THE   KESPIEATORY   ORGANS. 

Prognosis. — The  prognosis  in  this  form  of  pleurisy  varies  with  its  dura- 
tion and  extent.  If  the  adhesions  are  not  extensive  and  are  of  recent  date, 
the  process  may  be  arrested  and  complete  recovery  is  possible  ;  but  if  they 
are  extensive  and  the  inflammatory  process  has  continued  for  a  long  time,  it 
is  generally  progressive  and  recovery  is  impossible.  If  it  is  attended  by 
great  emaciation  and  progressively  failing  health  it  may  cause  death  with- 
out complications.  The  majority,  however,  die  from  the  complication  of 
chronic  bronchitis,  emphysema,  and  chronic  interstitial  pneumonia  (''fibrous 
phthisis").  In  some  cases  the  disturbance  of  the  general  circulation  from 
dilatation  of  the  right  ventricular  cavity  leads  to  general  dropsy  and  all 
the  conditions  which  result  from  heart  insufficiency. 

Treatment. — The  first  and  most  important  thing  to  be  accomplished  in 
the  treatment  of  this  affection  is  to  improve  the  nutrition  of  the  patient. 
In  accomplishing  this  the  diathesis  of  the  patient  must  be  carefully  consid- 
ered. The  diet  must  be  regulated  according  to  the  indications  ;  the  diet  of 
gouty  subjects  must  he  very  different  from  that  of  the  enfeebled,  broken- 
down  alcoholic  subject.  While  iron  and  the  mineral  acids  will  be  indicated 
in  one  class,  cod-liver  oil  and  the  hypophosphites  will  be  indicated  in  the 
other.  In  all  cases,  the  bichloride  of  mercury  in  minute  doses  will  be  found 
of  service.  Climatic  conditions  are  very  important  in  its  successful  man- 
agement ;  as  a  rule  high  altitude  with  a  warm,  dry  atmosphere,  such  as  is 
obtained  in  New  Mexico,  will  be  found  most  favorable.  The  external  ap- 
plication to  the  chest  which  has  seemed  to  me  to  have  a  desired  effect  in 
arresting  its  progress  and  removing  its  results,  is  the  oleate  of  mercury — 
its  use  must  be  continued  for  a  long  time,  care  being  taken  not  to  bring 
the  patient  under  the  constitutional  effects  of  the  mercury. 

CAlSrCER    OF    THE   PLEURA. 

Cancer  of  the  pleura  and  sub-pleural  tissue  is  never  primary,  and  is  only 
met  with  in  advanced  cancerous  infection.  It  appears  either  as  circum- 
scribed grayish  thickenings  of  the  pleura  or  in  the  form  of  distinct  papular 
elevations  on  the  pleural  surface.  As  the  papules  enlarge,  they  form  pe- 
dunculated outgrowths,  which  vary  in  size  from  a  pea  to  a  small  orange.  Ac- 
companying these  developments  there  is  interstitial  pleurisy,  which  causes 
extensive  thickening,  adhesion,  and  induration  of  the  pleura,  attended  by 
the  effusion  of  fluid  into  the  pleural  cavity. 

Etiology. — It  most  frequently  complicates  cancer  of  the  mamma,  medi- 
astinum, aud  lungs. 

Symptoms. — The  signs  of  pleural  cancer  are  always  obscure.  The  history 
of  the  case  is  always  important.  If  the  tumors  are  large,  or  the  fluid  effu- 
sion abundant,  so  as  to  cause  compression  of  the  lung,  there  will  be  dysp- 
noea, cyanosis,  and  vertigo,  with  the  physical  signs  of  fluid  accumulation 
and  the  slow  development  of  solid  tumors  in  the  pleura.  Should  the  evi- 
dence of  a  tumor  with  slow  accumulation  of  fluid  in  the  pleural  cavity  oc- 
cur in  a  case  of  long  standing  cancer  of  the  breast,  accompanied  by  gradual 
emaciation  and  dyspnoea  on  slight  exertion,  cancer  of  the  pleura  may  be 
suspected.    If  a  cancerous  tumor  is  developed  in  the  pleura  posteriorly,  with 


PYOPNEUMOTHORAX.  165 

the  aorta  in  front,  there  may  be  a  pulsation  and  bruit  which  will  cause  it 
to  be  mistaken  for  thoracic  aneurism.  The  prognosis  is  always  unfavora- 
ble, and  the  treatment  is  only  palliative. 

PYOPNEUMOTHOKAX. 

This  a  condition  characterized  by  the  presence  of  both  air  and  fluid  in 
the  pleural  cavity.  The  entrance  of  air  into  the  pleural  cavity  is  usually 
promptly  followed  by  the  effusion  of  liquid,  for  it  excites  suppurative  in- 
flammation of  the  pleural  membrane. 

Morbid  Anatomy. — The  morbid  changes  which  may  occur  in  the  pleural 
membrane  and  in  the  pleural  cavity  in  pyopneumothorax  very  nearly  cor- 
respond to  those  described  as  occurring  in  empyema ;  they  are  increase  of 
tissue,  granular  appearance  of  the  surface  of  the  pleura,  and  the  development 
of  pus.  By  the  entrance  of  air  into  the  pleural  cavity,  the  lung  is  allowed  to 
collapse,  to  contract  toward  its  base  near  the  spinal  column,  in  the  same 
manner  as  when  the  cavity  is  filled  with  fluid,  although  the  opening  (as  from 
rupture  in  an  emphysema)  may  be  no  larger  than  a  jDin-hole.'  The  heart 
may  be  considerably  displaced.  The  quantity  of  fluid  varies  in  different 
cases  ;  at  one  time  the  cavity  will  be  nearly  filled  with  fluid  and  contain 
little  air; — again  it  will  be  distended  with  air  and  contain  little  fluid. 
"When  extensive  and  firm  adhesions  of  the  pleural  surfaces  exist  prior  to  the 
entrance  of  air  into  the  pleural  cavity,  collapse  of  the  entire  lung  does  not 
take  i^lace,  but  the  escaped  air  is  contained  in  a  small  space  enclosed  by  ad- 
hesions on  all  sides.  This  condition  is  usually  present  when  pyopneumo- 
thorax is  developed  from  the  perforation  of  an  empyema,  or  suppurative 
pleuritis.  The  air  in  the  cavity  is  always  deoxidized  and  rich  in  carbon 
dioxide  ;  it  may  also  contain  sulphuretted  hydrogen. 

Etiology. — Eegarding  the  source  of  the  air  in  the  pleural  cavity  different 
views  have  been  entertained.  Some  have  claimed  that  gas  escapes  into  the 
pleural  cavity  from  the  tissues  or  blood,  in  the  same  manner  as  it  is  claimed 
to  escape  into  the  intestines  from  the  mucous  membrane  ;  this  may  be  pos- 
sible, but  it  is  by  no  means  probable.  Others,  again,  have  claimed  that 
it  is  the  product  of  decomposition  of  fluid  in  the  pleural  cavity ;  this  ib 
rarely,  if  ever,  the  case,  for  fluid  effused  into  closed  cavities  resists  de- 
composition in  a  surprising  manner,  although  when  taken  from  such  cavi- 
ties or  exposed  to  the  contact  with  air  within  them,  it  rapidly  decomposes. 
Pus  or  serum  will  resist  decomposition  in  a  pleural  cavity  so  long  as  it  is  not 
exposed  to  air. 

There  can  be  little  question  but  that  in  pneumothorax  and  pyopneu- 
mothorax there  is  always  an  opening  between  the  air-passages  of  the  lung 
and  the  pleural  cavity,  an  opening  which  is  the  result  of  an  ulcerative  proc- 
ess which  may  begin  within  the  lung  and  work  outward,  or  in  its  pleura] 
surface  and  work  inward.  In  rare  instances  air  enters  the  pleural  cavity 
through  an  external  opening  in  the  chest  wall.  Hydatids  sometimes  rupt- 
ure into  the  pleural  cavity.     In  most  cases  of  traumatic  pneumothorax 

i  But  them  need  he.  no  pleurisy  :  although  a  secondary  pleuritia  may  light  up  around  the  opening  and  close 
it,  thus  efifecting  a  cure. 


166  DISEASES    OF   THE    RESPIRATORY   ORGAISTS 

air  does  not  enter  the  pleural  cavity  tliroagli  the  opening  in  the  chest  wall, 
but  comes  from  the  lung  through  an  opening  in  the  pulmonary  pleura,  the 
lung  being  torn  at  the  same  time  that  the  opening  is  made  through  the 
walls  of  the  chest.  The  commonest  example  is  in  connection  with  fracture 
of  the  ribs,  in  which  the  lung  is  sometimes  torn  by  the  broken  end  of  the 
bone,  and  air  escapes  through  the  rent  into  the  pleural  cavity.  Entrance  of 
air  into  the  pleural  cavity  usually  occurs  either  in  connection  with  pulmo- 
nary phthisis,  gangrene  of  the  lung,  empyema,  or  pulmonary  emphysema. 
It  is  most  frequently  met  with  in  connection  with  pulmonary  phthisis.  Ab- 
scess of  the  bronchial  glands,  and  ulceration  of  the  oesophagus  or  stomach, 
may  lead  to  it.  When  an  empyema  has  existed  for  a  long  time  an  opening 
may  be  established  by  ulceration  through  the  lung  into  a  bronchial  tube, 
thus  permitting  the  fluid  to  be  expectorated,  and  air  to  enter  the  pleural 
cavity.  In  pulmonary  emphysema,  a  sac  containing  air  which  has  been 
formed  upon  the  surface  of  the  lung  may  rupture,  and  air  enter  the  pleural 
cavity  and  develop  pneumothorax ;  the  consequent  pleurisy  will  rapidly 
develop  a  pyopneumothorax.  At  the  post-mortem  examination  of  one  who 
has  died  of  pyopneumothorax,  it  is  often  difficult,  and  sometimes  impos- 
sible, to  find  the  opening  in  the  pulmonary  pleura,  for  the  reason  that  in 
some  instances  it  becomes  covered  with  a  fibrinous  deposit,  and  in  others  the 
opening  has  been  closed  some  time  before  death  by  an  inflammatory  process 
in  the  lung  substance  about  the  opening. 

Symptoms. — The  symptoms  which  attend  perforation  of  a  lung,  and  the 
escape  of  air  into  a  pleural  cavity,  are  usually  well  marked,  but  they  are 
somewhat  variable.  First,  there  is  a  class  of  cases  in  which  the  symptoms 
are  severe  in  character,  the  patient  is  suddenly  seized  with  a  sense  of  faint- 
ness  followed  by  hurried  respiration  and  great  dyspnoea.  Pain  may  or  may 
not  be  a  symptom  ;  its  existence  indicates  inflammation.  The  dyspnoea  is 
in  part  mechanical,  in  part  reflex.  It  is  extreme,  comes  on  suddenly,  is 
soon  followed  by  well-developed  cyanosis,  the  patient  passes  rapidly  into  a 
state  of  collapse,  and,  in  some  instances,  death  occurs  in  a  few  hours. 
Usually,  however,  the  patient  survives  the  shock  of  the  perforation,  and, 
after  a  time,  becomes  comparatively  comfortable,  suffering,  however,  from 
more  or  less  dyspnoea.  He  is  unable  to  lie  down,  able  only  to  recline  upon 
the  affected  side.  Some  say  they  experienced  a  sense  of  "tearing,"  and 
felt  as  if  a  fluid  "were  being  poured  inside  the  chest." 

As  the  pleural  cavity  becomes  filled  with  the  fluid  effusion  (which  may  re- 
sult from  the  attending  pleuritic  inflammation),  the  dyspnoea  and  cyanosis 
increase,  and  general  dropsy  gradually  develops.  Aseptic  air  alone  will  not 
cause  inflammation  or  rise  in  temperature.  It  is  a  purulent  accumulation 
in  the  pleural  cavity  which  proves  fatal,  and  not  the  pneumothorax,  for  with 
its  development  the  temperature  rises  and  the  patient  becomes  more  mani- 
festly hectic,  if  hectic  has  previously  existed.  When  the  purulent  accumu- 
lation becomes  very  abundant  the  patient  dies  from  the  exhaustion  produced 
by  the  intensity  of  the  fever  or  from  collateral  hypergemia  and  oedema  of  the 
opposite  lung.  In  some  cases  the  symptoms  which  attend  the  entrance  of 
air  into  the  pleural  cavity  come  on  more  insidiously.  The  difficulty  of 
breathing  may  be  gradually  developed,  and  the  existence  of  air  in  the  pleu- 


PYOPNEUMOTHORAX. 


167 


ral  cavity  may  not  be  recognized  until  after  considerable  fluid  has  collected 
in  the  pleural  cavity.  When  pneumothorax  occurs  in  connection  with  pul- 
monary phthisis,  its  occurrence  is  marked  by  very  active  symptoms,  pain 
being  prominent,  followed  by  all  the  evidences  of  collapse.  When  oc- 
curring in  connection  with  pulmonary  emphysema  its  development  is  very 
insidious. 

Physical  Signs. — The  physical  signs  of  pyopneumothorax  are  very  charac- 
teristic, and,  if  properly  appreciated,  will  always  enable  one  to  recognize  its 
existence.    By  ins;pection  there  will  be  noticed  a  bulging  of  the  intercostal 


Tympanitic  resonance.... 
Amphoric  respiration.... . 

Metallic  tinkling 

Succussion  sound 

Absent  vocal  fremitys . 

Flatness ^ -jj, 

Absent  voice • 

Absent  respiration 


Fia.  35. 
Diagram  illustrating  the  Physical  Signs  of  Pyopneumothorax. 

space  and  an  increase  in  the  size  of  the  affected  side,  which  becomes  more 
prominent  than  in  sub-acute  pleurisy  and  has  a  ''rounded"  look.  There 
will  be  the  displacement  of  viscera  seen  in  sub-acute  pleurisy  when  the  pleu- 
ral cavity  is  distended  with  fluid,  and  there  will  be  absence  of  motion  on  the 
affected  side,  while  upon  the  unaffected  side  the  respiratory  movement  will 
be  also  decreased  in  force  and  frequency,  but  to  no  such  great  extent,  the 
breathing  being  almost  wholly  abdominal. 

Upon  palpation  there  will  be  entire  absence  of  vocal  fremitus  upon  the 
affected  side,  unless  there  are  old  adhesions.  The  heart,  at  the  same  time, 
is  felt  pushed  from  its  normal  site.  Thus  far  there  is  no  difference  between 
the  physical  evidences  of  pyopneumothorax  and  sub-acute  pleurisy. 

On  percussion,  when  the  patient  is  sitting  or  standing  there  will  be  tym- 
panitic resonance  from  the  summit  of  the  affected  side  to  the  level  of  the 
fluid.  Below  the  level  of  the  fluid  there  will  be  complete  flatness.^  A 
change  in  the  position  of  the  patient  will  change  the  level  of  the  fluid,  and 
also,  of  course,  the  character  and  site  of  the  percussion  note. 

Upon  auscultation  there  will  be  found  an  entire  absence  of  all  respiratory 
and  vocal  sounds  below  the  level  of  the  fluid  ;  but,  as  soon  as  its  level  is 
reached,  if  the  opening  from  the  bronchial  tube  which  admits  the  air  into 
the  pleural  cavity  still  remains  pervious,  amphoric  respiration  or  "echo  " 
will  be  heard,  and  it  will  be  metallic  in  character.  Metallic  tinkling  is  al- 
most uniformly  associated  with  amphoric  respiration,  and  is  produced  in  a 

'  Except  in  pyopneumothorax  it  is  rare  to  find  an  exactly  horizontal  line  of  demarcation  with  pleural 
effusions. 


168  DISEASES   OF  THE   RESPIRATORY   ORGANS. 

variety  of  ways.  It  may  be  produced  by  agitation  of  tbe  liquid  from  tbe 
vibration  of  the  voice,  or  by  coughing  and  full  inspiration,  or  by  dropping 
of  liquid  from  the  walls  of  the  cavity  upon  the  surface  of  the  fluid.  It  is 
more  frequently  produced  by  agitation  of  the  fluid  from  speaking  and 
coughing.  The  characteristic  physical  sign  of  this  disease  is  the  succussion 
sound,  which  is  a  metallic,  splashing  sound,  produced  by  abruptly  shaking 
the  chest  while  the  ear  is  resting  upon  the  surface.  Over  the  affected  side 
no  vesicular  breathing  can  be  heard,  while  over  the  healthy  side  the  vesicu- 
lar breathing  is  exaggerated. 

Differential  Diagnosis. — When  pyopneumothorax  is  fully  developed,  it  is 
scarcely  possible  to  confound  it  with  any  other  disease,  but  it  is  possible  to 
confound  pneumothorax  with  some  other  conditions.  The  only  physical 
evidences  of  a  perforation  which  permits  the  entrance  of  air  into  the  pleural 
cavity,  are  tympanitic  percussion,  absence  of  all  respiratory  sounds  on  the 
affected  side,  and  intense  dyspnoea  ;  the  same  development  of  signs  might 
occur  in  connection  with  complete  obstruction  of  a  large  'bronchus.  Again, 
it  is  said  that  pneumothorax  maybe  confounded  with  extreme  pulmonary 
emphysema.  Patients  suffering  from  these  diseases  present  a  somewhat 
similar  appearance  ;  in  both  classes  there  is  tympanitic  percussion,  but  in 
the  emphysematous  patient  the  tympanitic  percussion  is  present  over  both 
lungs,  while  in  a  patient  suffering  from  pneumothorax  it  is  present  only 
upon  the  side  on  which  the  perforation  has  occurred.  Besides,  there  is  a 
vesicular  element  to  the  tympanitic  note  in  emphysema  never  found  in 
pneumothorax.  In  emphysema  there  will  also  be  heard  some  respiratory 
sounds.  The  expiration  is  prolonged  and  low  pitched  in  emphysema  ;  not 
so  in  pneumothorax.  The  breathing  is  broncho-vesicular  in  emphysema  ; 
not  so  in  pneumothorax,  where  respiratory  sounds  are  absent.  Succussion 
is  present  in  pyopneumothorax  ;  not  in  emphysema.  If  errors  in  the  dif- 
ferential diagnosis  of  these  two  conditions  are  possible,  they  will  be  made 
at  the  commencement  of  the  attack. 

A  large  cavity  in  the  lung  substance  may  be  mistaken  for  pyopneumo- 
thorax. I  have  never  met  with  a  pulmonary  cavity  of  sufficient  size  and 
with  the  conditions  to  produce  the  succussion  sound.  Amphoric  res- 
piration and  metallic  tinkling  may  be  developed  in  a  large  cavity,  but  the 
succussion  sound  will  be  absent  ;  on  the  other  hand,  when  amphoric  re& 
piration  and  metallic  tinkling  are  present  in  hydropneumothorax  the  suo. 
cussion  sound  will  also  be  present.  In  a  cavity  rales  would  be  loud  and 
numerous  ;  vocal  fremitus  is  very  often  exaggerated;  the  chest  wall  above  it 
would  probably  be  slightly  depressed,  and  fiinally,  the  heart,  etc.,  would  not 
be  displaced. 

With  a  knowledge  of  the  history  of  the  patient  and  a  proper  appreciation 
of  the  physical  signs,  it  is  hardly  possible  to  confound  pyopneumothorax 
with  any  other  form  of  disease.  In  no  other  disease  are  the  physical  signs 
so  characteristic  and  unequivocal,  and  in  a  large  proportion  of  cases  the 
rational  symptoms  are  equally  diagnostic. 

Prognosis. — The  prognosis  in  pyopneumothorax  is  always  unfavorable. 
All  authorities  agree  that  when  it  occurs  in  connection  with  advanced  pul- 


HTDROTHOEAX.  169 

monary  phthisis  or  gangrene  it  generally  proves  fatal  within  five  or  six  days  ; 
but  in  pneumothorax  without  pleurisy  the  prognosis  is  favorable.  Every 
day  the  patient  lives  betters  the  outlook ;  the  majority  of  fatal  cases 
die  within  two  days,  the  period  of  survival  in  the  remainder  rarely  extend- 
ing beyond  the  sixth  day.  When  recovery  has  taken  place  in  cases  of 
pyopneumothorax,  either  they  have  been  of  traumatic  origin,  the  result 
of  great  muscular  strain  in  connection  with  extensive  pulmonary  emphy- 
sema, or  an  empyema  has  discharged  itself  through  a  bronchus.  There  is 
record  of  a  few  recoveries  where  the  rupture  occurred  in  the  early  stage 
of  phthisis.  When  recovery  does  take  place  it  is  reached  in  the  following 
manner  : — plastic  material  is  poured  out  in  the  tissue  surrounding  the  open- 
ing in  sufficient  quantities  to  completely  close  it ;  the  air  and  fluid  are  thus 
imprisoned  in  the  pleural  cavity  ;  the  air  is  rapidly  absorbed  by  the  pleural 
membrane,  and  if  the  closure  is  sufficiently  firm  to  persist  after  the  air  has 
been  removed,  the  case  will  be  thus  changed  from  one  of  pyopneumo- 
thorax to  one  of  empyema.  Cases  have  been  related  in  which  perforation 
of  the  lung  and  pneumothorax  were  present  without  any  fluid  collecting  in 
the  pleural  cavity.  Such  cases  are  of  such  rare  occurrence  that  they  can 
hardly  be  taken  into  consideration  as  regards  prognosis. 

Treatment. — The  treatment  of  this  affection  is  almost  necessarily  pal- 
liative. At  the  very  onset  of  the  attack,  when  the  patient  is  suffering  from 
the  shock  of  the  perforation,  a  full  hypodermic  injection  of  morphine 
will  be  found  of  service,  and  it  may  be  repeated  once  or  twice  a  day  for 
the  first  few  days.  If  the  patient  survives  for  a  few  days,  stimulants 
may  be  advantageously  administered,  and  he  must  be  sustained  by  a 
most  nutritious  diet.  Among  drugs,  musk  and  chloroform  are  recom- 
mended by  so  good  an  authority  as  Dr.  Walshe.  Hot  poultices  and  sooth- 
ing fomentations  give  relief  when  applied  over  the  chest.  The  que- 
bracho bark  is  now  given  for  relief  of  the  dyspnoea.  When  the  dyspnoea 
is  extreme  and  the  distress  of  the  patient  is  very  great,  and  a  considerable 
quantity  of  fluid  has  accumulated  in  the  pleural  cavity,  the  question  will 
arise  whether  a  free  opening  shall  be  made  through  the  chest  walls.  As  a 
rule,  this  must  be  regarded  as  a  palliative  measure,  and  should  be  resorted 
to  only  in  extreme  cases.  If  it  be  resorted  to,  a  fine  trochar  sliould  be  in- 
serted into  the  chest,  and  the  air  permitted  to  escape  through  a  connecting 
tube  under  water,  until  an  equilibrium  has  been  established.  It  may  give 
relief  for  a  time,  and  it  is  justifiable  to  resort  to  it  when  the  fluid  collec- 
tion is  abundant  and  the  febrile  excitement  is  intense.  It  may  delay  the 
fatal  termination.     Walshe  recommends  general  bleeding  or  dry  cupping.' 

HYDEOTHOEAX. 

Uydrotliorax  is  anon-inflammatory  fluid  effusion  into  one  or  both  pleural 
cavities  ;  it  often  accompanies  general  dropsy.  The  fluid  is  generally  clear, 
of  a  yellowish-green  color,  and  may  be  sufficient  in  quantity  to  compress  to 
a  considerable  extent  one  or  both  lungs.     It  may  occur  in   any  chronio 

1  JJis.  of  Heart,  etc. 


170  DISEASES   OF  THE   EESPIEATORY   ORGAKS. 

exhausting  disease  which  causes  general  hydraemia.  It  rarely  occurs  as  the 
sole  morbid  process  in  the  human  body.  In  a  large  number  of  autopsies 
a  small  amount  of  clear  or  bloody  serum  will  be  found  in  the  pleural  cavi- 
ties, which  is  merely  the  result  of  post-mortem  changes  ;  such  conditions 
should  not  be  regarded  as  evidence  of  hydrothorax. 

Etiology. — Any  disease  or  condition  {e.  g.,  mitral  disease  especially)  that 
impedes,  and  raises  the  pressure  in,  the  venous  circulation  will  cause  it. 
Thus  it  may  be  caused  by  the  pressure  of  enlarged  glands ;  tumors  and 
venous  thrombi  may  induce  it ;  also  diseases  of  the  heart  and  kidneys,  the 
cancerous  and  other  cachexise.  Hydrothorax  generally  occurs  in  connec- 
tion with  general  anasarca,  such  as  is  developed  in  Bright's  disease. 

Symptoms. — It  generally  comes  on  insidiously,  and  its  development  is 
attended  by  no  febrile  symptoms.  Its  occurrence  is  marked  by  steadily  in- 
creasing dyspnoea,  until  the  patient  reaches  a  condition  of  extreme  distress, 
and  orthopnoea  ;  the  lips  become  livid,  the  finger-ends  blue,  and  the  res- 
piration gasping.  He  is  unable  to  lie  down  and  can  speak  only  in  mono- 
syllables. On  physical  examination  there  will  be  found  the  signs  of  fluid 
in  both  pleural  cavities.  There  may  be  a  short,  dry  cough.  If  the  effusion 
is  large,  the  action  of  the  heart  will  be  embarrassed,  as  shown  by  a  small, 
feeble  pulse.  All  the  phenomena  which  attend  this  condition  are  due 
to  mechanical  pressure  caused  by  the  presence  of  fluid  in  the  pleural  cavi- 
ties, and  patients  die  cyanosed  as  the  result  of  diminished  breathing 
capacity. 

Differential  Diagnosis. — Ordinarily  the  diagnosis  of  hydrothorax  is  readily 
made.  It  may  be  confounded  with  suh-acute  pleurisy,  but  generally  the 
history  of  the  case  will  determine  the  character  of  the  effusion.  Then,  its 
simultaneous  occurrence  on  both  sides  in  connection  with  general  dropsy, 
without  any  irritant  or  attendant  fever,  will  be  sufficient  to  enable  one  to^ 
make  the  diagnosis  of  hydrothorax.  It  may  be  mistaken  for  pulmonary 
oedema  ;  the  two  conditions  are  very  likely  to  occur  together,  but  in  pul- 
monary oedema  a  crackling  sound  will  be  heard  over  the  oedematous  lung, 
which  sound  is  not  present  in  hydrothorax,  and  there  will  be  copious, 
watery  (perhaps  blood-stained)  expectoration,  which  is  absent  in  hydro- 
thorax. In  emphysema  the  increased  resonance,  and  in  bronchitis  the 
sputum  and  rales,  will  suffice  to  differentiate  the  three  conditions.  An 
enlarged  (painless)  liver  will  not  be  mistaken  for  dropsy  of  the  chest.  The 
physical  sign  of  hydrothorax  is  fluid  in  both  pleural  cavities  which  is  freely 
movable  by  a  change  in  the  position  of  the  patient,  and  is  not  attended  by 
friction  sounds  or  vocal  fremitus.  The  introduction  of  a  trochar  and  with- 
drawal of  the  fluid  will  decide  the  case. 

Prognosis. — The  danger  attending  hydrothorax  will  depend  to  a  great 
extent  on  the  general  condition  of  the  patient  at  the  time  of  its  occurrence. 
When  it  occurs  in  connection  with  general  anasarca  in  Bright's  disease,  oT 
in  extensive  heart  disease,  it  may  prove  the  direct  cause  of  death.  The 
majority  of  cases  yield  readily  to  treatment,  and  life  may  be  prolonged 
months,  even  years,  by  judicious  management. 

Treatment. — The  general  treatment  of  hydrothorax  corresponds  to  that 


H^MOTHOEAX. — PULMOZsTARY    PHTHISIS.  171 

for  the  removal  of  dropsical  accumulations  in  other  parts  of  the  body.  It 
is  a  simple  dropsical  elfusion,  and  can  be  removed  by  the  administration  of 
remedies  which  diminisli  the  quantity  of  water  in  the  blood.  Such  reme- 
dies are  the  hydragogue  cathartics,  diuretics  and  that  general  class  of 
agents  employed  for  the  removal  of  fluid  from  the  areolar  tissue.  Elaterium 
is  the  best.  Digitalis  should  be  given  (P.  Anstie),  and  as  soon  as  its  effects 
show,  the  muriated  tincture  of  iron  (gtt.  xx  every  six  or  seven  hours)  should 
be  given.  In  many  cases  it  will  be  impossible  to  wait  for  the  effects  of  diu- 
retics and  hydragogue  cathartics,  as  the  patient  will  die  unless  immediate 
relief  from  the  pressure  of  the  fluid  is  afforded.  Under  such  circumstances 
the  aspirator  may  be  used  with  advantage.  Those  remedies  may  be  em- 
ployed which  are  of  service  in  the  treatment  of  general  anasarca. 


HEMOTHORAX. 

Hmmothorax  is  the  escape  of  blood  into  the  pleural  cavity  ;  it  is  never  a 
primary  affection.  The  escape  of  any  considerable  quantity  of  blood  into 
the  pleural  cavity  may  occur  in  connection  with  cancer  of  the  lung  or 
pleura,  from  the  bursting  of  an  aneurism,  the  rupture  of  the  pleura  follow- 
ing an  extensive  pulmonary  apoplexy  and  accompanied  by  escape  of  blood 
from  the  lung,  and  the  rupture  of  a  vessel.  It  may  be  due  to  traumatic 
causes,  a  vessel  being  injured,  as  in  fracture  of  the  ribs.  Sometimes  blood 
is  mixed  with  pleuritic  effusion,  the  product  of  pleuritic  inflammation  in 
those  of  a  scorbutic  or  purpuric  diathesis.  Fluid  blood  in  the  pleural  sac 
soon  excites  inflammation,  whose  products  are  usually  serum  with  a  varia- 
ble admixture  of  pus. 

The  symptoms  of  haemothorax  are  those  of  liquid  accumulation  in  the 
pleural  cavity  with  the  accompanying  evidences  of  internal  hemorrhage, 
pallor,  syncope,  etc.,  etc.  In  haemothorax,  dyspnoea  is  sometimes  greatest 
at  the  onset,  diminishing  gradually. 

In  those  cases  where  there  is  no  appreciable  traumatic  cause  for  the  bleed- 
ing, all  that  can  be  done  is  to  keep  the  patient  at  rest.  Opiates  are  not 
contra-indicated.  Stimulants  may  be  necessary.  In  some  instances  relief 
may  be  obtained  by  the  performance  of  paracentesis. 

PFLMOlSrAEY    PHTHISIS. 

At  the  present  day  there  is  no  subject  in  the  domain  of  practical  medi- 
cine concerning  which  competent  observers  differ  so  widely  as  in  the  inter- 
pretation of  the  anatomical  changes  which  are  met  Avitli  in  pulmonary 
phthisis.  For  one  class  of  observers  phthisis  is  an  inflam7natory  process 
which  may  or  may  not  be  secondarily  complicated  by  tubercle ;  another 
class  maintain  that  tubercle  is  the  primary  and  essential  lesion  of  all  phthi- 
sis. Still  more  recently  certain  investigators  maintain  that  there  is  a 
specific  material  in  phthisical  processes,  which  may  or  may  not  be  accom- 
panied by  the  histological  elements  of  miliary  tubercle,  but  which  always 


172  DISEASES    OF   THE    EESPIRATORT    OEGAISTS. 

has  a  specific  form  of  bacteria — the  tulerch  hacillus — as  the  sole  exciting 
cause  of  its  development. 

Clinically  and  pathologically  two  varieties  of  phthisis  can  be  recognized 
— the  acute  and  clironic.  The  pathological  changes  of  the  former  are 
quite  well  settled ;  but  the  great  difference  of  opinion  which  exists  in 
regard  to  the  morbid  changes  of  chronic  phthisis  is,  to  say  the  least, 
confusing.  This  diversity  compels  to  the  opinion  that  tubercle  is  either 
absent  or  plays  but  a  secondary  part  in  a  large  proportion  of  cases. 

Acute  phtJiisis. — The  morbid  changes  of  acute  phthisis  are  a  complex  of 
inflammation  and  the  rapid  development  of  tubercular  tissue  in  the  lung 
substance. 

Clironic  phthisis. — The  essential  pathological  change  of  chronic  phthisis 
is  consolidation  and  induration  of  lung  substance.  Tubercles  may  or  may 
not  be  its  primary  lesion,  and  when  present  they  may  constitute  but  a  small 
part  of  the  morbid  processes.  It  is  difficult  and  perhaps  impossible  to 
draw  a  sharp  line  of  demarcation  between  the  different  varieties  of  chronic 
phthisis.  Yet  by  the  prominence  of  certain  lesions  it  is  possible  to  dis- 
tinguish :  flrst,  a  variety  in  which  bronchitis,  pneumonia,  and  pleurisy  are 
intimately  associated  with  the  development  of  tubercular  tissue  ;  this  has 
been  recently  called  "tuberculous  lobular  pneumonia  ;^'  the  old  term  "  ca- 
tarrhal phthisis  "  indicates  equally  well  the  nature  of  the  primary  changes. 
Secondly,  a  variety  where  the  chief  lesion  is  the  production  of  new  tissue 
in  the  substance  of  the  lung,  the  new  growth  being  arranged  either  as  dense 
nodules  in  a  firm  tissue,  or  as  a  diffuse  infiltration  ;  in  the  latter  case  much 
of  the  lung  is  converted  into  a  dense  fibrous-looking  mass.  "  Tuberculou\, 
interstitial  pneumonia^''  is  suggested  as  the  name  for  this  variety,  but  tht> 
term  "fibroid  phthisis"  better  indicates  its  essential  changes.  Thirdly,  a 
variety  which  has  received  the  name  of  chronic  tubercular  phthisis,  in 
which  numerous  disseminated  nodules,  larger  and  harder  than  those  met 
with  in  acute  phthisis,  are  found  scattered  throughout  the  lung. 

ACUTE    PHTHISIS. 

Acute  phthisis  usually  occurs  in  young  subjects.  Its  advent  and  br^ef 
course  are  marked  by  high  temperature,  a  rapid  pulse,  hurried  respiration, 
pain  in  the  chest,  rapid  emaciation  and  general  loss  of  strength,  haemopty- 
sis, and  the  physical  signs  indicative  of  rapid  pulmonary  consolidation. 

Morbid  Anatomy. — A  lung  in  acute  phthisis  appears,  on  section,  to  be 
consolidated  throughout  the  whole  or  a  part  of  its  extent ;  the  consolidated 
portions  have  a  gross  appearance  resembling  red  hepatization,  interspersed 
with  diffuse  yellow  and  grayish  spots.  The  external  surface  of  the  lung 
may  appear  normal,  or  show  spots  of  yellow-gray  solidification.  Scattered 
through  the  lungs  may  also  be  found  extensive  patches  of  consolidated  tis- 
sue, the  central  portions  of  which  exhibit  yellow  or  yellowish-white  masses. 
The  material  in  the  alveoli  is  inclosed  in  a  fibrillated  mesh-work  (similar  to 
that  in  lobar  pneumonia)  and,  microscopicall}^,  is  found  to  consist  of  pus 
and  epithelial  cells  that  have  become  granular,  fatty,  swollen  or  distorted  in 


ACUTE   PHTHISIS. 


173 


Fig.  36. 

Acute  Phthisis. 

Section  of  Lung  showing  a  single  alveolus. 

A.  Wall  of  alveolvs.—B.  Pus  ccymuscles.—  C.  Cavity  of 

alveolus.— D.  Fibrillar  mesh.—E,  E.  Distorted,  fatty  and 

granular  epithelial  cells,     x  300. 


shape,  associated  with  a  shining,  transhicent,  homogeneous  substance  ;  this 
fibrinous  exudation  is  less  solid  than  that  of  acute  lobar  pneumonia. 
Though  its  evolution  is  not  dissimilar  (as  there  is  no  tendency  to  cheesy 
degeneration,  and  complete  reso- 
lution can  take  place),  yet  mor- 
phologically it  is  distinct.  Both 
lungs  may  be  equally  involved. 
This  stage  of  so-called  "  red  hepa- 
tization "  is  rapidly  reached.  In 
some  cases  of  acute  phthisis  the 
only  change  found  may  be  an 
accumulation  of  epithelia  in  the 
alveoli,  with  more  or  less  cellular 
infiltration  of  the  alveolar  walls. 
In  the  hepatized  mass  are  nodules 
of  tubercle  tissue  that  vary  in 
size.  They  are  bloodless,  hard 
and  white,  and,  agglomerating, 
press  upon  and  obstruct  the  vessels 
in  the  alveolar  walls.  Similar 
nodules  surround  the  small  bron- 
chioles and  air-cells.  The  walls 
of  the  bronchioles  are  more  or 

less  implicated  and  are  infiltrated  with  cells.     Their  lumen  is,  in  the  major- 
ity of  cases,  filled  with  changed  epithelia,  pus  and  fibrin.     These  are  called 

"tuberculous  zones."  They 
are  bloodless.  A  peri-bronchitis 
which  may  be  tubercular  exists 
in  all  cases  and  advances  uninter- 
ruptedly from  the  smaller  to  the 
larger  bronchi.  Infiltration  of 
peri-bronchial  tissue  is  followed 
by  proliferation  of  the  lymph 
follicles  in  the  bronchial  walls. 
Infiltration  of  the  bronchial  walls 
by  tuberculous  material  prone  to 
caseous  degeneration  is  followed 
by  sub-epithelial  abscess'  and 
ulcers  that  gradually  extend. 
Dilatation  follows,  and  the  bron- 
chial wall  becomes  disorganized, 
and  cavities  of  considerable  size 
are  thus  formed. 

In  the  midst  of  the  hepatized 
or  tubercular  tissue  are  spots  that 
Tissue  that  has  become  necrotic 


Fi«.  37. 
Acute  Phthisis. 
Bection  of  Lung  showing  a  single  alveolus  in  stage  of  hepa- 
tization. 
A.  Wall  of  alveolus,  with  in  fllf  ration  of  pus  at  B,  B. 
C.  Cavity  of  alveolus  nearly  filled  with  changed  epithelia 
and  a  few  pus  corpuscles. 
J),  D.  Fibrillar  mesh  enclosing  the  cell  elements. 


300. 


have  undergone  "coagulation  necrosis. 


'  Called  "  tubercular  "  by  Rindfleiech. 


174 


DISEASES    OF   THE   RESPIRATORY   ORGANS. 


in  this  way  is  very  abruptly  and  distinctly  outlined  from  the  adjacent  con- 
solidated lung.  It  may  remain  thus  without  further  change,  or  it  may 
suffer  cheesy  degeneration.  Cheesy  nodules  may  remain  unchanged,  or 
they  may  soften  and  form  cavities  that  vary  in  size  according  to  the  extent 
of  the  original  "  coagulation  necrosis."  ^  The  nodules  may,  if  resolution  of 
the  alveolar  exudate  occurs,  pass  into  and  be  surrounded  by  firm  inter- 
alveolar  fibrous  tissue.  Occlusion  of  the  branches  of  the  pulmonary  artery 
is  one  of  the  explanations  that  have  been  advanced  to  account  for  the 
'* coagulation  necrosis."  Another  is  the  rapid  accumulation  of  tubercular- 
tissue,  that  shuts  off  the  adja- 
cent blood  supply,  and  thus 
induces  necrosis.  Neither  view 
as  yet  is  accepted ;  but  it  is 
evident  that  the  areas  of  coagu- 
lation necrosis  soften  and  cause 
a  rapid  destruction  of  lung- 
tissue  which  resultsin  theforma- 
tion  of  cavities.^ 

Etiology. — The  most  frequent 
cause  of  acute  phthisis  is  defec- 
tive nutrition,  associated  with 
lymphatic  and  glandular  en- 
largements. When  these  con- 
ditions exist  all  the  predisposing 
causes  of  chronic  phthisis  pre- 
dispose to  this  form  also.  The 
exact  nature  of  its  essential 
cause  is  still  obscure ;  efforts 
to  discover  the  peculiar  elements 
which  give  to  tubercle  a  specific 
character  have  been  abundant, 
but  the  statements  of  various 
observers  who  claim  to  have 
discovered  a  tubercle  bacillus  lacked  demonstrative  proof  until  the 
researches  of  Koch  were  made  public,  when  he  announced  the  discov- 
ery of  a  bacillus  which  is  found  in  tubercles  and  in  them  alone.  Basing  his 
statements  on  a  series  of  experiments  many  times  repeated,  in  which  this  ba- 
cillus was  isolated  from  tubercle,  cultivated  in  a  solid  menstruum  under  the 
microscope,  and,  finally,  shown  by  inoculation  to  produce  general  tubercu- 


Fis. 

Coagulation  Necrosis. 

Section  of  Lung  through  an  area,  near  a  bronchial  tube,  in 
which  the  vascular  supply  has  been  cut  off. 

A.  Area  of  coagulation  necrosis.  The  alveoli  are  so 
filled  with  inflammatory  products  that  their  wails 
are  obscwed. 

B,  B,  B.  Pulmonary  tissue  around  the  necrosed  area.     The 

alveoli  are  here  filled  with  catarrhal  products. 

C,  C,  C.  Normal  lung,     x  30. 


1  Cohnheim  and  Weigert. 

2  The  acnte  phthisis  described  by  Williams  (in  "  Quain's  Dictionary")  is,  according  to  that  investiga- 
tor, marked  by  consolidation  of  the  lungs,  adherent  pleurse,  indurations  consisting  of  red  hepatization  and 
caseous  infiltration  (the  latter  largely  predominating),  with  but  little  or  no  miliary  tubercle  present.  Exca- 
vation quickly  succeeds  consolidation,  and  pneumothorax  is  often  the  result.  Others  describe  an  acute 
tuherculo-vmiimonic  phthisis,  a  "  connecting  link,"  as  It  were,  between  the  acute  and  chronic  varieties. 
The  tubercle-tissue  aggregates,  caseates,  and  rapidly  forms  cavities,  while  fresh  tubercle-tissue  is  being 
developed  elsewhere  in  the  lung.— Fox,  in  "  Beynolds''  System;'  states  that  in  acute  phthisis  soft  dif- 
fluent miliary  tubercular  deposits  are  found  with  ulcerous  and  irregular  anfractuous  cavities.  Engorged 
"  pneumonic  "  lung  intervenes  ;  the  bronchi  are  loaded  with  pus.  The  disease  resembles  gray  hepati- 
zation, and,  like  it,  is  oftenest  irwst  developed  in  the  lower  lobe. 


ACUTE  PHTHISIS.  175 

losis,  he  concludes  that  the  active  etiological  element  in  tubercle  is  a  dis- 
tinct lacillus,  and  that  tubercle  is  not  found  where  this  organism  is  not 
present.  It  is  not  his  claim,  however,  that  all  those  anatomical  elements 
which,  from  a  purely  histological  classification,  have  been  called  tubercle, 
are  due  to  the  presence  of  this  bacillus,  but  only  that  those  pathological 
changes  which  are  preceded  by  the  presence  of  this  oi'ganism  should  be 
called  tubercle.  The  applicability  of  these  conclusions  to  tubercle  as  found 
in  man  rests  solely  upon  the  supposition  of  the  identity  of  the  two  condi- 
tions in  man  and  the  lower  animals,  an  identity  which,  while  it  may  be  very 
generally  accepted  by  pathologists,  has  been  proven  only  by  inoculations 
fro7n  man  and  not  inversely.  Observations  of  the  truth  of  Koch's  state- 
ments, in  part,  are  abundant,  and  it  is  the  universal  testimony  that  the 
bacilli  described  are  found  in  tuberculous  matter.  The  success  of  various 
observers  in  finding  these  bacilli  is  not  uniform.  Some  report  bacilli  pres- 
ent in  all  cases  of  tubercle,  while  others  find  them  absent  in  a  varying  per- 
centage of  cases.  Beyond  this  point  Koch's  experiments  have  not  been 
repeated. 

The  case  at  present  may  be  stated  as  follows  :  the  presence  of  a  distinct 
bacillus  in  connection  with  tubercle  and  its  absence  in  all  other  morbid 
conditions  are  generally  confirmed  by  the  most  competent  observers. 
The  etiological  relation  of  this  bacillus  to  phthisis  still  rests  solely  upon 
Koch's  demonstration.  Observers  are  not  wanting  who  deny  entirely  not 
only  any  etiological  relation,  but  even  that  this  bacillus  is  confined  to  tu- 
bercular tissues  ;  but  they  fail  to  present  satisfactory  experimental  proof  in 
support  of  such  statements.  German  pathologists,  on  the  other  hand,  among 
whom  are  Cohnheim,  Frankel  and  Schottelius, — at  one  time  the  most  able 
opponents  of  the  infectious  character  of  tubercle, — accept  its  specific  nature 
as  a  fact  entirely  proven. 

This  form  of  phthisis  is  oftenest  met  with  in  the  young  who  have  grown 
rapidly  and  who  have  a  strong  inherited  phthisical  taint.  Children  who 
have  been  nursed  by  phthisical  mothers  are  especially  liable  to  its  develop- 
ment. 

Symptoms. — A  young  adult  who  for  some  time 
has  had  a  dry,  hacking  cough  with  a  gradual 
but  steady  emaciation,  is  suddenly  seized  with  a 
sharp  pain  in  the  side  ;  the  pulse  becomes  rapid 
and  feeble,  and  the  temperature  rises  to  104°  in 
the  evening,  while  the  morning  temperature  may 
be  normal.  With  increase  in  pulse-rate  and 
temperature  the  skin  becomes  pungently  hot. 
The  fever  alternates  with  night  chills  and  profuse 
sweats.     The  cough  is  soon  accompanied  by  an  ^^^ 

opaque,   purulent  expectoration,    in   which   are  .  ^  '     ^^^^. .   , 

„•'     ^,    '     ^  .-,-,,        .,,.    '  T,  ,      ,.       Tubercle    Bacilli    from  Phthisical 

found  numerous  tubercle  bacilli  and  yellow  elastic    sputum,  stained  with  Fuchsin. 
fibres.     There  is  rapid  loss  of  flesh  and  strength  :  a.  miatea bacuu. 

, .       ,    ,  -^         ,  ■,  .  ?  <  1  B.  Groupn  of  the  same.   ^ 

the  patient  becomes  extremely  ansemic  ;  and  the      The  unstained  granular  deiH* 

,       ,   ,  .  ,  -,  J.    1  -I    of  nus  corpuscles  and  mucus  are 

constant  harassing  cough  causes  loss  oi  sleep  and  seekjaintiy  at  c,  d.   x  50o. 


176 


DISEASES    OF   THE   KESPIEATORY   OEGANS. 


extreme  exhaustion.  The  expectoration  is  usually  not  abundant  until  after 
breaking  down  of  the  lung-tissue  has  occurred.  Patients  ascribe  the  ema- 
ciation and  weakness  to  the  profuse  sweats.      The  respirations  and   the 


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Fig.  40. 
Temperature  in  a  case  of  Acute  Phthisis.    Patient  a3t.  25.    The  larger  falls  of  temperature,  on  the  5th,  9th, 

16th  and  24th  days  followed  the  administration  of  sulphuric  ether.     Falls  of  a  degree  and  a  degree  antf 

a  half  were  induced  by  large  doses  of  the  sulphate  of  quinine. 
Death  occurred  after  a  steady  rise  in  temperature  for  a  week  preceding. 


pulse-rate  increase  in  frequency  with  the  fever.  The  pulse  ranges  from 
120  to  135.  Cardiac  palpitation  and  sudden  acceleration  of  the  pulse-rate 
follow  excitement.  In  some  cases  the  chill,  fever  and  sweat  occur  with 
such  regularity  that  malarial  fever  is  suspected  or  a  malarial  element  is 


ACUTE   PHTHISIS.  177 

regarded  as  the  prominent  feature.  Nausea,  yotniting  and  diarrhoea  are 
often  prominent  symptoms,  and  greatly  add  to  the  exhaustion  which  is  so 
marked  a  feature  of  the  disease.  The  skin  assumes  a  pearly  pallor,  the 
hectic  flush  is  present,  and  the  eyes  are  bright  and  glistening.  HaBmopty- 
sis  may  mark  the  advent  of  the  disease  and  recur  at  intervals  during  its 
course.  It  is  rarely  absent  during  the  entire  course  of  the  disease. 
Anorexia  is  always  a  marked  symptom.  Not  infrequently  the  destructive 
processes  are  so  rapid  as  to  cause  pneumothorax.  Acute  phthisis  usually 
pursues  a  steadily  progressive  course,  but  it  may  assume  an  intermittent 
character,  and  have  periods  of  arrest  and  apparent  amendment,  followed 
by  periods  of  exacerbation  and  rapid  progress. 

Physical  Signs. — The  physical  signs  will  vary  with  the  seat  and  extent  of 
pulmonary  consolidation,  and  with  the  rapidity  with  which  destructive 
processes  are  established. 

Inspection,  during  its  early  stage,  shows  rapid  respiration  and  imperfect 
expansion  of  the  upper  part  of  the  chest  during  a  deep  inspiration  ;  as 
the  disease  advances  the  loss  of  expansion  becomes  more  and  more  ajoparent, 
but  there  is  no  infra-clavicular  retraction. 

On  palpation  the  loss  of  motion  in  the  infra-clavicular  spaces  is  more 
apparent;  and  if  the  pleuritic  changes  are  not  extensive  there  will  be 
increased  vocal  fremitus. 

On  percussion  there  will  be  more  or  less  dulness  over  the  infra-clavicu- 
lar spaces.  If  there  are  large  superficial  cavities  which  contain  little  fluid, 
there  will  be  amphoric  or  cracked-pot  resonance. 

Upon  auscultation,  in  the  early  stage,  expiration  is  notably  prolonged 
and  high  pitched,  and  fine  mucous  rdles  with  fine  crepitation  will  be  heard 
over  the  affected  district.  The  respiration  is  wavy  and  interrupted.  There 
may  be  distinct  bronchial  breathing  and  bronchophony  over  a  circumscribed 
space  posteriorly  in  the  scapular  region.  Excavations  take  place  rapidly  in 
the  consolidated  portions  of  the  lung  ;  they  are  of  varying  size  and  are  sit- 
uated at  varying  distances  from  the  surface  of  the  lung.  Deeply  seated  cav- 
ities, when  filled,  give  deep-seated  dulness,  and,  when  empty,  an  exaggerated 
percussion  resonance.  Over  sm.all  cavities  with  lax  walls  low-pitched  puff- 
ing, cavernous  respiration  will  be  heard.  This  is  very  frequently  heard 
in  acute  jjMliisis  wliere  soft  yielding  walls  result  from  rapid  'pulmonary  ne- 
crosis. Amphoric  breathing,  gurgles  and  metallic  tinklings  will  be  heard 
over  large  cavities  which  communicate  freely  with  bronchial  tubes.  The 
sub-clavian  murmur  (discussed  in  chronic  phthisis)  is  not  so  liable  to  be 
heard  in  acute  as  in  chronic  phthisis. 

Differential  Diagnosis. — Acute  phthisis  may  be  mistaken  for  croupous  pneu- 
monia, troncliiectasis  and  acute  general  capillary  bronchitis. 

In  pneumonia  the  prolonged  ushering-in  chill,  the  continuous  high 
temperature,  the  characteristic  sputum,  the  dulness  limited  to  a  lobe  and  the 
pneumonic  countenance,  are  symptoms  which  readily  distinguish  it  from 
acute  phthisis.  In  some  cases  the  differential  diagnosis  cannot  be  made 
during  the  first  week.  Bronchiectasis  accompanied  by  wasting,  fetid  ex- 
pectoration, haemoptysis  and  night  sweats,  with  the  physical  signs  of  con- 
12 


178  DISEASES    OF   THE   RESPIEATOEY   OEGAKS. 

■solidation,  may  well  be  mistaken  for  the  adyanced  stage  of  acute  plitlii»/k^. 
In  phthisis  the  signs  of  conso\ida,tion  precede  those  of  cavities  ; — in  bronchi- 
ectasis they  follow  them.  Fever  and  emaciation  are  always  greater  in 
phthisis  than  in  bronchiectasis,  and  the  symptoms  are  more  steadily  pro- 
gressive. In  capillary  hroncliitis  there  is  no  dulness  on  percussion,  sub- 
crepitant  rales  are  heard  on  both  sides  of  the  chest,  and  there  is  no  bron- 
chial character  to  the  respirations.  The  temperature  range  is  lower  than 
in  phthisis.  Emaciation  is  rapid  in  phthisis,  and  the  signs  of  the  forma- 
tion of  cavities  occur  early. 

Prognosis. — The  prognosis  in  acute  phthisis  is  always  unfavorable.  Its 
average  duration  is  from  five  weeks  to  five  months.  A  sudden  amelioration 
of  the  symptoms  may  occur  before  the  cavities  are  formed,  but  the  ameliora- 
tion is  one  of  short  duration  and  is  usually  followed  by  a  more  rapid  prog- 
ress of  the  disease.  It  may  be  complicated  by  pleurisy,  pneumothorax, 
hydrothorax,  peritonitis,  and,  rarely,  by  pericarditis.  Death  may  occur 
from  exhaustion,  asthenia,  or  complications.  Acute  capillary  bronchitis 
and  pulmonary  oedema  and  congestion  often  lead  to  a  rapidly  fatal  termina- 
tion. 

Treatment. — Most  cases  are  hopeless  ;  the  dietetic  and  climatic  meth- 
ods employed  in  chronic  phthisis  have  no  place  in  the  management  of  acute 
phthisis. '  Morphia  in  small  doses — one-twentieth  of  a  grain  hypodermic- 
ally  every  six  or  eight  hours — has,  in  my  hands,  been  more  satisfactory  in 
staying  the  progress  of  the  disease,  prolonging  life  and  keeping  the  patient 
comfortable,  than  any  other  plan. 


CHEONIC    PHTHISIS. 

The  first  variety  of  chronic  phthisis, — which  may  be  designated  as  tuber^. 
cular  pneumonia  or  catarrhal  phthisis, — is  preceded  or  accompanied  by 
the  pathological  changes  of  localized  bronchitis,  lobular  consolidation  and 
pleurisy. 

Morbid  Anatomy. — The  primary  changes  are  in  the  bronchi  and  in  the 
cavities  of  the  alveoli,  which  become  more  or  less  filled  with  cellular  ele- 
ments mingled  with  other  inflammatory  exudation  products.  The  bronchial 
exudation  is  usually  abundant  and  purulent.  It  has  been  recently  claimed 
that  the  tubercular  infection  is  contained  in  it.  After  a  time  amass  of  cells 
obstructs  the  bronchioles  and  becomes  cheesy.  The  nutrition  of  the  walls  of 
the  bronchial  tubes  at  the  site  of  the  obstruction  is  interfered  with  and  they 
become  attenuated,  or  a  peri-bronchitis  is  developed.  The  peri-bronchitis 
may  be  tuberculous,  fibrous,  or  purulent.  An  ulcerative  process  may  also 
be  established  at  the  site  of  the  obstruction.  Ulcers  thus  formed  in  the 
tubes  are  usually  sharply  defined  and  shallow  ;  sometimes  they  involve  the 


1  Dr.  McCall  Anderson  (in  London  Lancet,  June,  1877)  takes  a  more  hopeful  view  of  tliese  cases,  and 
claims  that  subcutaneous  injections  of  atropia  check  the  exhausting  sweats  ;  and  that  quinine,  digitalis 
and  opium  reduce  the  temperature,  and  if  they  fail,  ice-cloths  to  the  abdomen  will  accomplish  the  desired 
result.  His  reported  results  are  exceedingly  encouraging,  but  the  failure  of  his  treatment  as  tried  by  oth- 
ers causes  many  to  doubt  his  diagnosis. 


CHRONIC   PHTHISIS. 


179 


A,  A 
B. 


adjacent  lung  substance  as  well  as  the  bronchial  walls.  These  cheesy  masses 
are  found  in  patches.  The  air-vesicles  become  filled  in  one  of  two  ways  : 
(1)  by  polypoid  outgrowths  from  the  alveolar  walls,  consisting  of  round  and 
polygonal  cells  in  a  basement  substance; 
or,  (2)  a  mass  of  similar  cells — with  or 
without  giant-cells — not  in  connection 
with  the  alveolar  walls,  partially  fills 
the  vesicles  of  the  affected  lobules,  the 
intervening  space  being  filled  with 
catarrhal  products.  These  masses  vary 
in  size.  They  may  be  limited  to  a 
single  lobule  or  they  may  attain  the 
size  of  a  hazel-nut.  When  they  pass 
into  the  caseous  state  all  the  elements 
of  the  exudation  become  granular, 
and  are  agglutinated  by  a  slightly  trans- 
parent granular  substance  which  glis- 
tens like  fibrin  upon  the  addition  of 
acetic  acid.  These  foci  are  friable  and 
present  a  gray  homogeneous  appear- 
ance, resembling  the  so-called  yellow 
tubercle. 

The  gross  appearance  of  lung-tissue 
involved  in  this  form  of  phthisis  varies.  "^  '''^' 

It  may  be  of  a  gray  color,  hard  and  glistening,  described  by  Laennec 
as  "gray  infiltration;"^  or  it  may  appear  as  a  colloid  jelly-like  mass 
{" gelatiniform  infiltration"  of  Laennec,  or  the  "colloid  caseous  pneu- 
monia "  of  Thaon).  Early  in  this  process  lymphoid  cells  infiltrate  the  alve- 
olar septa,  which  may  break  down  or  become  hardened  and  thickened  from 
new  tissue  developments.  Similar  cellular  infiltrations  may  also  occur  in 
the  walls  of  the  bronchioles.  Pressure  causes  obliteration  of  the  vessels  and 
subsequent  caseation  ;  and  in  this  way  large  tracts  of  gray  pneumonia^  are 
converted  into  yellow  masses.  Charcot  claims  that  in  caseous  pneumonia 
he  finds,  as  in  gray  granulation,  two  zones  :  (1)  a  central  region  consisting 
of  exudation  products,  cheesy  debris,  and  fibres  of  lung-tissue  ;  and,  (3)  a  pe- 
ripheral region,  made  up  of  adenoid  growths  and  giant-cells — "  zone  ernbry- 
onnaire."  These  last  two  he  regards  as  the  basis  of  tubercle — always  a 
peri-bronchial  product — and  that  caseation  does  not  take  place  unless  they 
are  present.  When  a  few  lobules  only  are  involved,  they  may  become  en- 
capsulated, or,  by  a  proisess  similar  to  that  described  in  lobular  pneumonia, 
they  may  undergo  resolution.  It  is  rare,  however,  for  a  lung  to  return  to 
its  normal  condition  unless  the  nodules  are  small  and  few  in  number. 
Even  should  the  masses  be  removed,  obliteration  of  the  alveoli  which  they 
occupied  is  apt  to  occur.     If  a  cheesy  nodule  is  encapsulated,  cretaceous  or 


Fig.  41. 

Chronic  (Catarrlial)  Phthisis. 

Section  of  Lung  sfwwing  two  alveoli. 

Wall  of  alveoli  covered  with  changed  epithe- 
livm. 

"  Polypoid  wxtqrowth  "  frmn  the  alveolar 
wail  nearly  filling  the  air-vesicle — composed 
of  a  delicate,^  granvlar  basement  substance  in 
ivhich  are  imbedded  round  and  polygonal 
cells. 
C,  C.  Epithelial  cells  between  the  last  and  wall  of 
the  air-vesicle. 
D.  Alveolus  partly  filled  with  epithelial  and 
lymphoid  cells  in  the  basement  substance. 


'  The  infiltrated  tubercle  of  Laennec  is  considered  as  desquamative  pneurrwnia  by  Buhl  and  scrofulous, 
inflammation  by  Rindflemch. 
*  Called  "gray  infiltration." 


180 


DISEASES    OF    THE    RESPIRATOKY   ORGAN'S. 


chalky  material  is  found  in  the  centre  of  the  fibroid  tissue.  The  lung-tis. 
sue  between  these  nodules  may  be  anaemic,  hypergemic,  cedematous,  or  em- 
physematous, or  the  seat  of  atelectasis.  The  larger  the  nodule  and  the 
more  rapidly  it  has  formed,  the  more  liable  is  it  to  soften.  Cheesy  masses 
may  soften  and  by  a  process  of  ulceration  be  removed  through  the  bronchi. 
Absorption  of  caseous  matter  by  tlie  lymphatics  is  attended  by  more  or  less 
adenoid  hyperplasia,  and  a  group  of  miliary  granules  may  be  deyeloped 
about  a  caseous  centre,  the  remainder  of  the  lung  not  being  involved.  Some- 
times softening  and  ulceration  are  so  rapid  that  the  process  becomes  dis- 
tinctly gangrenous. 

Cavities.— The  walls  of  a  phthisical  cavity  are  always  irregular.  At  first 
they  are  soft  and  friable ;  later  they  become  tough,  smooth  and  fibrous. 
Bands  of  dense  connective-tissue  traverse  them,  sometimes  covered  by  a 

layer  of  granulation- 
tissue,  and  vessels  and 
large  bronchi  often 
extend  across  them. 
Sharply  "  cut-off"  stubs 
of  bronchi  often  project 
half  an  inch  from  their 
walls ;  portions  of  the 
wall  may  stand  out  like 
the  columnse  carnese  of 
the  heart;  or  the  sur- 
face may  be  uneven  or 
ragged.  The  connec- 
tive-tissue trabeculse  ex- 
tending across  a  cavity 
frequently  contain 
blood-vessels,  whose 
rupture  may  cause  fatal 
hsemoptysis.  When 
„  ^       ^  cavities  are  formed  the 

A.  Stump  of  small  bronchus.— B,  B.  Bands  of  flbnn.—  C.  Loop  of  j     xi 

blood-vessels  in  bed  of  cavity.— D.  Smaller  cavities  ope?iing  into  a    luUg-tlSSUe    arOUnd    the 
larger  one.  .,  -mi       •     -,         ,    j 

cavity  Will  be  indurated 
and  the  cavities  will  be  separated  from  one  another  by  bands  of  firm 
fibrous  tissue,  and  the  peri-bronchial  and  peri  vascular  connective-tissue 
sheaths,  and  the  thickened  pleura,  will  all  be  involved  in  an  indurative 
process.  Cavities  increase  in  size  by  peripheral  disintegration,  or  several 
small  ones  may  coalesce  and  form  one  large,  irregular  excavation.  Phthis- 
ical cavities  contain  air  and  a  grumous  purulent  fluid  of  a  yellowish  or 
greenish  color,  with  which  shreds  of  lung-tissue  may  be  mingled.  If  the 
growth  of  a  phthisical  cavity  becomes  arrested,  a  "limiting  membrane 
forms  on  its  inner  surface."  The  purulent  secretion  from  it  at  first  is 
abundant,  later  it  diminishes,  and  the  case  becomes  one  of  a  "quiescent 
cavity."  A  large  cavity  may,  by  contraction  of  the  fibrous  tissue  around 
it,  have  its  walls  approximated  but  not  united.     True  cicatrization  of  a 


Fig.  42. 
A  Lung  Cavity. 


CHROlSriC   FIBEOUS   PHTHISIS. 


181 


chronic  cavity  which  has  a  distinct  lining  membrane  rarely  if  ever 
occurs. 

Ulcerating  cavities  are  those  which  having  been  long  quiescent  take  on, 
for  some  reason,  an  ulcerative  process.  A  small  cavity  at  the  surface  of  the 
lung,  after  having  caused  a  localized  pleurisy  and  a  thinning  of  the  friable 
wall  of  consolidated  lung-tissue  which  separates  the  pleura  from  the  cavity, 
may  break  through  into  the  pleural  cavity  and  cause  pyopneumothorax. 
Pleurisy  is  rarely  absent  in  this  variety  of  chronic  phthisis  ;  firm  adhesions 
form,  and  the  pleura  may  be  from  three-quarters  of  an  inch  to  one  inch 
thick.  These  changes — pulmonary  and  pleuritic — are  best  marked  at  the 
apices. 

The  broncliial  glands  may  be  softened,  cheesy,  chalky,  pigmented  and 
enlarged.     The  right  heart  is  frequently  dilated  and  hyijertrophied. 


CHEOlSriC    FIBEOUS   PHTHISIS. 


Clironic  fibrous  pMliisis,  or  interstitial  tubercular  pneumonia,  is  charac- 
terized by  the  diffuse  development  in  the  lungs  of  dense  fibrous  tissue^ 
which  may  be  associated  with  tubercles. 

Morbid  Anatomy. — The  affected  lung  is 
diminished  in  size.  The  pleural  surfaces  are 
adherent  and  greatly  thickened.  A  section 
of  a  portion  of  lung  that  is  the  seat  of  this 
variety  of  phthisis  presents  a  smooth  or  granu- 
lar surface,  or  it  has  a  striated  appearance. 
If  granular,  the  granules  are  imbedded  in 
the  fibrous  mass.  The  fibrous  tissue  contains 
more  or  less  pigment  material,  which  gives 
to  the  cut  surfaces  a  bluish  or  gray  color. 
If  the  process  is  old  the  lung  will  be  tough  ; 
if  recent  it  is  less  resistant  and  less  leathery. 
When  the  disease  has  existed  for  a  long  time 
the  apex,  and  sometimes  the  whole  lung,  is 
converted  into  fibrous  tissue,  all  traces  of  the 
normal  lung-tissue  being  obliterated.  The 
indurated  tissue  may  be  studded  with  nodules. 
The  nodules  may  be  small  masses  of  dense 
fibrous  tissue  containing  a  few  cells  at  their 
centre,  masses  of  tubercular  tissue,  granu- 
lation-tissue enveloping  tubercles,  or  cheesy 
masses  with  tubercles  and  interlacing  fibrous 
bands.  Giant-cells  may  or  may  not  be  present  in  the  nodules.  The  con- 
nective-tissue growths  may  begin  in  the  walls  of  the  bronchi,  alveoli,  or 
blood-vessels,  in  the  septa,  or  in  the  pleura.  The  alveoli  are  at  times 
dilated,  at  times  narrowed  ;  they  are  always  deformed.  The  alveolar  epi- 
thelium undergoes  slight  multiplication  and  swelling.     New  cells  also  form 


Fig.  43. 
Chronic  (Fibrous)  Phtliisis. 

Part  of  a  section  of  pulmonary  tvberch 
showing  change  into  fibrous-tissue  with 
obliteration  of  contiguous  alveoli. 

A.  Centre  of  the  tubercle. — B.  Periphery 
of  the  same  altered  into  fibrous  co7inec- 
tive-tissue. — C.  Growth  of  the  fibrous 
tissue  in  the  alveolar  walls.— D  D.  Two 
air-vesicles  in  process  of  solidification, 
X  100. 


183 


DISEASES   OF   THE   RESPIEATORY   ORGAN'S. 


in  the  walls.     Cheesy  masses,  specks  of  cretaceous  material  and  cayitied 
of  varying  size  are  found  in  the  hard  lung. 

The  bronchi  are  at  times  thickened,  at  times  thinned.  Bronchiectatic 
cavities  (cylindrical,  fusiform  or  sacculated)  are  found,  chiefly  in  the  apex. 
The  appearance  of  these  cavities  is  similar  to  that  described  in  chronic  in- 
terstitial pneumonia.  Through  ulcerative  processes  cavities,  often  of  large 
size,  result  from  these  bronchiectases.  As  the  disease  progresses,  more  and 
more  of  the  tubercle-tissue  is  changed  into  connective-tissue.  But  while  the 
growth  of  connective-tissue  is  extra-alveolar,  the  tubercle-tissue  is  both 
extra  and  intra-alveolar.  The  early  stage  of  connective-tissue  development 
consists  in  the  accumulation  of  a  large  number  of  small  cells  looking  like 
granulation-tissue  and  lymphoid  cells,  while,  in  the  later  stages,  we  find 
dense  fibrillated  tissue  containing  a  few  cells — and  those  spindle-shaped — 
and  an  abundant  supply  of  irregular  blood-vessels.  Tubercles  may  also  be 
found  in  the  pleura. 

Anthracosis — from  the  deposit  in  the  lungs  of  inhaled  particles  like  coal- 
dust,  causing  the  development  of  interstitial  pneumonia — is  a  form  of  fibrous 
phthisis.     One  or  both  lungs  may  be  involved,  the  diseased  portions  being 

dense  and  of  a  slaty  or  black  color. 
They  are  usually  elevated  above  the 
surface  of  the  lungs. 

Upon  section  the  indurated  portions 
present  a  smooth,  shining  solid  surface 
of  slate,  gray,  black,  or  ebony  color. 
When  the  lesion  is  pronounced  the  finger 
is  soiled  by  contact  with  it,  and  a  thick 
fluid  of  the  same  color  is  obtained  on 
scraping  it  with  a  scalpel.  The  bronchi 
contain  a  dark  muco-pus. 

Under  the  microscope  the  inter-alveolar 
septa  are  seen  to  be  much  thickened  and 
contain  small  black  particles  scattered 
along  the  vessels,  in  the  cells  and  between 
the  fibres  of  the  connective-tissue.  The 
„  vv   .,    ,        „   ,      ,     alveoli  are  diminished  in  size,  and  con- 

verse  section.— C,  C.  Alveolar  walls  largely-         .  ■   i     t      i  _e  • 

piqmented.—D,  D.  Alveolar   epithelium  con-    tam  CClls  With  dark  granules  01  irregular 
taming  pigment  granules,     x  250.  ,,.  ^  ,,  ,  r>i-.i       -,i 

outline.  Soon  the  septa  are  nlled  with 
black  particles,  some  of  which,  entering  the  lymphatic  circulation,  reach 
tlie  bronchial  and  even  the  mesenteric  glands,  which  suffer  enlargement. 
Iron  and  steel  workers  have  a  brown  discoloration  of  the  lung  (siderosis). 
In  stone-cutters'  phthisis  (chalicosis)  a  slaty-gray  appearance  is  found,  due 
to  the  lodgment  of  inhaled  dust  and  silica. 


FiQ.  44. 

Anthracosis. 

Section  from  a  Coal-tniner's  Lung, 

A,  A,  A.  Alveoli.— B,  B.  Small  arteries  in  trans- 


CHRONIC   TUBERCULAR   PHTHISIS. 


183 


CHRONIC    TUBERCULAE    PHTHISIS. 


Chronic  tubercular  phthisis  is  characterized  by  gray  granules  scattered 
more  or  less  abundantly  throughout  the  affected  portion  of  the  lung,  or  by 
masses  of  them  agglomerated  by  fibrous  "tubercle-tissue." 

Morbid  Anatomy. — The  lungs  are  large,  emphysematous  and  pale,  unless 
pneumonia,  congestion  or  oedema  is  present.  The  surface  of  the  lungs  is 
often  marbled.  The  apex  of  the  lung  is  studded  with  firm,  hard,  gray  or 
cheesy  nodules,  varying  in  size  from  a  pin's  head  to  that  of  a  pea. 

Ul3on  section  of  a  lung  which  shows  these  changes  muco-pus  flows  from 
the  cut  bronchi.  Peri-bronchitic  and  inter-alveolar  interstitial  pneumonia 
is  developed  to  a  greater  or  less  degree  around  these  nodules,  with  irregular 
dilatation  of  the  alveoli.  These  nodules  originate  chiefly  in  the  lymph- 
sheaths  of  the  arterioles,  in  the  peri-bronchial  adenoid  tissue,  or  in  the 
small  masses  of  cytogenic  tissue  in  the  alveolar  walls.'  These  bloodless 
nodules  are  incapable  of  suppuration,  resorption,  or  organization.  As  the 
'Hubercle-tissue"  about  the  vessels  increases,  it  causes  occlusion  of  their 
lumen.  The  lumen  of  the  occluded  vessel  is  occupied  by  granular  fibrin, 
and  on  transverse  section  a  row  of 
white  blood-corpuscles  and  of  en- 
dothelial cells  is  often  seen  between 
the  coagulum  and  the  vessel  wall. 
In  recent  cases  the  walls  of  the 
vessels  are  very  easily  distinguish- 
ed. But  if  the  centre  of  the 
tubercle  has  become  caseous  the 
vessel  wall  is  also  altered  and  is 
very  indistinct.  Thickening  of 
the  alveolar  walls  may  also  result 
from  the  development  of  ''tuber- 
cle tissue  "  in  them.  Many  claim 
that  the  commencement  of  the 
process  is  a  small  cellular  projec- 
tion on  one  side  of  an  alveolus, 
which,  as  it  grows,  pushes  the 
capillaries  and  the  epithelium  with 
it  into  the  alveolar  cavity.  The 
bronchioles  are  thickened  and  diminished  in  calibre  ;  sometimes  there  are 
complete  peri-bronchial  cylinders  of  new  embryonic  or  tubercle-tissue. 
The  alveolar  cavity  maybe  filled  by  the  new  formation,  the  walls  remain- 
ing distinct ;  or  the  wall  may  be  destroyed  by  the  growth  of  the  projecting 
nodule,  and  thus  communication  opened  between  adjoining  air  vesicles." 
After  coalescence  of  masses  of  tubercle-tissue  anaemic  necrosis  occurs  ; 

1  Rindfleisch  states  that  the  points  at  which  the  smalleat  tjronchioles  become  contimioyf  with  alveolar'  sacs 
are  the  situations  of  the  first  eiv.ption.  of  the  tubercles,  and  that  the  first  lesion  is  a  tuberculous  infiltratiion  of 
all  the  angles  and  projections  situated  at  these  points. 

=  Hamilton  states  that  this  appearance,  which  so  resembles  the  condition  of  the  lobules  in  catarrhal 
pneumonia,  has  caused  the  mistake  of  regarding  tubercle  and  catarrhal  pneumonia  as  identical. 


Pig.  45. 

Chronic  (Tubercular)  Phthisis. 

Section  of  Lung  shoirlng  a  small  miliary  tubercle,  with 

surrounding  pulmonary  alveoli. 

A.  Cheesy  centre  of  tvbercle. 

B,  B.  Trabeculce  of  the  basement  tissue  of  the  tubercle, 

containing  lymphoid  elements,  large  cells,  etc. 
C,  C.  Divided  'arteries  with  inflltration  of  their  walls 
with  tubercular  tissue. 
D.D,D.  Lung  alveoli  filled  with  catarrhal  products.  x50 


184 


DISEASES  OF  THE   EESPIEATOET  OKGANS. 


the  cellular  elements  become  granular,  atrophied  and  fatty,  and  form  cheesy 
yellow  masses.  These  caseous  masses  are  easily  removed  from  the  paren- 
chyma in  which  they 
are  imbedded.  Sur- 
rounding these  masses 
are  found  groups  of 
gray  miliary  tubercles. 
The  mode  of  this  for- 
mation of  cavities  and 
their  appearance  are 
the  same  as  already 
described.  Between  the 
ulcerous  cavities  of 
chronic  tubercular 
phthisis  the  lung-tis- 
sue may  be  emphyse- 
matous, engorged,  oi 
pneumonic.  The  iron- 
chi  are  filled  with 
muco-pus ;  their  mu- 
cous membrane  is  the 
seat  of  a  catarrh,  and 
is  congested  and  tra- 
beculated.  Their  walls 
are  thickened,  tuber- 
cle-tissue is  found  in 
them,  and  ulcers  are 
not  infrequent. 

The  pleura  is  con- 
gested and  covered  with  fleshy,  soft  vegetations  over  the  parts  involved 
in  the  chronic  phthisical  processes.  Organized  adhesions  are  common; 
in  them  tubercles  may  be  found,  and  also  in  the  pleura.  Tubercles 
may  be  found  in  the  larynx,  trachea,  mesenteric  and  lymphatic  glands,  and 
in  the  mucous  surfaces  of  the  alimentary  tract,  peritoneum,  spleen,  kidney, 
liver,  brain,  bladder  and  testes.  Thus  a  chronic  local  disease  of  slow  and 
seemingly  intermittent  progress  is  found  associated  with  evidence  of  some 
sort  of  general  infection.  Fatty  heart  is  not  uncommon.  The  recent  dictum 
is  that  chronic  tubercular  growths  may  heal.  Many,  however,  believe  that, 
once  established,  the  process  can  never  become  ''quiescent."  '  Ulceration, 
dilatation  of  the  bronchi,  and  the  formation  of  large  cavities  are  not  infre- 
quent attendants  on  this  process.'' 

'  Rindfleisch  advances  a  new  doctrine  of  the  "healing  processes  in  tuberculosis  of  the  lung,"  viz.:  it 
consists  in  a  shrinkage  of  the  infiltration,  combined  with  a  formation  of  new  vessels.  These  vessels  do  not 
penetrate  deeply  into  the  infiltration,  but  surround  it  and  supply  it  with  constant,  though  scanty,  nourish- 
ment.   It  is  a  "fibrinous  shrinkage  ;"  the  capsule  not  only  encloses  but  nourishes. 

=  In  a  variety  called  by  O.  Clark  and  Rindfleisch  "■  Broncho-phlMsis  Pulmonalls  "  the  central  feature  of 
the  change  is  f  ■-■  extensive  vlceraiion  of  all  the  bronchi  of  medium  size  down  to  the  intra-lobular  branches. 
Spaces  of  all  sizes  are  seen— on  section— connected  with  one  another.  Rindfleisch  states  that  a  ' 
mative  pneumonic  process  "  accompanies  this  peculiar  form  of  tuberculosis  of  the  lungs. 


Fig.  46. 
Chronic  (Tubercular)  Phthisis. 

Section  of  Lung  showing  a  small  tubercular  nodule  with  surrounding 
alveoli. 
A.  Cheesy  centre  of  nodtde. 

B,  B.  Fibrillar  basement  substance  containing  cells  and  nuclei. 

C,  C.  Giant-cells. 
1).  Vacuoles. 

E,  Ey  E.  Alveoli,  surrounding  the  tubercle,  containing  pneumonic  products. 
F.  Part  of  wall  of  an  artery  infiltrated  with  tubercle-tissue,     x  250. 


CHEONIC   PULMONARY    PHTHISIS.  185 

Etiology. — The  causes  of  chronic  phthisis  are  general  and  local. 

The  most  effective  general  causes  are  hereditary  or  g-cquired  feebleness  of 
constitution,  anti-hygienic  influences,  climate,  and  soil. 

The  local  causes  are  pneumonia,  pleurisy,  bronchitis,  mechanical  irri- 
tants, and  noxious  vapors. 

Inherited  tendency. — The  influence  of  heredity  is  so  decided  that  many 
observers  claim  that  phthisis  can  never  be  developed  by  those  who  have  no 
such  tendency.  Every-day  expei'ience  disproves  such  sweeping  statements. 
My  own  statistics  show  a  direct  transmission  in  more  than  18  per  cent.  ;  it 
is  stronger  in  women  than  in  men  in  the  proportion  of  57  to  43.  Mothers 
transmit  phthisical  tendencies  more  certainly  than  fathers.  But  when  one 
parent  alone  is  affected  the  mother  is  more  apt  to  transmit  to  the  daughters 
than  to  the  sons,  and  vice  versa.  The  stronger  the  hereditary  predispo- 
sition the  earlier  will  be  the  development  of  the  disease  and  the  more  acute 
its  course.  A  phthisical  vice  of  constitution  may  be  inherited  by  the 
children  of  the  aged,  of  drunkards,  of  those  enervated  by  excesses,  and  of 
,  those  who,  at  the  time  of  the  birth  of  their  children  were  suffering  from 
some  form  of  constitutional  disease  such  as  cancer,  syphilis,  or  gout.  It  is 
therefore  necessary,  in  order  to  fully  determine  the  influence  of  an  heredi- 
tary tendency  in  any  given  case,  to  know  the  condition  of  the  parents  at  the 
time  of  the  individual's  birth.  Children  of  the  scrofulous  are  apt  to  be 
tuberculous  early  in  life.  Children  of  consanguineous  marriages  are  es- 
pecially liable  to  pulmonary  phthisis. 

Anti-hygienic  surroundings. — Second  only  to  hereditary  influence  are 
anti-hygienic  surroundings.  Impure  air,  improper  quality  and  insufficient 
quantity  of  nutritious  food,  are  among  the  most  prolific  of  this  class  of 
causes.  Bad  ventilation  and  impure  air,  an  indoor  life,  especially  when 
large  numbers  are  crowded  into  a  small  space,  are  strong  predisposing 
causes.  The  frequency  of  phthisis  in  clerks,  printers,  tailors,  milliners, 
seamstresses,  factory  employes— -^ho  live  in  a  hot,  close,  dust-laden  atmo- 
sphere—proves this.  Of  indoor  workers  those  are  most  liable  to  phthisis 
who  exercise  least  at  their  vocations.  Compositors  suffer  oftener  than  the 
press-hands  in  the  same  room.  The  moister  the  air  and  the  higher  the  tem- 
perature of  the  apartment  the  more  liable  is  phthisis  to  be  developed.  If, 
in  addition  to  these  anti-hygienic  conditions,  are  added  insufficient  and  im- 
proper clothing,  want  of  cleanliness,  alcohol  drinking,  prolonged  lactation, 
and  repeated  miscarriages,  it  is  evident  that  the  feebleness  of  constitution 
which  predisposes  to  phthisis  can  be  acquired  as  well  as  inherited. 

I  am  convinced,  from  a  careful  analysis  of  my  records,  that  the  phthisi- 
cal developments  depend  as  much  upon  the  anti-hygienic  influences  under 
which  childhood  has  been  passed  as  upon  hereditary  tendencies.  These 
predisposing  anti-hygienic  influences  embrace  the  important  problem  of 
infantile  diet.  Few  mothers,  especially  among  the  wealthier  classes,  are  in 
a  condition  properly  to  nourish  their  own  offspring.  The  habit  which  pre- 
vails of  feeding  children  until  they  are  one,  two,  or  even  three  years  of  age 
upon  barley-water  and  pap  has  a  great  influence  upon  the  future  physical 
development  of  the  child.     In  determining  the  influences  which  have  pre- 


186  DISEASES   OF   THE   RESPIRATOEY   ORGAN'S. 

disposed  to  the  phthisis  in  any  case,  it  is  important  to  consider  not  only  the 
condition  of  the  parents  at  the  time  of  the  birth  of  the  individual,  but  also 
the  hygienic  influences  under  which  his  childhood  and  early  life  were 
passed.  One  of  the  great  objects  of  early  physical  training  should  be  to 
overcome  hereditary  physical  tendencies ;  this  can  be  accomplished,  in  the 
majority  of  cases,  by  good  hygienic  surroundings  and  systematic  physical 
training  during  infantile  and  early  life.  It  is  especially  important  that  the 
children  of  phthisical  parents  should  be  placed  under  such  influences,  dur- 
ing infancy  and  childhood,  as  shall  insure  the  greatest  physical  vigor.  All 
these  predisposing  influences  tend  to  arrest  physical  development. 

Climate  has  long  been  regarded  as  an  important  factor  in  the  develop- 
ment of  phthisis.  We  know  of  no  climatic  condition  which  renders  its 
development  a  necessity,  or  that  makes  its  development  impossible ;  yet 
there  is  no  question  but  that  it  occurs  with  greater  frequency  in  one  cli- 
mate than  in  another.  It  is  rare  in  the  torrid  and  frigid  zones,  and  fre- 
quent in  the  temperate.  It  is  a  question,  however,  if  climate  alone  can 
properly  be  regarded  as  a  cause  of  phthisis.  There  is  something  more  than 
climatic  changes  which  renders  certain  localities  especially  powerful  in  its 
development.  Altitude  is  more  important  than  climate,  for  most  high  ele- 
vations are  antagonistic  to  its  development.  The  condition  of  the  soil  of  a 
region  or  locality  favors,  or  is  antagonistic  to,  phthisis  :  light,  sandy,  por- 
ous soils  are  antagonistic;  while  heavy,  hard,  clayey  and  impermeable  soils 
are  favorable.  A  damp,  cold  atmosphere,  an  impermeable  soil,  and  sudden 
changes  in  temperature  are  the  most  favorable  conditions  for  developing 
phthisis.     Want  of  sunlight  acts  also  as  a  strong  predisposing  cause. 

Local  causes. — One  who  carefully  studies  the  clinical  features  of  a  large 
number  of  cases  of  phthisis  must  be  convinced  that  bronchitis  of  the  smaller 
tubes  and  chronic  lobular  [catarrhal)  pneumonia  are  the  starting  points  of  a. 
large  number  of  cases  of  phthisis.  Some  call  these  "exceptional "  catarrhs. ' 
That  an  apparently  simple  catarrh  leads  to  the  development  of  phthisis  in- 
one  case  and  not  in  another  may  be  explained  by  the  fact  that  one  individ- 
ual is  in  a  condition  to  resist  the  bronchitis,  while  in  another  all  the  predis- 
posing causes  of  phthisis  are  in  operation  and  the  catarrh  then  results  in 
the  phthisical  developments.  The  relation  which  pneumonia  bears  to  the 
development  of  phthisis  has  been  sufficiently  considered  under  the  head  of 
its  morbid  anatomy.  From  a  clinical  standpoint  there  seems  to  be  no  ques- 
tion but  that  a  non-resolved  pneumonia  is  the  starting  point  of  phthisis  in 
quite  a  large  proportion  of  cases.  The  question  which  it  seems  difficult  ta 
decide  is  : — are  such  pneumonias  tubercular  ? 

That  pulmonary  phthisis  not  infrequently  dates  from  a  pleurisy  is^ 
evident  to  every  careful  observer.  Phthisis  which  is  preceded  by  pleu- 
risy is  often  attended  by  an  extensive  development  of  fibrous  tubercular- 
tissue.  Bronchial  hemorrhage  is  frequently  the  first  and  only  sign  of 
phthisical  developments.  It  is  claimed  that  bronchihis  precedes  and  causes 
the  hemorrhage.     Unquestionably  such  bronchial  hemorrhages  indicate  a, 

'  Winiams  found  In  1,000  cases  of  phthisis  that  bronchitis  was  the  origin  in  12  per  cent.  Niemeyer  regards, 
bronchitis  ae  the  primary  and  essential  developing  cause  in  the  majority  of  cases. 


CHRONIC    PULMONARY    PHTHISIS.  187 

vice  of  constitution  which  favors  phthisical  developments  ;  but  it  requires 
no  argument  to  prove  that  the  hemorrhage  is  not  an  evidence  that  tuber- 
cles exist  in  the  lung  at  the  time  of  tlie  hemorrhage.  The  connection 
which  exists  between  phthisical  developments  and  bronchial  hemorrhage  is 
not  always  clear. 

The  mechanical  irritation  of  the  bronchi  produced  by  the  constant  in- 
halation of  an  atmosphere  laden  with  dust  leads  to  phthisis.  The  phthisis 
of  knife-grinders,  stone-cutters,  potters,  silk- workers,  cigar-makers  and 
coal-miners,  are  examples  of  this.  The  constant  inhalation  of  noxious  gases, 
such  as  are  generated  in  overcrowded,  badly  ventilated  apartments,  is  a  fre- 
quent exciting  cause  of  phthisis. 

Pregnancy,  instead  of  preventing  phthisis,  as  was  at  one  time  supposed, 
predisposes  to  it,  and  renders  its  course  more  rapid  in  those  who  are  already 
phthisical. 

Empliysema  and  goitre  have  been  by  some  supposed  to  afford  an  immunity 
against  phthisis,  but  my  observations  lead  me  to  the  conclusion  that  it  is  a 
very  frequent  attendant  of  both  these  conditions.  The  notion  that  malaria 
and  marsh  fevers  are  antagonistic  to  phthisis  is  disproved  by  every-day 
experience.  The  relation  between  dialetes  melUtus  and  pulmonary  phthisis 
is  not  well  understood,  but  that  one  complicates  the  other  very  frequently 
is  a  clinical  fact.  At  the  present  day  many  claim  that  phthisis  is  commu- 
nicable, that  those  who  live  intimately  together,  occupying  the  same  apart- 
ment and  the  same  bed — husband  and  wife,  children  in  nurseries,  and  sol- 
diers in  barracks — can  contract  the  disease  one  from  the  other.  It  seems  to 
me  that  the  question  of  the  communicability  of  phthisis,— either  by  per- 
sonal contact,  inoculation,  or  the  ingestion  of  tuberculous  matter, — is  one  to 
which  clinical  observation  has  as  yet  given  no  conclusive  answer,  and  ex- 
perimental observations  upon  man  are  wanting,  save  in  a  single  questiona- 
ble case.  The  proof  of  isolated  or  collated  cases  upon  either  side  are  but 
presumptive.  In  animals  the  case  is  different,  and  the  results  of  experi- 
mental research  seem  to  prove  conclusively  that  tubercle  is  communicable 
by  inoculation  through  inhalation  of  tuberculous  matter.  The  tuberculosis 
thus  produced  is  identical  histologically  with  that  caused  by  various  irrita- 
ting substances,  but  is  entirely  distinct  in  its  power  to  produce  general  tu- 
berculosis upon  inoculation,  a  power  which  the  tubercle  of  irritation  has  in 
but  small  degree  if  at  all.  Cohnheim  strongly  believes  in  infection  ;  and 
Virchowand  many  English  physicians  believe  in  the  communicability  from 
person  to  person.  Some  English  physicians  go  so  far  as  to  forbid  kissing. 
The  frequency  with  which  young  women  become  phthisical  after  pregnancy 
has  given  rise  to  the  idea  that  they  may  have  been  infected  by  phthisical  off- 
spring." 

Symptoms.  — There  are  certain  symptoms  which  characterize  the  early  stages 
of  each  variety  of  chronic  phthisis.  Catarrhal  or  tuhercular  pneumonic' 
phthisis  usually  commences  with  a  bronchial  catarrh.     The  cough  is  par- 

>  Reginald  Thompson,  in  London  Jymcfi/,  January,  1881,  Art.  "  The  Tnfectirmof  PhfMw,"  makes  a  spe- 
cial form  of  "  infectivf'  phtliisin,"  not  "ordinary  phthisis."  He  calls  the  former  "  rather  an  ulcerative  proc- 
ess capable  of  privirig  rise  to  pyaemia."  His  cases  would  certainly  lead  one  to  a  belief  in  the  communi- 
cability of  phthisis. 


188  DISEASES   OF  THE   EESPIRATORT   ORGANS. 

oxysmal  and  accompanied  by  tenacious  muco-purulent  sputa,  now  and  then 
blood-stained.  There  is  a  gradual  but  steady  loss  of  flesh  and  strength  ;  the 
patient  grows  pale  and  has  an  occasional  night-sweat.  These  symptoms  are 
accompanied  by  the  physical  signs  of  slight  consolidation  at  the  apex  of  one 
or  both  lungs,  with  those  of  localized  bronchitis  of  the  small  tubes.  Some- 
times this  variety  begins  with  more  acute  symptoms,  and  the  physical  signs 
of  apical  lobular  pneamonia  are  present.  In  such  cases  the  pneumonia  does 
not  resolve  and  the  fever  takes  on  a  distinctly  remittent  type,  with  a  more 
raj)id  loss  of  flesh  and  strength,  and  a  copious  purulent  expectoration,  often 
blood-streaked.  Night  sweats  become  profuse  and  exhausting,  and  there 
are  the  physical  signs  of  progressive  consolidation  of  lung-tissue.  At  any 
time  during  the  early  stage  the  physical  processes  may  be  arrested.  And 
during  the  period  of  arrest  there  may  be  a  great  improvement  in  the  gen- 
eral condition  of  the  patient,  and  complete  recovery  is  possible.  But  in  a 
large  proportion  of  cases  a  return  to  the  anti-hygienic  conditions  in  which 
its  primary  development  occurred,  or  a  fresh  bronchitis,  lights  up  anew  the 
phthisical  process. 

Tuberculous  interstitial  pneumonia— or  fibroid  phthisis — comes  on  very 
insidiously ;  it  may  be  ushered  in  by  one  or  more  attacks  of  haemoptysis. 
In  most  cases  it  commences  with  the  physical  signs  of  a  localized  bronchi- 
tis and  pleurisy  at  the  apex  of  one  lung.  Cough  and  a  muco-purulent  ex- 
pectoration, with  more  or  less  pain  in  the  affected  lung,  may  exist  for  a 
long  time  before  there  is  any  marked  impairment  of  the  general  health. 
After  a  variable  period  the  patient  begins  to  lose  flesh  and  strength,  the 
cough  increases,  and  the  expectoration  becomes  more  abundant.  There  is 
a  progressive  loss  of  appetite,  but  at  no  time  is  the  temperature  high  or  the 
pulse  rapid.  Dyspnoea  becomes  more  and  more  marked,  especially  on  ex- 
ertion. Eetraction  of  the  chest  walls  under  the  clavicle  commences  quite 
early  and  is  steadily  progressive.  The  limited  play  of  the  chest  walls  is  the 
most  distinctive  early  sign.  This  variety  of  phthisis  rarely  occurs  in  young 
persons,  and  it  is  often  associated  with  a  rheumatic,  gouty  or  syphilitic 
taint,  or  is  the  result  of  mechanical  irritation. 

Chronic  tubercular  phthisis  may  for  a  long  period  give  no  distinctive 
signs,  for  interstitial  pleurisy,  chronic  bronchitis  and  emphysema  nearly 
always  accompany  it,  their  prominent  symptoms  masking  those  of  phthisis. 
Patients  with  this  form  become  emaciated  ;  their  dyspnoea  resembles  that 
of  emphysema.  The  expectoration  is  in  the  earlier  stages  mucous,  and  later 
it  becomes  muco-purulent.  Hsemoptysis  is  common  ;  and  hectic  fever  is 
more  pronounced  than  in  any  other  variety.  There  are  no  periods  of  im- 
provement, though  there  may  be  periods  during  which  the  disease  remains 
stationary.  Pleurisy,  laryngitis,  and  intestinal  catarrh  are  more  marked 
than  the  pulmonary  symptoms.  As  the  disease  advances  its  symptoms 
resemble  those  of  fibroid  phthisis. 

In  analyzing  the  symptoms  which  are  common  in  all  varieties  of  chronic 
phthisis  I  shall  first  consider  the  cough.  It  is  the  earliest  and  most  constant 
of  all  the  phthisical  symptoms.  It  is  present  early  and  continues  through- 
out the  whole  course  of  the  disease.    At  first  it  is  dry  and  hacking.    It  may 


CHRONIC    PULMONARY    PHTHISIS.  189 

exist  before  there  are  any  physical  signs,  and  then  there  is  little  or  no  ex- 
pectoration ;  it  may  amount  only  to  a  "  clearing  of  the  throat."  The  sever- 
ity of  the  cough  without  expectoration  is  a  measure  of  the  extent  to  which 
the  pleura  is  involved.  The  younger  and  more  excitable  the  patient,  the 
more  paroxysmal  is  the  cough.  It  is  usually  worse  in  the  morning  on  rising, 
or  just  after  lying  down  at  night.  Lying  on  the  affected  side  often  brings 
on  violent  paroxysms.  Some  cough  after  the  slightest  exertion ;  others  have 
a  varying  number  of  paroxysms  during  the  day  and  can  estimate  how  long 
an  interval  of  rest  they  will  have  between  the  paroxysms.  The  loss  of  sleep 
occasioned  by  the  cough  may  add  much  to  the  discomfort  and  wasting  of  the 
patient.  In  advanced  phthisis,  when  cavities  have  formed,  the  cough  be- 
comes ''hollow"  in  character.  Expectoration  may  accompany  cough  from 
its  commencement.  At  first  it  is  tenacious,  glairy,  frothy  and  mucous; 
then  yellow  purulent  spots  are  found  in  it.  It  is  always  important  to  ascer- 
tain whether  pallor,  fever,  and  emaciation  have  been  preceded  by  cough 
and  expectoration,  or  whether  emaciation  preceded  cough  and  expectora- 
tion. The  sputa  are  gelatinous  and  faintly  pink  when  the  infiltration  is  ex- 
tensive. Vitreous,  gelatinous  rounded  masses  may  be  mingled  with  yellow 
catarrhal  expectoration,  and  these  are  evidences  of  a  recent  pneumonia. 
Dots  and  streaks  of  blood  in  catarrhal  sputa  indicate  a  lobular  pneumonia, 
and  when  this  occurs  fatty,  swollen,  and  granular  bronchial  and  alveolar 
epithelium  will  be  found  intermingled  in  the  mass.  The  sputa  in  the  ear- 
lier stages — often  for  months — are  muco-purulent.  When  shreds  of  elastic 
tissue  are  found  it  indicates  softening  and  destruction  of  lung-tissue.  Elas- 
tic fibres  are  generally  found  in  compact,  airless,  uneven  masses,  which  read- 
ily sink  in  water.  As  cavities  form,  the  sputa  becomes  more  purulent,  some- 
times being  wholly  composed  of  fluid  pus,  which  may  be  fetid  and  greenish, 
and  contain  elastic  fibres  coming  from  the  alveolar  wall,  organic  matter, 
fat-crystals,  pigment,  young  cells,  and  small  masses  of  cheesy  matter,  and 
the  tubercle  bacillus  ;  the  latter  are  present  in  the  sputa  of  all  varieties  of 
advanced  phthisis.  The  quantity  of  matter  expectorated  varies  with  the 
extent  of  the  bronchial  catarrh  and  the  number  and  size  of  the  cavities.  It 
may  be  expectorated  readily,  or  only  with  difficulty.  Usually,  the  more  fee- 
ble the  patient  the  more  difficult  the  expectoration.  In  rapidly  formed 
cavities  the  expectoration  may  contain  fragments  of  bronchioles  and  blood- 
vessels, with  shreds  of  lung-tissue. 

Hmmoptysis  is  a  very  important  symptom  of  phthisis,  and  may  occur 
during  any  stage  of  the  disease  ;  the  blood  may  simply  streak  the  sputa, 
or  a  pound  or  more  may  be  expectorated  at  one  time.  Hemorrhages  that 
occur  in  the  early  stage  of  pulmonary  phthisis  are,  in  the  majority  of  in- 
stances, bronchial ;  and  the  blood  expectorated  is  arterial  in  color.  When 
streaks  of  blood  appear  in  the  sputa,  the  bleeding  usually  comes  from  the 
vessels  of  the  alveolar  walls.  Profuse  hemorrhages  in  the  later  stages  of 
phthisis  have  their  origin  in  cavities  in  the  lung  substance.  Hemorrhages 
that  occur  in  the  early  stages  may  be  profuse,  but  they  are  rarely  danger- 
ous ;  hemorrhages  in  advanced  phthisis  may  be  the  immediate  cause  of 
death.     Haemoptysis  usually  comes  on  with  coughing.     There  is  a  sen- 


190  DISEASES    OF    THE    RESPIRATORY    ORGAiq'S. 

sation  as  if  a  fluid  were  trickling  underneath  the  sternum,  and  there  may 
be  violent  cardiac  palpitation,  oppressed  breathing,  and  a  peculiar  sweetish 
taste  in  the  mouth.  In  profuse  hemorrhage  the  rapid  flow  of  blood  into 
the  mouth  may  excite  vomiting  and  be  mistaken  for  hsematemesis.  For 
some  time  after  the  primary  hemorrhage  blood  is  coughed  up,  and  the 
color  of  the  spitting  becomes  darker  and  darker.  Sometimes  without 
warning  there  is  a  sudden  filling  of  the  mouth  with  hot  arterial  blood. 

Many  English  writers  describe  a  hemorrhagic  phthisis.  In  this  variety  an 
apparently  healthy  man  has  a  sudden  and  profuse  hemorrhage,  recurring 
daily  for  some  time,  and  followed  by  cough  and  slight  expectoration  for  a 
few  days,  with  no  physical  signs  of  consolidation.  These  cases  often  con- 
tinue for  years  without  any  other  phthisical  symptoms,  but  sooner  or  later 
phthisis  is  developed.'  Haemoptysis  often  occurs  in  those  who  have  no 
physical  or  rational  signs  of  phthisis  at  the  time  of  its  occurrence,  and  who 
do  not  become  phthisical  after.  Although  haemoptysis  occurs  more  fre- 
quently in  phthisis  than  in  any  other  pulmonary  affection,  and  there  are  few 
phthisical  subjects  who  do  not  have  one  or  more  hemorrhages,  yet  its  oc- 
currence is  by  no  means  a  certain  indication  that  an  individual  afterward 
will  develop  phthisis. 

Fever.  —Rise  in  temperature  is  so  constant  a  symptom  of  phthisis  that  it 
has  led  to  the  expression,  "  there  is  no  consumption  without  fever  ;  "  but 
in  no  two  cases  is  the  fever  course  exactly  ttie  same.  In  some  cases  the 
temperature  in  the  morning  may  be  subnormal,  only  reaching  normal  in 
the  evening  ;  in  others  the  rise  commences  at  2  p.m.,  continues  until  8  p.m., 
and  then  falls  until  5  in  the  morning.  Between  10  and  11  A.M.  the  tem- 
perature is  nearly  normal.  As  cavities  form,  the  post-meridian  rise  occurs 
later,  i.  e.,  10  to  12  at  night.  Toward  the  end  of  the  disease  the  fever 
type  resembles  that  of  pyaemia.  Night  sweats  temporarily  lower  the 
temperature.  When  the  alveoli  are  involved  in  pneumonic  processes  the 
temperature  rises  rapidly  to  103°-104°  F. ;  should  it  continue  high,  it 
indicates  that  the  pneumonia  is  tubercular  in  character.  Hectic  fever  may 
occur  in  any  stage  of  phthisis,  but  is  usually  confined  to  the  stage  of  soften- 
ing and  excavation.  It  has  three  stages :  first,  at  some  time  during  the 
day  there  is  a  well-marked  chill  or  chilly  sensation,  which  may  last  from 
half  an  hour  to  an  hour,  followed  {second)  by  a  dryness  and  heat  of  the  sur- 
face, the  temperature  rising  from  102°  F.  to  104°  F.,  the  face  assuming  a  pe- 
culiar brilliant  appearance,  and  the  cheeks  having  a  peculiar  rosy  tint  called 
the  *^ hectic  flush."  After  a  time  the  fever  gradually  subsides,  and  some 
time  in  the  night  (it  may  be  toward  morning)  the  tliird  or  sweating  stage 
comes  on.  The  night  sweats  are  usually  profuse  and  exhausting,  and 
always  indicate  the  existence  of  hectic  fever.  The  chilly  feeling  may  be  ab- 
sent, the  subsequent  fever  may  be  so  slight  as  to  be  overlooked,  but  sweats 
are  constant.  A  steady  and  continuous  low  temperature  indicates  that  the 
phthisical  processes  are  retrogressive ;  a  steady  and  continuous  high  tem- 
perature indicates  that  they  are  progressive.  In  fibroid  phthisis  the  tem- 
perature rarely  rises  more  than  a  degree  or  two  above  the  normal.     In  the 

1  Fox  claims  that  tubercular  disease  of  the  vascular  walls  is  the  primary  and.  chief  ev»n'-  in  such  cases. 


CHROIS'IC    PULMONARY   PHTHISIS.  191 

absence  of  local  symptoms,  the  thermometer  alone  may  detect  pulmonary 
phthisis  in  the  aged.'  An  intermittent  temperature  indicates  a  milder  proc- 
ess than  a  remittent  or  continuous  febrile  action. 

The  pulse  in  chronic  phthisis  bears  no  uniform  relation  to  the  temper- 
ature ;  it  is  always  feeble.  It  varies  greatly  in  frequency  and  force,  but 
rarely  in  rhythm ;  it  is  accelerated  by  slight  exciting  causes.  In  the  early 
stages  its  excitability  is  one  of  its  most  characteristic  features.  The  ar- 
terial tension  is  below  the  normal.  In  the  early  stage  of  fibroid  phthisis 
it  is  rarely  over  100.  In  a  few  cases  it  is  abnormally  slow.  An  improvement 
in  the  other  symptoms  is  not  always  accompanied  by  an  improvement  in 
the  pulse.  In  the  last  stage  of  all  varieties  of  phthisis  the  pulse  becomes 
very  rapid  and  feeble. 

The  respirations  are  more  or  less  accelerated,  and  after  exertion  there  is 
dyspnoea.  When  the  patients  are  quiet,  unexcited,  and  resting  in  bed, 
the  respirations  may  be  normal  or  but  slightly  increased.  But  on  exertion 
the  breathing  becomes  accelerated  and  labored.  The  accelerated  breathing 
is  due  to  the  fever,  the  diminished  breathing  area,  to  bronchial  obstruction 
and  to  pain  in  the  chest.  Anaemia  and  heart  failure  may  also  contribute 
to  it.  In  the  absence  of  fever  the  dyspnoea  and  accelerated  breathing  dimin- 
ish. The  extent  to  which  the  lungs  are  involved  influences  the  frequency 
of  the  respirations.  Dyspnoea  is  usually  not  marked  except  after  exercise 
and  during  periods  of  excitement.  In  young  subjects  the  dyspnoea  is  fre- 
quently periodical.  During  the  whole  course  of  fibroid  phthisis  shortness 
of  breath  on  exertion  is  a  constant  symptom. 

Pain  in  the  chest  is  not  a  prominent  or  constant  symptom  of  chronic 
phthisis,  except  in  connection  with  pleuritic  changes.  Dry  and  intersti- 
tial pleurisies  are  common  ;  yet  they  seldom  cause  severe  pain,  but  rather  a 
sense  of  tightness  and  constriction  on  taking  a  full  inspiration.  Intercostal 
neuralgia  is  frequent  and  may  be  confounded  with  the  pain  of  a  localized 
pleurisy.  Dragging  pains  in  the  side  are  most  marked  in  fibroid  phthisis. 
Pain  on  swallowing  should  always  cause  one  to  carefully  examine  the  lar- 
ynx.    It  usually  announces  the  co-existence  of  laryngeal  phthisis. 

Emaciation  is  an  early  and  constant  symptom  of  phthisis  ;  but  it  is  not 
always  progressive.  Fever  is  the  chief  cause  of  the  wasting  and  pallor  that 
are  so  common  in  all  varieties  of  phthisis.  The  higher  the  average  range 
of  temperature,  the  more  rapid  the  emaciation.  The  pulmonary  change 
may  he  preceded  by  progressive  emaciation,  but  in  all  such  cases  the  aver- 
age temperature  is  a  degree  above  the  normal.  Emaciation  may  be  a  part 
of  the  constitutional  tendency  of  the  individual,  but  such  emaciation  forms 
no  part  of  the  phthisical  wasting.  While  emaciation,  loss  of  strength  and 
progressive  anaemia  are  recognized  premonitory  symptoms,  they  cannot  be 
regarded  as  diagnostic.  Emaciation  may  not  be  continuous  in  all  cases  ; 
there  are  periods  when  the  patient  may  even  regain  lost  weight  and  mus- 

1  Sir  William  .Tenner  makes  three  clinical  types  of  chronic  phthisis  in  reference  to  temperature— the 
insiclimn,  the  ac/ive  febrile,  and  the  adynamic.  In  the  first  the  morning  temperature  is  normal ;  in  the 
second,  the  morning  temperature  will  be  about  100°  or  101",  and  the  eveninn;  temperature  10fi°-in4''.  In 
the  third,  morning  and  evening  temperatures  are  both  high  and  not  very  diflEerent ;  but  between  these 
times  irregular  fluctuations  occur. 


19iiJ  DISEASES   OF   THE   EESPIEATORY   OEGANS. 

cular  strength.  The  anorexia,  dyspepsia,  diarrhoea,  profuse  expectora- 
tion and  hsemoptysis  are  all  causes  of  the  emaciation.  Phthisical  wasting 
occurs  not  only  in  the  fat  and  muscle,  but  in  the  organs  and  blood  as 
well.'     Slow,  gradual  wasting  belongs  to  the  history  of  fibroid  phthisis. 

The  symptoms  indicating  disturbances  in  the  alimentary  tract  are  im- 
portant. Anorexia  is  often  for  a  long  time  one  of  the  most  prominent 
symptoms.  It  may  be  accompanied  by  nausea,  vomiting  and  pain  in  the 
stomach,  due  either  to  reflex  causes  or  sub-acute  or  chronic  gastric  catarrh. 
At  the  autopsy  we  often  find  a  normal  gastric  mucous  membrane  in  one  who 
during  life  gave  the  symptoms  of  acute  gastric  catarrh.  The  most  common 
cause  which  acts  in  a  reflex  manner  to  produce  vomiting  is  a  violent  fit  of 
coughing.  It  is  important  to  distinguish  between  the  vomiting  due  to  re- 
flex causes  and  that  due  to  gastric  catarrh.  With  dyspeptic  symptoms  the 
tongue  and  pharynx  are  frequently  covered  with  aphthae.  The  most  im- 
portant interference  with  digestion  which  occurs  during  the  progress  of 
phthisis  is  due  to  changes  which  take  place  in  the  small  and  large  in- 
testine. These  intestinal  changes  are  marked  by  more  or  less  tympan- 
itis and  by  diarrhoea  which  is  often  very  troublesome  and  difficult  to 
relieve  ;  few  altogether  escape  these  symptoms.  Diarrhoea  may  occur  in 
any  stage,  but  it  is  more  likely  to  occur  during  the  later  stages ;  in  some 
cases  it  alternates  with  hectic  fever.  It  is  usually  most  severe  at  night. 
The  profuse  watery  diarrhoea  which  comes  on  late  in  phthisis  is  called 
colliquative  diarrhoea.  Hemorrhoids  and  fistulce  in  ano  are  frequent 
troublesome  complications  of  phthisis,  and  should  always  be  relieved  by 
surgical  interference  in  the  early  stages  of  the  disease.  The  cure  of  a 
fistula  in  ano,  or  the  healing  of  an  old  ulcer  is  often  followed  by  phthisical 
developments  ;  and  scrofulous  joint  disease,  psoas  and  lumbar  abscesses  in 
children  are  often  followed  by  phthisis  in  early  adult  life. 

Cerebral  symptoms  are  rarely  pronounced  in  any  stage  of  phthisis  ;  there 
is  no  chronic  disease  in  which  the  mind  is  so  clear.  The  hopefulness 
and  buoyancy  of  spirits  which  attend  its  development  are  remarkable. 
The  least  improvement  is  hailed  by  the  patient  as  an  indication  of  com- 
mencing recovery.  He  speaks  lightly  of  his  unpleasant  symptoms,  and  is 
very  reluctant  to  admit  that  his  disease  is  of  a  serious  nature  ;  rarely  will 
a  phthisical  patient  admit  that  recovery  is  not  possible. 

Laryngeal  symptoms  of  phthisis  have  been  considered  under  the  head  of 
Chronic  Laryngitis.  The  pharynx  is  sometimes  the  seat  of  tuberculous 
processes.  Arrest  of  menstruation  is  a  very  frequent  occurrence  in  females 
who  are  consumptive.  In  young  females  this  is  sometimes  the  first  notice- 
able symptom.  Its  occurrence  in  advanced  phthisis  indicates  extreme  ex- 
haustion, and  it  is  often  followed  by  a  more  rapid  progress  *of  the  disease. 

The  shin  is  pale  and  traversed  by  prominent  blue  veins.  Sudamina  and 
pityriasis  versicolor  are  often  observed.  The  nails  curve  and  become  claw- 
like.    The  terminal  phalanges  of  the  fingers  become  "clubbed,"  and  this 

1  Malassez  states  that  the  red  discs  are  diminished  in  number.  The  haemoglobin  is  also  diminished. 
Leucocytes,  fibrin,  and  calcic  phosphate  are  in  excess.  Gr.'inular  masses  agglomerate  into  patches  vary- 
ing greatly  in  size ;  and,  on  a  warm  stage,  they  appear  to  develop  into,  or  give  rise  to  organisms  which 
move  about  in  the  blood. 


CHRONIC    PULMONARY   PHTHISIS.  193 

is  by  some  regarded  as  an  important  diagnostic  symptom,  but  it  occurs  fre- 
quently in  other  chronic  thoracic  affections.  It  has  been  regarded  as  (1)  a 
form  of  scleroderma  beginning  in  the  phalanges  and  extending  centrally 
over  the  body ;  (2)  as  due  to  interference  with  peripheral  return  circu- 
lation ;  and  (3)  as  an  hypertrophy  of  connective-tissue/  The  hair  becomes 
thin,  dry,  gray,  and  falls  out.  (Edema  of  the  feet  and  legs  is  not  an  infre- 
quent symptom  during  the  last  stage,  and  its  gravity  is  well  recognized  by 
the  non -professional.  Its  occurrence  indicates  that  a  fatal  issue  is  not  far 
distant.  It  may  be  due  to  secondary  changes  in  the  vessels,  but  in  a  large 
proportion  of  cases  it  is  due  to  thrombosis  of  the  veins  of  the  lower  extrem- 
ities, the  result  of  an  enfeebled  heart. 

Physical  Signs. — There  are  thi-ee  recognized  stages  in  chronic  phthisis  :  a 
stage  of  consolidation,  a  stage  of  softening,  and  a  stage  of  excavation. 

The  physical  signs  of  the  stage  of  consolidation  vary  with  the  extent  of 
the  consolidation  according  as  it  involves  large  areas  or  small  disseminated 
patches.  As  a  rule,  phthisical  developments  have  their  seat  at  the  upper 
portion  of  the  lungs. 

Inspection  reveals  diminished  expansion — on  inspiration — in  the  supra- 
and  infra-clavicular  regions  of  the  affected  side.  If  there  are  extensive 
pleuritic  thickenings  and  adhesions,  or  if  extensive  fibroid  changes  exist, 
flattening  and  retraction,  most  marked  at  the  end  of  a  full  inspiration, 
will  be  found  on  the  affected  side  or  over  the  seat  of  ^the  phthisical 
development. 

Palpation  shows  more  distinctly  the  loss  of  expansion  on  the  affected 
side.  Vocal  fremitus  is  slightly  increased  over  the  affected  lung,  although 
extensive  pleuritic  changes  may  render  the  vocal  fremitus  less  distinct. 

Percussion. — The  percussion  sound  will  vary  with  the  extent  of  the  con- 
solidation and  the  condition  of  the  lung-tissue  surrounding  the  consolidated 
portion.  There  is  always  more  or  less  pulmonary  resonance.  If  the  con- 
solidation is  slight  the  percussion  sound  may  remain  normal,  and  local- 
ized emphysema  may  give  rise  to  exaggerated  resonance  even  when  consoli- 
dated lung-tissue  exists.  When  practising  percussion,  to  recognize  a  slight 
consolidation  at  the  apex  of  the  lung,  it  is  important  to  percuss  from  the 
trachea  rather  than  toward  it.  In  all  cases  percussion  should  be  performed 
at  the  end  of  a  full  inspiration  and  at  the  end  of  a  full  expiration.  Dul- 
ness  usually  appears  first  under  the  scapula,  next  over  the  sternal  end  of  the 
clavicle,  and  gradually  extends  down,  being  limited,  for  a  long  time,  to  the 
apex  of  the  lung.  If  the  dulness  is  slight  at  first  it  gradually  increases  and 
may  reach  complete  flatness. 

Auscultation. — The  auscultatory  signs  vary  greatly  in  different  cases,  and 
at  different  times  in  the  same  ease.  Over  the  affected  portion  the  respira- 
tory sounds  may  be  feeble  or  exaggerated,  interrupted,  '' cog-wheeled  "  or 
wavy.  The  breathing  may  be  rude  or  IroncMal ;  or,  when  rude  in  charac- 
ter, it  may  be  rude  and  wavy,  rude  and  interrupted,  at  the  same  time  being 
exaggerated,  or  it  may  be  feeble  and  rude.  The  pitch  indicates  the  extent 
of  the  consolidation.     At  the  commencement  there  may  be  only  a  loss  in 

'  In  1,776  cases  Pollock  found  clubbing  of  the  finger-ends  in  about  25  per  cent. 


194  DISEASES    OF    THE   BESPIRATORY    OEGANS. 

the  vesicular  character  of  the  inspirations,  with  a  slight  rise  in  the  pitch  of 
the  expiration. 

Prolonged  expiration,  when  MgJi  pitched,  is  very  significant.     The  expi- 

increased  vocal  fremitus... ^^       ration    is   prolonged   in    cmphy- 

siightduiness  on  percussion ..:^^K,      scma,  but  low  pitched.      Wavy 

E^xaggeratea vocal  resonance.....   ^g^R      or  jerking  respiration  is  regarded 

Jxuae  or  broncho-vesicular  resjnration.    jj^^^^hM^^       -■  4;  •    j.-  j      u 

Moist  rales  may  ormay  not  be  pres-      J^^^^^^^       by  SOme   aS   a  iriction   SOUnd,    by 

eni .^^^^^^^M      others  as  the  result  of  a  narrow- 

^1^  ing  of  the  bronchi  which  inter- 
feres with  the  entrance  of  air  into 
the  lung  substance.  Accom- 
panying or  preceding  changes  in 
the  respiratory  murmur,  crepita- 
^^^^^^^  ting  sounds  are  heard  ;  they  may 
be  crumpling  or  creaking  in 
character.  Small  mucous  and 
sub-crepitant    rales,    if    present, 

"Tig-  47.  are    heard    loudest    after    cough- 

Diagram  illustrating  Physical  signs  of  first  staee  of        •  1     --e  j-u  TJ    i- 

Chronic  PhthisTs.         ="  »i»K«  "^      jj^g.^  ^ud,  if  the  Consolidation  is 

Partial  InJUtratlon  at  the  Apex  of  the  Lvng.  extcusive,    they   haVG    a    metallic 

ring.  It  is  claimed  by  some  that  all  the  rdles  that  are  heard  in  this 
stage  of  phthisis  are  produced  upon  the  surface  and  not  in  the  sub- 
stance of  the  lung.  This  statement  is  too  sweeping,  for  these  sounds  are 
usually  circumscribed.  They  can  be  changed  by  coughing,  and  are  often 
entirely  removed  by  violent  coughing,  and  can  be  heard  before  the  inspira- 
tion is  completed.  If  they  were  pleuritic  they  would  remain  after  cough- 
ing, and  would  not  be  changed  in  size,  character  or  position,  at  different 
examinations.  Pleuritic  sounds  are  present  in  a  large  proportion  of  cases, 
but  they  can  be  very  readily  distinguished  from  rdles  produced  in  lung  sub- 
stance. Carefully  conducted  post-mortem  examinations  show  that,  in  a 
large  proportion  of  cases  of  phthisis  the  pleuritic  changes  are  secondary  to 
the  changes  in  the  lung  substance.  Besides,  by  inflating  phthisical  lungs 
after  they  are  removed  from  the  body,  sounds  similar  to  those  heard  during 
life  are  distinctly  audible  if  a  stethoscope  is  pressed  firmly  upon  their  sur- 
face. A  systolic  murmur  over  the  subclavian  artery  of  the  affected  side, 
heard  loudest  during  expiration,  indicates  that  the  pleural  surfaces  at  the 
apex  of  the  lung  on  that  side  are  adherent.  Vocal  resonance  is  usually 
increased  in  proportion  to  the  percussion  dulness ;  the  more  marked  the 
dulness  the  more  intense  the  vocal  resonance. 

In  the  second  stage,  or  stage  of  softening,  the  physical  signs  of  consolida- 
tion become  more  marked,  and  new  auscultatory  signs  are  developed. 

Inspection  shows  a  greater  frequency  of  respiration  and  a  more  marked 
(depression  above  and  below  the  clavicle  on  the  affected  side,  as  well  as  an 
increased  difficulty  in  local  expansion.  In  fibroid  phthisis  the  retraction 
is  more  marked  than  in  any  other  variety. 

Percussion  elicits  more  uniform  and  widely-spread  dulness,  which 
assumes  a  wooden  or  tubular  character. 


CHRONIC    PULMONARY    PHTHISIS. 


195 


Palpation  shows  a  more  marked  diminution  in  expansion  of  the  affected 
side.  On  forced  inspiration — both  hands  being  placed  on  the  chest  equally 
far  from  the  median  line — the  fingers  that  rest  over  the  affected  lung  will 
move  but  slightly  compared  with  those  on  the  opposite  side.  Vocal 
fremitus  is  increased. 

AuscuItatio7i. — Bronchial  breathing  and  bronchophony  become  more 
distinct ;  numerous  moist  crackling  rdles,  unchanged  by  coughing,  are 
heard  over  a  circumscribed  space,  and  have  a  distinct,  shai-p,  metallic 
character,  unlike  the  crepitation  and  bubbling  sounds  which  were  heard 
during  the  first  stage. 

In  the  third  stage,  inspection  shows  greater  depression  in  the  infra- 
clavicular region  than  existed  in  either  of  the  preceding  stages,  and  there 
is  more  complete  absence  of  expansive  movements  during  the  respiratory 
acts. 

Palpation  gives  results  similar  to  those  of  the  second  stage.  Over  large 
cavities  containing  air  and  communicating  with  a  bronchus,  vocal  fremitus 
is  intensified. 

Percussion. — The  percussion  sound  will  vary  according  to  the  condition 
of  the  cavities  and  their  surroundings  ;  over  large  superficial  cavities  partly 
filled  with  liquid  there  will  be  amphoric  or  "  cracked-pot "  resonance,  if 
there  is  a  free  communication  with  a  bronchial  tube.  Deeply  seated 
cavities,  when  filled,  will  give  deep-seated  dulness,  and,  when  empty,  an 
exaggerated  percussion  sound.  A  metallic  amphoric  note  is  obtainable  only 
from  a  cavity  whose  transverse  diameter  is  at  least  1^  to  1|  in.^  Occasion- 
ally, cracked-pot  resonance  will  disappear  and  remain  absent  for  some 
time,  and  no  evidence  of  a  cavity  can  be  found  where  one  was  known  to 
have  previously  existed.  This  happens  when  the  bronchial  tube  which  has 
communicated  with  the  cavity 
becomes  obstructed  in  such  a 
manner  as  to  prevent  the  in- 
gress of  air  and  the  egress  of 
fluid. 

Auscultation. — Over  small 
cavities  with  lax  walls,  low- 
pitched,  puffing,  cavernous  res- 
piration will  be  heard.  When 
cavities  are  surrounded  by 
firm,  tense  walls,  and  are  of 
large  size,  communicating  free- 
ly with  a  larger  bronchus  and 
are  situated  near  the  surface, 
a  musical,  or  amphoric,  respi- 
ration is  heard.  The  amphoric 
echo  is  sometimes  most  marked 


Cracked-pot  resonance 
Cavernous  respiration. 
Cavernous  whisper. . . , 


Amphoric  respiration 

Gurgles 

Pectoriloquy 


Diagram  illusirating  Physical  Signs  of  Cavities  in  the  third 
stage  of  Chronic  Phthisis. 


on  inspiration  ;  at  other  times  on  expiration.  The  clearness  of  the  amphoric 
note  is  no  way  influenced  by  the  presence  of  a  moderate  amount  of  fluid  in 


'  Merbach  and  Leichtenstern. 


196  DISEASES    OF   THE   KESPIRATORY   ORGANS. 

the  cavity.  But,  when  the  fluid  in  the  cavity  has  its  level  at  or  above  the 
opening  of  the  bronchus,  the  incoming  air  may  bubble  up  and  cause 
gurgles.  These  have  a  metallic  quality  and  vary  according  to  the  character 
of  the  fluid — the  thinner  and  more  watery  the  fluid  the  more  bubbling  the 
sounds  ;  the  thicker  the  fluid  the  more  crackling  are  the  sounds.  Gurgles 
are  always  most  distinct  and  abundant  during  and  after  cough.  When  very 
large  cavities  with  rigid  walls  contain  thin  liquid,  metallic,  tinkling  sounds 
may  be  produced  by  coughing  and  speaking.  The  vocal  sounds  over  large 
cavities  have  a  metallic  or  musical  quality.  Whispering  pectoriloquy  is 
a  diagnostic  sign  of  a  cavity. 

Differential  Diagnosis. — The  early  stage  of  chronic  phthisis  may  be  con- 
founded with  'bronchitis,  ^pulmonary  infarction,  pleurisy,  acute  lohar  pneu- 
monia, anwmia  with  cough  and  expectoration,  and  cancer  of  the  lung.  The 
evidence  of  consolidation  of  lung-tissue  is  essential  to  the  diagnosis  of 
phthisis.  So  long  as  bronchitis  is  accompanied  by  a  temperature  of  100° 
R,  and  the  physical  signs  show  that  the  bronchitis  is  general,  phthisis  ia 
readily  excluded  ;  but  if  the  temperature  rises  to  103°  F.,  and  localized 
crepitant  rales  develop  at  the  apex  of  either  lung,  accompanied  by  dulness 
on  percussion  over  the  seat  of  the  rdles,  with  a  bronchial  character  to  the 
respirations,  then  there  is  reason  to  believe  that  phthisis  is  being  developed. 
If,  with  these  signs,  there  is  gradual  loss  of  flesh  and  strength,  the  cough 
becoming  hacking  in  character,  and  the  expectoration  containing  fine 
yellow  streaks  and  blood  stains,  it  is  almost  certain  that  phthisis  is  develop- 
ing. The  diagnosis  between  chronic  bronchitis  and  fibrous  phthisis  rests 
upon  the  evidences  of  consolidation  and  retraction  in  phthisis,  and  their 
absence  in  bronchitis. 

Infarctions  are  attended  by  haemoptysis  and  localized  areas  of  dulness. 
Their  etiology,  however,  is  very  different  from  phthisis,  heart  disease  being 
their  chief  cause.  The  blood  expectorated  in  phthisis  is  of  a  bright  scarlet 
color ;  in  infarctions  it  is  dark  and  in  the  form  of  coagula.  Infarctions  are 
most  frequently  situated  in  the  lower  lobes  ;  in  phthisis  the  dulness  is 
apical.     The  temperature  is  normal  in  infarction,  elevated  in  phthisis. 

In  pleurisy  ivith  effusion,  flatness  will  exist  from  the  base  of  the  lungs 
to  the  level  of  the  fluid  ;  the  line  of  flatness  will  change  with  a  change  in 
the  position  of  the  patient ;  the  breathing  will  be  exaggerated  above  the 
line  of  dulness  ;  the  range  of  temperature  is  lower  and  does  not  undergo 
such  marked  diurnal  changes  as  in  phthisis.  The  cough  is  more  hacking 
and  is  not  accompanied  by  expectoration,  and  vocal  fremitus  is  dimin- 
ished or  absent.  If,  after  the  disappearance  of  the  fluid,  the  lung  remains 
compressed  and  bronchial  or  broncho-vesicular  breathing  is  present,  with 
feebleness  of  the  patient,  hacking  cough  and  "short  breath,"  the  differen- 
tial diagnosis  between  it  and  fibrous  phthisis  is  difficult.  A  localized 
pleurisy  at  the  apex  of  the  lung,  not  the  result  of  a  general  pleurisy, 
is  indicative  of  phthisical  developments. 

Anmnia  with  cough  and  expectoration  is  attended  by  no  febrile  symp- 
toms, and  by  none  of  the  physical  evidences  of  pulmonary  consolida- 
tion. 


CHRONIC    PULMONARY   PHTHISIS.  197 

In  cancer  of  the  lung  there  is  usually  bulging  of  the  chest  at  the  seat  of 
the  cancerous  development ;  in  phthisis  there  is  retraction.  In  cancer 
the  temperature  is  often  sub-normal,  in  phthisis  it  is  more  or  less  elevated. 
The  currant-jelly  expectoration  of  cancer  is  diagnostic.  Pain  is  constant  in 
cancer  and  intermittent  in  phthisis.  The  cancerous  cachexia  and  swollen 
lymphatic  glands  also  aid  in  the  diagnosis  of  cancer. 

Whenever  cavities  have  formed  in  phthisis  the  diagnosis  is  not  difficult 
if  the  physical  signs  are  properly  appreciated  ;  they  can  be  confounded  only 
with  those  of  bronchiectasis.  The  rules  for  the  diagnosis  of  hroncMectatic 
cavities  are  given  under  the  head  of  chronic  bronchitis. 

Prognosis. — Chronic  pulmonary  phthisis  is  not  necessarily  a  fatal  disease. 
Its  morbid  processes  may  be  arrested  in  their  early  stage  in  a  large  propor- 
tion of  cases.  In  the  advanced  stage,  or  stage  of  cavities,  proper  treatment 
will  prolong  life,  and  in  some  eases  permanently  arrest  the  progress  of  the 
disease.  Eecovery  has  occurred  in  one-sixth  of  my  recorded  cases  during 
the  past  ten  years.  Its  duration  depends  on  the  variety  and  treatment ; 
in  Laennec's  and  Bayle's  statistics,  its  average  duration  is  from  one  to  two 
years.  My  records  of  chronic  phthisis  give  an  average  duration  of  three 
years  and  four  months.  The  younger  the  subject  the  shorter  its  dura- 
tion. Phthisis  can  in  no  sense  be  regarded  as  a  self-limiting  disease. 
Some  cases,  after  a  period  of  activity,  become  stationary  and  then  slowly  re- 
cover ;  others  slowly  but  steadily  progress  to  a  fatal  termination  ;  others, 
again,  pursue  a  more  rapid  and  fatal  course.  The  course  that  any  case  will 
take  is  determined  more  by  the  conditions  under  which  it  is  developed  than 
by  the  natural  history  of  the  disease.  If  an  individual  has  suffered  from 
phthisical  developments  from  which  he  has  apparently  recovered,  his  chances 
for  recovery  from  a  second  attack  are  greatly  diminished.  The  history  of 
phthisical  manifestations  in  early  life  renders  the  prognosis  unfavorable 
when  the  disease  develops  during  middle  life. 

The  prognosis  is  unfavorable  when  there  is  a  strong  hereditary  tendency, 
when  phthisis  develops  early  in  life,  when  scrofulous  or  glandular  disease 
has  existed  in  childhood,  when  the  patient  is  narrow  chested  or  dissipated, 
when  the  ordinary  pulse-rate  is  high,  and  when  there  is  great  variation  in 
weight  without  any  apparent  cause.  Opinions  in  regard  to  haemoptysis 
vary.  Many  think  its  occurrence  renders  the  prognosis  favorable,  and  that 
there  is  a  larger  percentage  of  recoveries  when  frequent  haemoptysis  occurs. 
My  own  experience  leads  me  to  the  opinion  that  frequent  haemoptysis  in  an 
early  stage  of  the  disease  is  not  unfavorable.  When  oedema  of  the  feet  and 
lower  extremities  comes  on  in  advanced  phthisis  the  prognosis  is  very  un- 
favorable, and  a  fatal  issue  is  not  far  off.  The  following  complications  ren- 
der the  prognosis  unfavorable  : — pleurisy,  pneumothorax,  emphysema, 
pneumonia,  secondary  eruptions  of  miliary  tubercles,  pericarditis,  meniu' 
gitis,  diarrhoea,  intestinal  ulceration,  peritonitis  (with  or  without  perforation) 
sub-acute  gastric  catarrh,  amyloid  degeneration  of  liver,  intestines,  spleen, 
or  kidneys,  chronic  laryngeal  catarrh  and  bronchitis. 

But  there  is  no  general  law  that  can  be  applied  to  all  cases.  The  general 
condition  of  the  patient,  the  rapidity  of  the  emaciation,  the  pulse-rate  and 


198  DISEASES   OF  THE   BESPIRATORY   ORGANS. 

temperature,  the  amount  of  consolidation,  the  age  of  the  patient,  a  knowL 
edge  of  the  progress  of  the  disease  in  other  members  of  the  family,  and  the 
character  of  the  phthisical  process  will  indicate  the  probable  course  of  the 
disease.  In  chronic  phthisis  of  long  standing  the  future  course  may  be  de- 
termined in  some  degree  by  the  past  history  of  the  case.  It  must  be  remem- 
bered that  phthisical  patients  who  seem  to  be  progressing  favorably,  may 
suddenly  develop  some  complication  which  rapidly  terminates  the  case. 
Again,  a  case  that  presents  symptoms  which  indicate  a  rapid  course  may 
suddenly  be  arrested  and  a  retrogressive  process  be  established.  Advanced 
cases  may  die  suddenly  from  heart  failure  or  syncope.  The  majority  waste 
to  a  skeleton,  but  the  mind  is  perfectly  clear  and  the  patient  is  hopeful  of 
recovery,  and  makes  plans  for  the  future  as  if  perfectly  well. 

Treatment. — I  shall  consider  the  treatment  of  pulmonary  phthisis  under 
three  heads,  viz. : 

(1)  Prophylactic;  (2)  Medicinal — internal  and  local  (as  inhalations);  and 
(3)  Hygienic,  including  the  climatic  treatment. 

Prophylactic. — During  the  period  when  prophylaxis  can  be  success- 
fully employed  it  is  possible  to  prevent  the  development  of  phthisis.  In  one 
who  is  delicate  and  leads  a  sedentary  life,  or  is  engaged  in  an  occupation 
where  the  surroundings  are  unhealthy  and  depressing,  or  whose  family  his- 
tory strongly  predisposes  him  to  phthisical  developments,  the  occurrence  of 
emaciation  or  loss  of  strength  should  immediately  lead  to  such  a  change  in 
habit  of  life,  occupation  and  surroundings  as  shall  arrest  defective  nutrition, 
invigorate  his  constitution,  and  thus  counteract  his  marked  tendencies. 
Children  born  of  phthisical  or  decrepit  parents  should  not  be  nourished  in 
infancy  by  their  own  mothers,  but  should  be  placed  with  healthy  wet  nurses. 
During  childhood  they  should  be  fed  chiefly  on  good  cow's  milk,  and  the 
greatest  care  should  be  taken  in  their  exercise  and  general  hygiene.  Change 
of  climate  and  surroundings  is  often  of  the  greatest  prophylactic  importance 
in  this  class  of  children — ^let  the  child  be  removed  from  the  city  to  the 
country.  There  is  no  other  agent  so  powerful  in  correcting  phthisical 
tendencies  in  childhood  as  systematic  physical  exercise  in  the  open  air.  This 
training  should  be  commenced  in  infancy  and  continue  to  adult  life.  All 
those  agencies  which  tend  to  develop  pulmonary  hyperaemia  and  bronchial 
catarrh  should  be  avoided.  Individuals  with  phthisical  tendencies  should 
not  breathe  air  laden  with  foul  vapors  or  fine  particles  of  dust.  Sudden 
changes  in  temperature  must  be  avoided,  also  hot  crowded  apartments. 
They  should  have  the  largest  amount  of  fresh  air,  not  only  during  the  day 
but  also  at  night ;  their  sleeping  apartments  should  be  large  and  well  ven- 
tilated. Pulmonary  hyperaemia  may  be  the  result  of  speaking  a  few  hours 
in  a  crowded  and  badly  ventilated  apartment,  and  then  may  be  followed  by 
broncho-  or  lobular  pneumonia,  which  maybe  the  exciting  cause  of  phthisis. 
Flannel  should  be  worn  next  the  skin  the  whole  year.  It  is  important  that 
such  individuals  should  not  engage  in  excessive  physical  exercise — as  jump- 
ing, running  and  violent  gymnastics. 

The  diet  should  be  simple  and  nutritious,  and  taken  with  regularity  ;  and 
the  digestive  process  should  never  be  overtaxed  by  taking  a  large  quantity 


CHRONIC    PULMOKAKY    PHTHISIS.  199 

of  food  into  the  stomach  at  one  time.  Alcohol  is  not  to  be  taken,  except 
after  severe  mental  or  physical  work,  when  there  is  a  sense  of  exhaustion,  or 
after  the  body  has  been  chilled.  The  functions  of  the  skin  must  be  most 
carefully  preserved.  The  soil  on  which  the  dwelling-house  is  built  must 
also  be  carefully  chosen  ;  a  sandy,  porous  earth  is  the  best.  All  bronchial 
catarrhs  must  be  carefully  and  promptly  treated  until  complete  recovery  is 
reached.  I  know  of  nothing  so  certain  to  assist  in  the  removal  of  bronchial 
catarrhs,  in  this  class  of  subjects,  as  a  change  of  climate.  Those  living  in 
the  mountains  should  go  to  the  sea  ;  those  at  the  sea  to  the  mountains.  The 
"  milk  "  and  "  grape-cure  "  so  strongly  advocated  by  some  for  the  arrest  of 
early  phthisis,  will  often  be  useful  in  those  who  have  feeble  digestive  pow- 
ers. The  whole  object  of  prophylaxis  is  to  sustain  and  improve  the  nutri- 
tion, and  to  guard  against  bronchial,  pleuritic  or  pulmonary  complications. 
Medicinal  Treatment. — The  most  constant  and  important  symptom  of 
phthisis  is  fever,  and  its  reduction  is  therefore  one  of  the  most  important 
thiligs  to  be  accomplished  in  the  management  of  a  case,  for  the  wasting, 
the  cough,  the  expectoration,  and  the  rapidity  of  the  phthisical  processes, 
are  closely  connected  with  the  fever.  Of  all  the  anti-pyretics  in  the  treat- 
ment of  the  fever  of  phthisis  the  sulphate  of  quinine  is  the  most  reliable, 
but  it  must  be  remembered  that  rest  is  equally  important.  I  have  often 
found  that  when  quinine  had  little  anti-pyretic  power  while  the  patient 
was  "  taking  exercise,"  a  reduction  of  temperature  was  effected  by  the  same 
dose  if  he  were  put  to  bed.  Twenty  grains,  on  alternate  mornings,  I  have 
found  most  efficacious.  Even  when  cavities  are  forming,  its  administra- 
tion will  often  be  followed  by  a  lower  temperature.  It  seems  to  check 
the  process  of  consolidation  and  limit  bronchial  catarrhs.  Digitalis  exer- 
cises no  anti-pyretic  power,  and  only  temporarily  increases  heart-power  in 
phthisis.  Salicylate  of  soda  is  recommended  as  an  anti-pyretic  by  English 
physicians,  but  my  experience  does  not  favor  its  use.  Arsenic  will  act  as 
an  anti-pyretic  in  some  mild  cases  when  all  others  fail.  One-tenth  of 
a  grain  of  morphine  combined  with  quinine  increases  its  anti-pyretic 
power,  so  much  so  that  now  I  rarely  give  quinine  as  an  anti-pyretic  to 
phthisical  patients  without  it.  Aconite,  veratrum,  gelsemium,  and  anti- 
mony I  seldom  use  on  account  of  the  disturbance  of  digestion  which  they 
cause.  In  many  cases  after  the  disease  has  passed  the  first  stage  the  fever 
cannot  be  controlled.  When  the  first  elevation  of  temperature  occurs,  qui- 
nine rarely  fails  to  control  the  fever.  Its  administration  should  be  contin- 
ued until  cinchonism  is  produced,  or  until  the  temperature  falls  ;  after  the 
temperature  commences  to  fall  the  dose  may  be  diminished.  If  the  fever 
can  be  controlled,  the  additional  beneficial  influences  of  a  change  of  cli- 
mate may,  in  very  many  instances,  carry  the  phthisical  patient  on  to  recov- 
ery, or,  if  not  to  complete  recovery,  life  may  be  prolonged,  and  the  patient 
made  comfortable.  In  some  cases,  even  when  cavities  exist,  phthisical 
patients  may  be  much  improved  by  the  judicious  administration  of  qui- 
nine. I  am  confident  that  no  drug  has  equal  power  in  arresting  phthisical 
processes  during  its  early  stage.  In  fibroid  phthisis  its  use  is  only  indicated 
during  those  slight  attacks  of  febrile  excitement  which  attend  its  progress. 


300  DISEASES    OF   THE    RESPIRATORY   ORGAl«rS. 

Another  medicinal  agent  which  has  been  extensively  employed  in  the 
treatment  of  phthisis,  and  which,  for  the  past  twenty  years,  has  enjoyed 
the  reputation  of  curing  this  disease,  is  cod-liver  oil.  It  has  been  claimed 
that  if  this  remedy  is  commenced  very  early  it  has  the  power  of  arresting 
the  phthisical  processes.  I  am  not  among  those  who  advocate  its  indis- 
criminate use.  I  doubt  if  it  exerts  any  specific  influence  upon  the  disease  ; 
it  is  more  than  probable  that  all  its  beneficial  influence  is  due  to  the  fact 
that  it  furnishes  some  element  essential  to  the  digestion  and  assimilation 
of  certain  nutritive  elements.  In  very  many  cases  the  exact  manner  in 
which  it  acts  remedially  is  not  well  understood.  There  are  three  facts 
which  seem  to  me  to  afford  some  clue  to  the  mode  of  its  action  :— first, 
unless  the  patient  gains  in  weight  while  using  the  oil,  it  seldom  or  never 
proves  remedial ;  secondly,  flesh  and  weight  may  be  gained  during  its  ad- 
ministration, and  still  the  phthisical  processes  steadily  progress;  and. 
thirdly,  when  it  does  act  remedially  the  weight  gained  is  far  greater 
than  would  result  from  the  oil  as  a  mere  element  of  nutrition.  A  great 
gain  in  weight  will  sometimes  immediately  follow  the  administration  of  a 
small  quantity  of  oil.  It  always  acts  remedially  with  more  certainty  in 
young  persons  and  children  than  in  the  aged ;  generally,  old  persons  are 
not  much  benefited  by  its  use.  Those  patients  who  improve  under  its 
use  take  more  food  than  they  have  been  accustomed  to  previous  to  its 
employment,  and  digest  it  more  perfectly.  In  some  instances  diarrhoea 
will  be  arrested  by  its  use,  and  also  vomiting  of  food  after  eating.  In  other 
cases  the  oil  itself  will  be  rejected  and  its  administration  rendered  impos- 
sible. If  possible,  it  should  be  given  in  connection  with  an  alkali.  At 
first  small  doses  should  be  given,  not  often  repeated.  A  teaspoonful  once 
or  twice  a  day  is  sufficient  to  commence  with,  the  dose  being  gradually 
increased  to  a  tablespoonful  three  times  a  day.  No  special  benefit  is  to  be 
derived  from  the  administration  of  large  doses.  Most  patients  take  the  oil 
best  immediately  or  soon  after  meals.  If  it  disagrees  with  the  stomach, 
lying  down  a  short  time  after  taking  it  will  often  prevent  any  disagreeable 
sensation.  Some  can  better  take  it  upon  going  to  bed  at  night.  It  should 
not  be  administered  in  connection  with  stimulants  unless  the  patient  cannot 
take  it  in  any  other  way.  Regularity  and  perseverance  in  its  use  are  essen- 
tial in  order  to  obtain  the  full  benefit  it  is  capable  of  producing.  If,  at 
times,  it  seems  to  disagree  with  the  digestive  organs,  it  may  be  tem- 
porarily omitted,  especially  during  the  summer  months.  The  best  oil 
in  the  market  is  '^Holler's,"  or  what  is  termed  ISTorwegian  oil.  Fish- 
oils  of  various  kinds,  cream,  glycerine,  oils  from  vegetables,  koumyss, 
malt  extracts,  pancreatic  and  pepsin  emulsions,  etc.,  etc.,  have  all 
proved  inferior  to  the  simple  cod-liver  oil.  Phosphorus,  sulphur,  the 
hypophosphites  of  lime,  soda  and  iron,  sulphurous  acid,  the  sulphites,  are 
all  excellent  adjuvants  to  the  oil,  but  cannot  take  its  place.  When  intes- 
tinal digestion  is  imperfect,  the  hypojDhosphites  are  especially  beneficial. 
When  phthisical  subjects  become  anaemic,  iron  may  be  given  at  each  meal 
if  the  temperature  is  below  100°  F.  ;  it  may  be  combined  with  quinine, 
arsenic  and  the  mineral  acids  as  tonics. 


CHEONIC    PULMONARY   PHTHISIS.  201 

There  is  a  great  diversity  of  opinion  as  regards  the  use  of  alcohol  in 
the  treatment  of  phthisis.  Some  claim  for  it  a  curative  power;  others 
maintain  that  its  daily  use  does  harm.  The  question,  therefore,  arises  : — 
under  what  circumstances  has  experience  taught  that  it  is  of  service,  and 
when  is  it  hurtful  ?  I  am  convinced  that  benefit  may  be  expected  from 
the  use  of  alcoholic  stimulants  only  when  they  increase  the  desire  for  food 
and  assist  digestion,  or  when  their  use  is  followed  by  an  increase  in 
strength  and  a  disposition  to  take  exercise.  On  the  other  hand,  if  their 
use  causes  a  rise  in  temperature  and  an  acceleration  of  the  pulse,  followed 
by  a  feeling  of  increased  weakness  and  nervous  depression,  they  will  cer- 
tainly do  harm.  The  belief  that  alcohol  has  the  power  of  arresting 
phthisical  development  is  one  which  experience  does  not  sustain.  The 
daily  use  of  alcohol  for  a  time  may  mask  phthisical  symptoms,  and  the 
patient  and  his  friends  may  fancy  that  the  progress  of  the  disease  is  stayed; 
but  soon  he  reaches  a  condition  in  which  the  disease  will  make  rapid  prog- 
ress, and  in  which  a  large  quantity  of  stimulants  will  not  give  relief.  It 
is  unfortunate  for  a  phthisical  patient  to  become  addicted  to  the  daily  use 
of  stimulants.  If  an  individual  with  developed  phthisis  reaches  complete 
recovery  while  taking  alcoholic  stimulants  freely,  I  am  confident  that  he 
would  have  reached  it  more  rapidly  and  safely  without  them.  The 
quantity  and  kind  of  stimulants  to  be  used  must  be  determined  by  the 
effects: — no  rule  can  be  given;  each  case  is  a  law  unto  itself.  Malt 
liquors  and  wines  do  less  harm  than  whiskey  and  brandy,  and  are  usu- 
ally more  serviceable.  Phthisical  patients  tolerate  alcohol  to  a  marked 
degree. 

Cough-mixtures  are  prescribed  by  physicians  to  phthisical  patients  more 
frequently  than  any  other  medicinal  agents.  Such  mixtures  are  usually 
composed  of  substances  which  are  more  or  less  nauseating ;  and  as  the 
future  well-being  of  every  phthisical  patient  depends  upon  his  powers  of 
digestion,  everything  that  may  interfere  with  the  healthy  performance  of 
this  function  must,  as  far  as  possible,  be  avoided.  Although  a  distressing 
symptom  may  temporarily  be  relieved  by  a  cough-syrup,  its  administration 
will  certainly  cause  digestive  disturbances  which  will  do  positive  harm. 
The  relief  obtained  by  cough-mixtures  is  due,  for  the  most  part,  to  the 
opium  which  they  contain. 

This  brings  us  to  the  question  : — should  opium  be  given  to  phthisical 
patients  ?  In  answer  to  this  question,  I  would  say  that  opium  should 
neyer  be  given  in  any  stage  of  phthisis,  unless  the  cough  is  distressing  and 
the  patient  is  unable  to  obtain  the^  required  amount  of  sleep.  Under  such 
circumstances  the  milder  narcotics  should  first  be  tried.  Opium  should  be 
reserved  for  the  later  stages  of  the  disease.  Its  use  should  be  commenced 
with  the  smallest  dose  that  will  give  rest.  In  the  majority  of  instances  I 
have  found  that  more  speedy  and  satisfactory  relief  will  be  obtained  from 
the  cough  and  restlessness  during  the  early  stages  of  phthisis  by  the  inhal- 
ation of  a  few  drops  of  chloroform  than  from  the  use  of  opium;  besides, 
chloroform  is  less  liable  than  opium  to  dist^^rb  digestion.  One  must  be 
careful  in  the  use  of  chloroform  ;  there  is  danger  that  phthisical  patients 


302  DISEASES   OF  THE   RESPIEATOEY  ORGANS. 

may  become  addicted  to  its  excessive  use.  Chloral  hydrate,  hydrobromie 
acid,  '^chlorodyne,"  creosote,  stramonium  and  belladonna  sometimes  act 
better  than  opium.  Quite  recently  oxalate  of  cerium  has  been  employed. 
All  narcotics  act  only  as  palliatives,  and  should  be  employed  only  when 
the  symptoms  become  suflBciently  distressing  to  demand  relief.  In  those 
cases  where  a  constant  hacking  or  violent  paroxysmal  cough  is  excited 
or  kept  up  by  an  inflamed  or  irritable  condition  of  the  fauces,  the  topical 
application  of  sedative  or  astringent  remedies  by  means  of  sprays  will  be 
found  of  great  service.  It  is  sometimes  imperative  to  give  a  stimulating 
expectorant.  Ammonium  carbonate  in  the  infusion  of  wild  cherry  bark 
is  one  of  the  best.     It  never  nauseates. 

Night  sivents  are  a  part  of  hectic.  When  quinine  does  not  control 
them,  quinine  with  opium  may  do  so.  Oxide  of  zinc  (gr.  ij-iv),  gallic 
or  suljjhuric  acids,  arseniate  of  iron  (gr.  ^  -  ^),  ext.  of  belladonna  or  sul- 
phate of  atropia  (hypodermically),  muscarine,  picrotoxine,  ergot, — all  may 
be  tried  at  different  times.  Atropia  is  the  most  reliable.  Cold  spongings, 
and  sponging  with  acidulated  or  astringent  waters  (alum  in  alcohol)  are- 
always  agreeable  and  sometimes  efficacious.  Capsicum  in  the  sponging 
water  is  sometimes  serviceable. 

Gastric  and  intestinal  disturbances  are  a  part  of  the  history  of  nearly 
every  case  of  phthisis,  and  there  are  two  conditions  upon  which  the  diar- 
rhoea and  distress  after  eating  may  depend  : — viz.,  either  upon  a  hypersemic 
condition  of  the  gastro-intestinal  mucous  membrane  produced  by  indigesti- 
ble food,  or  upon  ulceration  of  the  large  or  the  small  intestine.  If  it  depend 
upon  gastro-intestinal  hypersemia,  the  quantity  and  quality  of  the  food 
must  be  carefully  attended  to,  and  a  mild  saline  laxative  rather  than  an 
astringent  must  be  administered  ;  this  should  be  followed  by  the  daily  use 
of  the  lacto-phosphate  of  lime.  If  the  diarrhoea  is  dependent  upon  ulcer- 
ations in  the  small  intestine,  cod-liver  oil  and  the  hypophosphites  of  lime 
and  soda  will  often  be  of  service.  If  these  fail  to  give  relief,  ten  grains  of 
bismuth,  combined  with  the  twelfth  of  a  grain  of  morphine  after  each 
movement,  will  almost  certainly  control  the  diarrhoea  for  a  time.  If  the 
diarrhoea  depends  upon  ulceration  of  the  large  intestine,  all  that  can  be 
done  is  to  give  temporary  relief  by  opium  suppositories.  Vomiting  after 
meals  is  often  a  troublesome  attendant  of  phthisis.  Champagne  with  the 
food,  hydrocyanic  acid,  pepsin,  and  a  long  list  of  other  remedies  are  rec- 
ommended for  its  relief.  The  most  certain  relief  is  obtained  by  giving 
the  patient  a  glass  of  hot  water  every  two  hours,  followed  in  half  an  hour 
by  a  teaspoonful  of  raio  scraped  beef  made  into  a  sandwich,  at  the  same 
time  keeping  him  absolutely  quiet  in  a  recumbent  posture. 

The  most  valuable  remedies  for  the  arrest  of  Ticemoptysis  are  rest  and 
opium.  Lead,  ergot,  ice  and  a  long  list  of  astringents  are  recommended. 
Ergotin  hypodermically  is  much  employed.  Turpentine  is  more  relia- 
ble than  any  remedy  except  opium.  Local  pains  in  the  chest  may  be  re- 
lieved by  blisters  and  counter-irritants  ;  strapping  the  chest  so  as  to  render 
the  chest  walls  immovable  often  gives  marked  relief  from  the  pains  in  the 
chest  caused  by  the  circumscribed  pleurisies  which  attend  phthisical  proc- 


CHRONIC    PULMONARY    PHTHISIS.  203 

esses.  Dry  cupping  often  gives  marked  relief  from  the  dyspnoea  which 
accompanies  acute  phthisical  processes. 

The  antiseptic  treatment  of  phthisis  has  thus  far  given  no  satisfactory 
results;  carbolized  inhalations  have  been  quite  extensively  employed  with 
very  favorable  results,  according  to  the  statements  of  some  recent  observ- 
ers, but  after  quite  an  extensive  trial,  my  experience  is  decidedly  against 
their  use.  The  internal  or  hypodermatic  use  of  antiseptics,  notwithstand- 
ing the  strong  statements  made  in  their  favor  by  some  of  their  enthusias- 
tic advocates,  I  have  found  to  fail  not  only  in  counteracting  the  sepsis  of 
advanced  phthisis  but  in  reducing  the  high  temperature  which  so  rapidly 
exhausts  the  phthisical  patients.  The  injection  of  cavities  through  the  chest 
walls  has  not  been  followed  by  satisfactory  results.^  The  injecting  of  cav- 
ities through  canulse  passed  into  the  larynx  and  trachea  seems  to  me  not 
only  dangerous  but  futile. 

The  Hygienic  Treatment  of  Phthisis. — The  quantity  and  quality  of  the  air 
habitually  respired  is  a  most  important  consideration  in  the  hygienic  treat- 
ment of  phthisis.  Phthisical  patients  should  sleep  in  large,  well  ventilated 
and  well  lighted  rooms  with  a  southerly  or  westerly  exposure.  Flannels 
should  be  worn  next  the  skin,  and  the  surface  must  never  be  exposed  to  sud- 
den changes  of  temperature  ;  cold  sponging  or  baths  often  act  as  tonics  when 
judiciously  employed.  The  diet  should  be  varied,  and  phthisical  subjects 
should  become  accustomed  to  drink  from  one  to  three  quarts  of  milk  each 
day.  The  quantity  of  food  taken  should  be  determined  by  the  power  of 
digestion  ;  a  phthisical  subject  should  never  take  more  food  at  a  time  than 
can  be  easily  digested.  Peptonized  foods  and  preparations  of  pancreatin 
will  often  aid  a  feeble  digestion.  The  patient  must  live  as  much  as  possible 
in  the  open  air,  and  should  avoid  sedentary  occupations,  taking  systematic 
daily  exercises,  but  never  to  fatigue.  It  is  a  very  great  mistake  for  a  phthis- 
ical subject  to  exercise  when  his  temperature  is  ranging  from  102°  P.  to 
104°  P. 

The  Climatic  Treatment  of  Phthisis  is  a  subject  which  has  recently  re- 
ceived much  attention,  but  it  is  to  be  remembered  that  its  usefulness  is  con- 
fined almost  exclusively  to  the  first  stage  of  the  disease  and  that  no  absolute 
rules  can  be  laid  down  in  regard  to  it.  It  is  well  known  that  some  consump- 
tives thrive  best  in  a  warm,  moist  air,  others  in  a  cool,  dry  atmosphere  ; 
some  are  most  vigorous  in  winter,  others  in  midsummer.  Each  year's  ex- 
perience impresses  on  me  the  conviction  that  while  climate,  more  than  any 
other  agent,  has  a  controlling  influence  over  phthisical  developments,^  each 
case  must  be  carefully  analyzed  before  any  definite  directions  can  be  given 
as  to  the  climate  best  suited  to  it.  Although  we  know  of  no  climatic  condi- 
tions which  render  phthisis  a  necessity  or  an  impossibility,  still  there  are 
conditions  which  are  known  to  be  antagonistic  to  its  development  as  well 
as  those  which  favor  its  development.     Scarcely  twenty  years  ago  the  great 

J  Dr.  Pepper,  American  Journal  Med.  Science.  The  modus  operandi  of  washing  out  hinf?-cavities  and 
the  use  of  drainage  tubes  in  such  cases  are  fully  discussed  by  Hosier  in  the  October  number  of  the  Bar. 
Kiln.  Woch.,  1878. 

2  Laennec  long  ago  wrote,  "  Of  all  the  means  hitherto  recommended  for  the  cure  of  phthisis,  none  have 
been  followed  more  frequently  by  complete  cessation  of  the  disease  than  change  of  climate.  " 


204  DISEASES   OF  THE   RESPIEATOKY   ORGAN'S. 

desideratum  was  thought  to  be  a  warm,  dry  atmosphere,  but  we  now  know 
that  a  cold  climate  not  only  does  not  hasten,  but  often  arrests  phthisical 
processes.  The  statement  has  been  made  that  "  the  higher  the  altitude  the 
less  prevalent  is  phthisis,"  but  the  altitude  at  which  such  immunity  exists 
varies  with  the  latitude  and  with  the  idiosyncrasy  of  the  individual. 

Mountains  and  elevated  districts  were  thought  to  be  beneficial  on  account 
of  their  elevation  alone.  But  recent  investigations  show  that  the  absence 
of  atmospheric  impurities  is  the  chief  element,  and  that  the  purity  of  the 
air  is  the  chief  reason  that  elevated  regions  are  so  beneficial  in  phthisis. 
Prof.  Tyndall's  experiments  are  of  special  interest  in  this  connection. '  Or- 
ganic germs  are  more  abundant  in  the  air  in  the  city  than  in  the  country. 
Eain  and  ozone  free  the  air  from  them,  the  latter  by  oxidation.  Rain 
cleanses  the  atmosphere  of  solid  particles  and  purifies  it  by  washing  down 
ammonia  and  carbonic  acid.  The  presence  of  ozone  in  the  air  is  presump- 
tive evidence  of  its  purity.  The  air  of  high  mountains  and  plateaux  and 
along  the  shore  of  the  ocean  is  richer  m  ozone  than  that  of  the  plains.  Prof. 
Tyndall's  experiments  show  that  in  early  summer,  the  mountains,  and  in 
late  summer  and  fall,  the  sea-shore,  have  their  purest  air.  The  benefit  which 
phthisical  patients  derive  from  living  near  pine-forests  has  long  been  known. 
Turpentine  exhaled  from  pine  or  hemlock  forests  converts  oxygen  into  ozone, 
and  thus  the  air  of  pine-forests  becomes  pure.  Direct  inhalation  of  ozone 
has  little  power  over  phthisis  ;  hence  it  is  not  the  ozone  but  the  purity  of 
air  it  induces  that  renders  the  air  of  certain  localities  so  salubrious.  It  was 
formerly  thought  that  resorts  where  no  rain  fell  for  weeks  and  months  were 
the  best  suited  to  phthisical  subjects,  but  experience  has  taught  the  reverse. 
Long-continued  rains  are  certainly  unfavorable,  but  cleansing  showers  act 
beneficially.  The  amount  of  rainfall  is  not  a  sure  indication  of  the  amount 
of  moisture  in  the  air  of  any  region,  the  latter  depending  more  upon  the 
dampness  of  the  soil.  The  atmosphere  of  a  region  with  a  loose,  porous, 
sandy  soil,  through  which  the  water  filters,  and  whose  surface  dries  quickly, 
is  never  damp  ;  but  hard,  compact,  rocky  or  clayey  regions  that  drain  but 
slowly  and  imperfectly,  hold  the  moisture  and  cause  a  dampness  which  is  a 
strong  predisposing  cause  of  phthisis.^ 

Atmospheric  temperature  is  an  important  element  in  the  climatic  treat- 
ment of  phthisis.  Some  patients  thrive  best  in  a  warm  sedative  climate,  oth- 
ers in  a  cool,  stimulating  climate.  Extended  clinical  observation  leads  one 
to  believe  that  it  is  neither  the  heat  nor  cold  of  a  certain  locality,  but  the 
absence  of  sudden  and  frequent  changes,  which  makes  it  so  beneficial  to 
phthisical  invalids. 

Altitude  is  regarded  by  many  at  the  present  time  as  of  more  importance 

1  After  boiling,  filtering  and  evaporating  a  vegetable  infusion  he  hermetically  sealed  it  in  flasks,  which 
he  transported  to  the  Alps  7,000  feet  above  sea  level.  Some  of  the  flasks  were  opened  during  transporta- 
tion, and  in  these  millions  of  organisms  developed  in  the  fluid,  while  the  fluid  in  the  flasks  that  were 
opened  on  the  mountain  remained  free  from  such  organisms.  By  further  experiments  he  showed  that  dust- 
laden  air  was  necessary  to  the  procreation  of  these  organisms,  and  that  they  are  diffused  through  the  atmos- 
phere, although  the  air  in  different  localities  may  be  infected  in  different  degrees. 

2  Laennec  states  that  the  dampness  arising  from  such  a  condit  ion  of  soil  is  one  of  the  most  certain  devel- 
oping causes  of  phthisis,  and  he  makes  mention  of  a  locality  having  such  a  soil,  in  which  the  dampness 
was  so  constant  and  of  such  a  character  that  two-thirds  of  the  resident  population  died  of  phthisis. 


CHRONIC    PULMONAEY    PHTHISIS.  205 

than  any  other  natural  element.  As  a  rule,  the  atmosphere  at  elevations 
of  1,500  or  1,800  feet  is  purer  than  on  the  plains  ;  yet  all  high  altitudes  are 
not  thus  pure ;  experiment  has  shown  the  atmosphere  of  some  elevated 
regions  to  be  impure,  and  that  consumptives  on  such  elevations  do  badly. 
Something  more  than  altitude  is  needed  to  make  a  given  locality  suitable  to 
plithisical  subjects.  Recent  investigations  show  that  the  similarity  in  the 
composition  of  sea  and  mountain  air,  at  certain  times  of  the  year,  is  far 
greater  than  was  at  one  time  supposed.  Mountain  air  is  less  dense,  less 
humid  and  lower  in  temperature  than  sea  air,  but  in  both  we  find  excess  of 
ozone  and  freedom  from  organic  impurities.  Both  sea  and  mountain  air  are 
cooler  and  less  subject  to  frequent  variations  in  temperature  than  the  air  of 
the  plains.  A  slight  diminution  in  atmospheric  pressure  produces  no  palpa- 
ble changes.  But  a  great  diminution  (say  one-quarter)  produces  serious  dis- 
turbances of  nutrition,  developing  a  condition  which  favors  rather  than 
retards  phthisical  developments.  The  effects  of  diminished  atmospheric 
pressure  vary  so  greatly  in  different  individuals  that  no  jjractical  deduc- 
tions can  be  made. 

The  question  arises  : — will  this  patient  be  benefited  by  sea  or  by  mountain 
air  ?  Beneke's  experiments  show  that  tissue  changes  take  place  more  rap- 
idly on  or  by  the  sea  than  in  the  mountains.  Hence  those  in  whom  the  proc- 
ess of  tissue-change  needs  no  hastening,  and  those  with  exhausted  nervous 
systems,  with  an  overtaxed  brain  from  excessive  mental  labor  or  an  all- 
absorbing  business,  and  who  still  retain  considerable  muscular  power — those 
should  go  to  the  mountains.  While  those  past  middle  life,  who  have  devel- 
oped phthisis  late,  who  are  incapable  of  much  muscular  activity,  and  who 
therefore  require  stimulation  in  order  to  the  production  of  tissue  change — 
such  patients  do  best  in  sea  air.  Sea  air  is  better  suited  than  mountain  air 
to  those  who  cannot  bear  sudden  changes  of  temperature,  while  the  suscepti- 
bility to  such  changes  is  greatly  lessened  by  mountain  air. 

On  our  own  continent  is  found  every  variety  of  climate.  Permanent  im- 
provement only  occurs  after  a  prolonged  residence  in  the  place  which  experi- 
ence proves  best  suited  to  each  case.  A  change  of  climate  should  not  be 
made  every  year.  The  limited  space  which  can  be  devoted  to  the  consid- 
eration of  the  localities  best  suited  to  the  phthisical  patients  in  this  and 
other  countries  will  only  allow  of  mention  of  the  most  important  ones. 
Every  stage  of  fibroid  phthisis,  no  matter  how  far  advanced  or  where  the 
fibroid  developments  began,  is  benefited  in  the  high  altitudes  found  in  Col- 
orado and  about  the  Rocky  Mountains.  But  there  is  one  grave  objection  to 
Colorado  as  a  winter  refuge  :— the  enormous  monthly,  and  also  the  diurnal, 
range  of  temperature  must  severely  try  any  invalid.  During  March,  1880, 
the  thermal  range  at  Denver  was  eighty-three  degrees,  and  in  December, 
1876,  it  amounted  to  ninety-three  degrees— a  change  in  a  single  month 
greater  than  occurs  at  London  in  a  whole  year,  and  greater  than  occurs  at 
New  York  in  a  whole  winter. 

In  my  experience,  catarrhal  phthisis  is  not  benefited  in  regions  of  very 
high  altitudes.  It  is  during,  or  before,  the  stage  of  consolidation  that  per- 
sons with  this  variety  of  phthisis  are  to  be  benefited  by  climatic  influences, 


206  DISEASES    OF    THE     RESPIRATORY    ORGANS. 

and  a  careful  analysis  of  each  case  is  important  before  directions  can  be 
given  as  to  the  region  most  likely  to  suit  the  special  requirements  of  each 
case.  The  patient  must  not  wander  around  till  he  hits  upon  the  place  which 
suits  him  ;  much  valuable  time  is  thus  lost.  Except  in  those  who  are  con- 
valescing from  some  acute  lung  disease,  a  sojourn  in  a  southern  climate  dur- 
ing the  winter  seems  after  a  time  to  hasten  the  degenerative  processes.  My 
favorite  resorts  in  the  winter,  for  those  recovering  from  acute  pulmonary  dis- 
eases, are  Aiken,  S.  C,  Palatka,  Enterprise  and  Gainsville,  Fla.,  Thomas- 
ville,  G-a.,  and  Nassau.  These  localities  are  also  favorable  for  those  in  whom 
there  are  evident  phthisical  tendencies,  but  in  whom  as  yet,  no  physical  evi- 
dences of  pulmonary  consolidation  exist.  My  best  results,  when  the  evi- 
dences of  consolidation  were  present,  have  been  obtained  in  those  who  have 
stayed  from  one  to  three  years  in  mountain  regions  1,500  to  2, 000  feet  above 
the  sea.  My  most  decidedly  beneficial  and  permanent  results  have  been 
obtained  in  Asheville,  N.  C,  in  New  Mexico,  and  in  the  Adirondack  region 
of  New  York  State.  The  temperature,  rainfall,  and  surroundings  of  the 
latter  region  are  all  at  variance  with  preconceived  notions  of  a  proper  "  re- 
sort for  consumptives,"  but  results  are  strong  in  its  favor.  A  camp  or  tent 
life  in  the  open  air  is  best  for  those  who  can  enjoy  such  life.  Excursions 
and  cheerful  social  intercourse  in  the  open  air  should  always  be  an  object. 
A  dreary  spot,  even  with  plenty  of  ozone  and  elevation,  is  not  of  great 
material  benefit. 

I  would  advocate  sanitariums  for  the  phthisical.  Not  overcrowded  hos- 
pitals, but  cottages  and  pavilions  in  sheltered  spots,  in  appropriate  climates, 
and  at  a  given  elevation,  where  privacy  and  quiet  are  possible,  and  where 
all  shall  be  supervised  by  a  capable  and  intelligent  physician.  Minnesota 
has  a  dry,  cool,  exhilarating  climate.  Southern  California,  Georgia  and 
South  Carolina  have  a  dry,  warm  atmosphere.  The  Bermudas,  Bahamas, 
Florida,  Turk's  Island,  Santa  Cruz,  and  St.  Thomas  have  a  warm,  moist 
and  usually  healthy  climate.  The  extraordinarily  dry  belt  of  country  which 
runs  northward  from  San  Antonio,  Texas,  has  begun  to  endanger  the  su- 
premacy of  Florida  as  a  winter  health  resort  for  the  consumptive.  That 
this  belt  offers  some  climatic  advantages  for  weak  lungs  over  the  mild  but 
rather  humid  air  of  Florida,  cannot  be  doubted.  Nassau,  the  capital  of  the 
Bahamas,  is  a  noted  resort  and  one  that  suits  most  phthisical  subjects  past 
middle  life  ;  Matanzas,  Cuba,  has  a  dry,  warm  climate,  suitable  for  a  win- 
ter home  for  the  enfeebled,  but  not  for  those  who  have  developed  phthisis. 
It  maybe  that,  for  various  reasons,  a  phthisical  patient  prefers  a  residence 
abroad.  Dry  climates  near  the  sea  are  Malaga,  Riviera  and  Algiers.  Egypt 
and  South  Africa  are  highly  recommended  by  the  English  physicians  for 
phthisis.  Sea  voyages  to  Australia  and  New  Zealand  are  recommended  in 
cases  of  "  hemorrhagic  pTitMsis.^^  J.  Hughes  Bennett  finds  the  lakes  of 
Scotland  the  best  resorts  for  consumptives  in  the  summer.  The  Engadine 
has  been  strongly  advocated  by  many. 

Recently,  Davos  am  Platz,  in  the  Swiss  Alps,  has  been  most  extensively 
visited.  Williams,  Albutt  and  other  English  physicians  give  very  favorable 
reports  of  it.    It  is  5,200  feet  above  the  sea,  very  dry,  but  not  windy,  and  not 


CHRONIC    PULMONAET   PHTHISIS.  207 

changeable.'  Davos  possesses,  also,  the  unique  climatic  characteristic  of  free- 
dom from  high  winds  (the  records  showing  that  from  October  1,  1880,  to 
March  31,  1881,  there  were  one  hundred  and  thirty-four  days  with  "no 
wind"),  while  its  "sun  temperature"  rises  even  in  January,  as  Dr.  Frank- 
lin notes,  as  high  as  150° — conditions  which  admit  of  much  invaluable  out- 
door exercise  by  invalids.  Doubtless  some  high  winter  resort  combining 
these  vitalizing  conditions  can  be  found  in  the  southwestern  Kocky  Moun- 
tain region  of  our  own  country. 

'  London  Lancet,  1878,  i.  884. 


SECTION  II. 
DISEASES  OF  THE  DIGESTIVE  SYSTEM. 

{Including  Diseases  of  the  Liver,  Spleen  and  Pancreas.) 

DISEASES  OF  THE  MOUTH. 
The  following  classification  may  be  made  of  the  diseases  of  the  mouth 


I.  stomatitis. 

II. 

Tlie  "  tliru&hr 

a.   Catarrhal. 

III. 

The  tongue-diseases. 

l.   Follicular. 

a.   Glossitis. 

c.    Gangrenous. 

b.    Cancer. 

d.   Ulcerative. 

IV. 

Injlammatio7i  of  the  parotid 
gland  or  "Mumps." 

OATAEEHAL    STOMATITIS. 

Catarrhal  stomatitis  is  an  inflammation  of  the  whole,  or  a  portion  of  the 
mucous  membrane  of  the  buccal  cavity  and  tongae.  It  may  be  acute  or 
chronic. 

Morbid  Anatomy. — At  its  onset  the  mucous  and  submucous  tissue  of  the 
tongue  and  inside  of  the  mouth  becomes  tumefied,  much  redder  than  nor- 
mal, and  dry.  Later,  the  mucous  and  salivary  secretions  are  very  much 
increased.  The  swelling  is  greatest  over  those  parts  disconnected  with 
bone,  as  the  tongue  and  cheeks.  The  tongue  becomes  covered  with  a 
whitish  coating,  and  the  red  papillae  are  visible  through  it.  A  copious- 
glairy  secretion,  slightly  acid  in  its  reaction,  containing  pus  and  epithelial 
cells,  covers  its  surface.  This  secretion  has  a  sourish,  but  not  a  fetid  odor. 
In  some  cases  the  changes  are  slight  and  superficial,  in  others  the  tongue 
is  so  swollen  that  it  presses  on  the  teeth  and  becomes  indented  by  them,  and 
the  mucous  membrane  of  the  cheek  and  gums  fills  the  space  outside  of 
them.  The  whole  surface  becomes  covered  with  a  tenacious,  opaque  secre- 
tion. 

If  the  process  becomes  chronic,  the  glands  of  the  mouth  become 
swollen  and  tender,  the  filiform  papillse  become  elongated  and  pale,  and 
give  what  is  called  the  "  hairy  tongue."  The  tongue  is  less  swollen  than 
in  the  acute  stage  ;  the  secretions  have  a  fetid  odor.  Occasionally, 
patches  of  exudation  form  over  the  tongue  and  sides  of  the  mouth,  which, 
tend  to  collect  about  the  teeth.  Large  diffuse  ulcers  sometimes  occur  in 
adults. 

Etiology. — The  acute  form  occurs  almost  exclusively  in  children  during 
th.e  period  of  dentition.     The  chronic  occurs  mainly  in  adults.     Decayed 


CATARRHAL   STOMATITIS.  209 

and  ulcerated  teeth,  acid  ingesta,  and  the  taking  frequently  of  too  hot  or 
too  cold  fluids,  often  excite  it.  The  i^rolonged  administration  of  mercury 
and  preparations  of  iodine  for  their  specific  effect,  causes  a  form  which  is 
termed  mercurial  stomatitis.  The  excessive  use  of  tobacco  is  a  frequent 
cause.  Gastric  catarrh  may  precede  or  follow  it.  It  may  be  an  ex- 
tension of  inflammation  from  wounds  of  the  tongue  and  fauces.  More  or 
less  severe  catarrhal  inflammation  of  the  mucous  membrane  of  the  mouth  is 
present  in  most  of  the  specific  fevers,  especially  in  scarlatina.  Improper 
food,  bad  air,  and  bad  hygienic  surroundings  will  induce  it  in  children. 

Symptoms. — The  acute  form  commences  with  a  burning,  smarting  pain 
in  the  mouth.  The  child  refuses  to  take  food,  or  allow  the  finger  to 
be  put  in  its  mouth  ;  it  will  take  freely  of  cold  drinks,  is  fretful  and  sleep- 
less, and  there  is  usually  a  slight  rise  in  temperature.  Vomiting  and  diar- 
rhoea often  accompany  it.  The  salivary  secretion  is  increased,  and  flows 
from  the  corners  of  the  mouth,  excoriating  the  parts  with  which  it  comes 
in  contact.  It  may  extend  into  the  larynx  and  cause  laryngeal  catarrh. 
When  it  occurs  in  adults,  there  is  a  slight  rise  in  pulse  and  temperature,  a 
general  feeling  of  malaise  and  much  difficulty  in  swallowing.  The  patient 
is  constantly  trying  to  get  rid  of  the  slimy  coating  on  the  tongue  and  mouth, 
by  hawking  and  spitting.  The  sense  of  taste  is  blunted,  and  there  is  usu- 
ally an  unpleasant  bitter  taste  in  the  mouth.  These  symptoms  are  usually 
accompanied  by  a  dull  frontal  headache. 

In  chronic  stomatitis  the  breath  in  the  morning  has  a  fetid  odor,  the 
taste  is  vitiated,  and  there  is  often  great  depression  of  spirits.  Earely  is 
the  digestion  interfered  with. 

Differential  Diagnosis. — Catarrhal  stomatitis  may  be  mistaken  for  the 
changes  which  take  ];)lace  m  the  tongue  and  mouth  in  some  of  the  specific 
fevers.  In  catarrhal  stomatitis  the  coating  of  the  tongue  is  soon  followed 
by  a  coj)ious  salivary  secretion;  while  in  fevers  the  tongue  becomes  dry, 
and  the  detachment  of  brown  crusts  leaves  a  glassy,  smooth  surface.  In 
catarrh,  the  appetite  for  solid  food  and  the  digestive  functions  are  not 
much  changed,  while  in  fevers  there  is  great  thirst  and  repugnance  for 
food.  There  are  slight,  if  any,  constitutional  symptoms  in  catarrh,  while 
in  incipient  fever  there  are  marked  constitutional  symptoms. 

Prognosis. — The  acute  form  generally  terminates  in  recovery  within  a  few 
days.  Chronic  oral  catarrh  is  very  persistent  and  stubborn,  and  rarely  yields 
to  treatment. 

Treatment. — In  young  children  the  diet  should  be  cold  milk  with  lime- 
water.  The  mouth  should  be  washed  with  a  slightly  alkaline  wash,  and 
chlorate  of  potash  given  internally.  In  all  cases  the  cause  should  be  re- 
moved, and  the  bowels  regulated  with  rhubarb  and  soda. 

In  chronic  catarrhal  stomatitis,  after  the  removal  of  its  exciting  causes, 
moderately  strong  alkaline  washes  should  be  frequently  used,  and  in  obsti- 
nate cases  a  weak  solution  of  nitrate  of  silver  will  be  found  most  effica- 
cious. Carbolic  acid  sprays  relieve  the  offensive  odor  and  other  unpleasant 
symptoms. 

14 


310  DISEASES    OP   THE    DIGESTIVE    SYSTEM. 


rOLLICIJLAE    STOMATITIS. 

Follicular,  aphthous,  sometimes  called  croupous,  stomatitis  is  a  vari- 
ety of  inflammation  of  the  mouth,  in  which  the  mucous  follicles  are  pri- 
marily and  chiefly  affected. 

Morbid  Anatomy. — On  the  anterior  portion  of  the  tongue,  and  on  the 
mucous  surfaces  of  the  gums  and  cheeks,  there  appear  small  vesicle-like 
elevations,  semi-transparent,  and  having  a  red  zone  about  their  base  ;  these 
are  called  ''aphthae  ;"  some  regard  them  as  a  peculiar  deposit,  others  as  a 
local  croupous  exudation.  They  are  often  numerous  ;  after  they  have  rupt- 
ured they  leave  an  irregular  gray  surface,  resembling  a  small  ulcer,  which 
heals  slowly.  Occasionally  a  number  of  aphthae  coalesce  and  form  irregular 
ulcer-like  or  excoriated  patches.  In  the  majority  of  cases  the  ulcers  soon  dis- 
appear, new  crops  appear  and  the  disease  may  run  a  tedious  course.  Dirty 
white  or  yellow  sloughs  cover  the  ruptured  aphthae,  and  gradually  separate, 
leaving  no  scar.  Follicular  ulcers  on  the  inner  side  of  the  lips  sometimes 
occur  at  the  menstrual  epoch,  or  during  pregnancy  and  lactation ;  ulcers 
like  these  rarely  occur  in  men. 

Etiology. — Aphthffi  may  accompany  any  disease  of  the  tongue  or  mouth. 
It  is,  like  most  oral  diseases,  chiefly  prevalent  among  children  during  den- 
tition, and  is  rare  after  five  years  of  age.  It  is  idiopathic,  or  a  sequela  of 
one  of  the  exanthemata.  Unripe  fruit,  candy,  and  indigestible  food  re- 
maining in  the  child's  mouth  will  cause  it.  Bad  hygienic  surroundings- 
and  a  weakly,  badly  nourished  state  of  the  body,  are  its  principal  predis- 
posing causes.     It  sometimes  prevails  epidemically. 

Symptoms. — Aphthous  stomatitis  shows  itself  in  very  young  children  by 
pain  on  taking  the  breast  and  in  swallowing.  Older  children  have  pain  on 
talking  and  masticating.  There  is  a  slight  febrile  excitement  and  enlarged 
and  tender  sub-maxillary  glands.  Salivation  occurs,  and  tJie  parts  about 
the  month  and  chin  become  excoriated  by  the  saliva,  which  continually 
runs  over  them.  Feculent  diarrhoea  is  common,  and  there  is  more  or  less 
interference  with  digestion. 

Differential  Diagnosis. — This  cannot  be  confounded  with  any  other  dis- 
ease. 

Prognosis. — It  is  never  fatal ;  it  generally  disappears  as  soon  as  the  causes 
that  produced  it  are  removed. 

Treatment. — Correct  any  intestinal  disturbance  that  may  exist  with  small 
doses  of  rhubarb  and  magnesia,  or  mild  salines  ;  restrict  the  diet  to  milk. 
Wash  the  mouth  with  a  weak  solution  of  glycerine  and  borax,  or  chlorate 
of  potash.  In  severe  cases  the  mouth  should  be  washed  every  few  hours 
with  a  dilute  mineral  acid,  or  nitrate  of  silver.  In  weak  children,  wlien  the 
general  health  is  impaired,  stimulants  may  be  given  with  benefit. 


GANGRENOUS   STOMATITIS.  211 


GANGRENOUS    STOMATITIS. 


Grangrenous  stomatitis,  ''cancrura  oris/'  or  sloughing  phagedgena  of  the 
mouth,  is  a  formidable  disease  of  childhood,  in  which  the  tissues  of  the 
cheek  are  prominently  involved. 

Morbid. Anatomy. — There  is  first  a  hard  swelling  developed  in  the  cheek, 
the  skin  over  it  being  red,  shining,  tense,  and  brawny.  In  the  mouth,  at 
the  side  of  the  indenture,  there  is  a  deep,  ragged,  angry,  unhealthy  ulcer 
covered  with  a  dark,  ashy,  or  brown  colored  slough.  The  adjacent  tissue  is 
cedematous,  and  hemorrhage  fi'om  the  livid  and  swollen  part  sometimes 
occurs.  The  ulcer  in  the  cheek  rapidly  extends  and  deepens,  emits  a 
very  fetid  odor,  and  often  perforates  the  walls  of  the  buccal  cavity.  The 
slough  may  occupy  the  whole  of  one  side  of  the  mouth,  the  teeth  may 
become  loosened,  and  caries,  or  necrosis  of  the  inferior  maxilla,  result.  If 
the  ulcerative  process  is  not  extensive,  separation  of  the  slough  may  occur, 
and  the  ulcer  heal  by  granulation  and  cicatrization.  The  facial  vein  may 
be  implicated,  and  then  pyaemia,  with  multiple  abscesses,  may  result. 

Etiology. — This  is  a  very  rare  disease.  It  occurs  principally  in  debilitated 
children  between  two  and  five  years  of  age  who  are  convalescing  from  some 
form  of  acute  disease,  such  as  scarlet  fever.  Whether  it  is  contagious  or 
not  has  never  been  determined.  It  sometimes  follows  the  prolonged  use  of 
mercurials.  Bad  air,  insufficient  food,  and  anti-hygienic  surroundings, 
predispose  to  it. 

Symptoms. — It  commences  with  pain  in  the  mouth,  which  is  increased  by 
movement  of  the  jaws.  Then  the  local  changes  already  described  appear 
on  the  cheek  and  gums,  and  an  abnormal  quantity  of  saliva,  mixed  with  a 
putrescent  fluid,  often  with  blood,  flows  from  the  affected  side  of  the 
mouth.  The  breath  has  a  peculiarly  offensive  odor.  The  adjacent  glands 
become  enlarged  and  tender.  As  the  disease  advances,  the  constitutional 
symptoms  of  septicaemia  are  developed.  In  most  cases  the  child  after  a 
time  becomes  drowsy,  passes  into  coma,  and  dies. 

Differential  Diagnosis. — Cancrum  oris  maybe  mistaken  for  "malignant 
fustuW  Malignant  pustule  attacks  the  skin  and  exposed  parts  -first, 
while  gangrenous  stomatitis  begins  in  the  mucous  membrane  of  the  cheek 
or  about  the  gums,  involving  the  skin  secondarily.  Malignant  pustule  is 
at  once  accompanied  by  constitutional  symptoms,  and  soon  followed  by  the 
phenomena  of  a  septic  or  typhoid  fever,  while  cancrum  oris  is  without 
pyrexia  or  loss  of  appetite  at  its  onset,  and  severe  general  symptoms  do  not 
come  on  till  late. 

Prognosis. — This  is  an  exceedingly  fatal  disease — nineteen  out  of  twenty 
die.  In  the  few  cases  where  the  process  has  been  mild,  recovery  has 
occurred  within  two  weeks  from  its  commencement.  The  complications 
are  pneumonia,  bronchitis,  and  pyaemia.  Death  may  occur  from  exhaus- 
tion or  from  one  of  the  above  named  complications. 

Treatment. — Prompt  measures  are  indicated  at  the  onset  of  this  affection. 
Nitrate  of  silver,  and  even  strong  nitric  acid,  should  be  thoroughly  applied 


212  DISEASES   OF   THE   DIGESTIVE   SYSTEM. 

to  the  slough,  and  the  mouth  frequently  washed  with  solutions  of  carbolic 
acid  and  chlorate  of  potash.  The  best  internal  remedies  are  quinine  and 
hydrochloric  acid.  The  diet  should  be  highly  nutritious  ;  stimulants  may 
be  freely  given,  if  indicated.  "When  the  child  cannot  swallow,  beef  tea  and 
brandy  enemata  should  be  administered. 

ULCERATIVE     STOMATITIS. 

Ulcerative  stomatitis,  or  noma,  is  a  variety  of  inflammation  of  the  mouth 
chiefly  affecting  the  gums  and  spreading  over  a  large  extent  of  surface. 

Morbid  Anatomy. — The  gums  are  hypera^mic  and  tumefied.  Sometimes 
they  assume  a  purplish  color,  separate  from  the  teeth,  and  are  covered  with 
a  pulpy  gray- white  material  which  disintegrates,  becomes  soft  and  dark, 
and  gradually  spreads  to  the  lips  and  side  of  the  cheek.  This  gangrene- 
like slough  may  gradually  extend  until  the  gums  are  destroyed.  In  some 
few  instances  little  vesicles  precede  the  slough.  If  the  slough  is  removed 
as  soon  as  it  appears,  the  gums  underneath  will  be  found  red,  bleeding  and 
granular.  The  teeth  become  loosened  and  often  drop  out,  the  tongue 
enlarges  and  has  a  sodden  a]3pearance,  and  the  mucous  membrane  of  the 
cheek  swells  so  that  it  often  receives  the  impression  of  the  teeth.  Some- 
times the  bones  about  the  face  lose  their  periosteum  and  exfoliate.  When 
recovery  takes  place  deep  cicatrices  may  remain  and  cause  more  or  less 
distortion  of  the  face. 

Etiology. — Noma,  or  ulcerative  stomatitis,  is  met  with  only  in  children 
from  one  to  ten  years  of  age.  It  occurs  among  those  who  inhabit  filthy 
localities,  who  are  badly  fed  and  compelled  to  breathe  unwholesome  air. 
Dampness  seems  to  exert  a  predisposing  influence,  and  the  disease  is  most 
prevalent  during  the  autumn  months.  It  is  probably  contagious,  for  well- 
marked  epidemics  of  it  are  recognized.  It  is  common  after  asthenic  in- 
flammation and  the  eruptive  fevers.  The  prolonged  use  of  mercurials  will 
cause  ulcerative  stomatitis. 

Symptoms. — The  mouth  is  hot  and  painful  for  some  time,  and  then  ap- 
pear the  changes  already  described.  There  is  pain  on  chewing  or  speaking, 
and  there  may  be  slight  febrile  excitement,  although  constitutional  symp- 
toms are  not  prominent.  There  is  an  increased  flow  of  saliva  which  has 
a  very  offensive  odor,  and  is  mixed  with  blood  and  shreds  of  the  pulpy 
mass.  There  is  enlargement  and  tenderness  of  the  sub-maxillary  glands. 
In  some  cases  the  child  will  pick  at  its  mouth  and  throat,  and  very  often 
loosens  and  swallows  some  of  the  shred-like  sloughs.  The  appetite  may 
not  be  impaired,  though  the  bowels  are  disordered,  and  the  child  is  restless 
and  sleepless.  The  upper  lip  becomes  swollen,  dark-red,  and  projects  out- 
ward, while  the  mouth  is  kept  widely  open  to  prevent  painful  contact  with 
the  lips  or  tongue.  The  excessive  salivation  soon  decreases,  but  the  un- 
pleasant fetor  of  it  and  of  the  breath  persists.  Late  in  the  disease  the  adja- 
cent glands  become  enlarged  and  tender. 

Differential  Diagnosis. — Ulcerative  stomatitis  maybe  mistaken  for  "  can- 
crum  oris,"  or  gangrenous  stomatitis.     It  is  a  local  disease,  while  cancrum 


THRUSH.  213 

oris  is  attended  by  constitutional  symiotoms  ;  it  begins  in  the  gums,  while 
gangrenous  stomatitis  begins  in  the  cheek.  The  j)rogress  of  noma  is  slow 
compared  with  the  very  rapid  extension  of  cancrum  oris.  The  livid  red- 
ness, the  dark  swelling,  and  the  ashy  slough  of  cancrum  oris  are  absent  in 
ulcerative  stomatitis. 

Prognosis. — This  is  good.  Its  duration  is  about  eight  days,  but  slough- 
ing about  the  gums  may  continue  for  weeks. 

Treatment. — The  treatment  is  the  same  as  in  aphthous  stomatitis.  The 
chlorate  of  potash  may  be  used  as  a  wash  or  gargle  and  internally,  and  will 
usually  arrest  it.  In  many  instances,  fresh  air,  cleanliness  and  a  restricted 
diet  are  all  that  is  necessary  to  effect  a  cure.  If  the  ulceration  spreads, 
the  application  of  nitric  acid,  and  sometimes  the  employment  of  the  ac- 
tual cautery,  must  be  resorted  to.  For  the  profuse  salivation  which  is 
sometimes  so  troublesome,  belladonna  has  proved  efficacious. 

THEUSH. 

Thrush,  sjjrtie  or  muguet  is  an  aphthous  disease  of  the  epithelium  of 
the  mouth  and  tongue,  due  to  the  growth  of  the  germs  of  the  thrush-fun- 
gus, the  oidiutn  albicans.  It  was  formerly  classed  as  an  exudative  inflam- 
mation. 

Morbid  Anatomy. — The  mucous  membrane  of  the  mouth  assumes  a  dark 
red  color,  and  upon  the  most  superficial  layer  of  the  epithelium  there  ap- 
pear numerous  small,  round  whitish  spots, — "  aphthas," — which  give  to  it  a 
flocculent  or  curdy  appearance.  These  spots  are  often  aggregated  in 
groups  of  two  or  three  ;  at  first,  as  they  enlarge,  they  fall  off  or  can  be 
readily  removed,  but  are  soon  reproduced  and  run 
together  m  patches.  The  development  in  thrush 
of  the  oidium  albicans  and  of  its  frequent  j)arasitic 
companion,  the  leptothrix  buccalis,  in  and  between 
the  epithelial  cells  may  continue  until  the  mucous 
tissue  is  invaded.  The  epithelium  becomes  swollen 
and  loosened,  the  tongue  and  inside  of  the  mouth 
are  covered  with  a  yellowish  pultaceous,  creamy 
mass,  underneath  which  the.  mucous  membrane  is 
of  deep  red  color,  and  the  papillfe  are  enlarged.  In 
the  new-born  it  occurs  most  abundantly  about  the 
boundary  line  between  the  hard  and  soft  palates  ; 
in  adults,  on  the  mucous  membrane  of  lips,  cheek  '*^'  ^^' 

,  ,      „    ,  -ri  -TIT  Oidium  Albicaiis.     From  the 

and  end  of  tongue.  It  may  invade  the  pharynx,  tongvein  a  case  of ''Thrush:'' 
oesophagus  and  stomach.  It  has  been  found  in  the  uai  tiireads^^''^  m.  '  ^^' 
lungs  and  air-passages  and  about   the  breasts  and 

genitals  of  infants.  A  microscopic  examination  of  a  patch  shows  it  to  con- 
tain mucous  and  epithelial  cells,  fat  spherules,  and  the  spores  and  filaments 
of  the  oidium  albicans.  The  spores  are  round  or  ovoid  and  form  masses  of 
varying  sizes,  while  the  filaments  coming  out  of  the  spores  are  cylindrical, 
curved  or  branched,  and  consist  of  long  cells,  which  are  constricted  where 
they  Join  one  another,  each  cell  being  filled  with  granules. 


314  DISEASES   OF  THE   DIGESTIVE   SYSTEM. 

Etiology. — In  children  this  disease  occurs  from  birth  to  the  second  year, 
and  is  very  rare  after  that  time  until  adult  life.  These  parasitic  plants 
grow  best  in  the  presence  of  acids,  hence  the  acid  secretion  of  the  mouth 
for  the  first  six  or  seven  months  predisposes  to  it.  All  food  or  drink  that 
will  produce  irritation  of  the  stomach  or  intestines,  and  make  the  intestinal 
contents  acid,  jDredisposes  to  it.  Want  of  cleanliness  in  the  care  of  nursing- 
bottles,  spoons,  etc.,  is  one  of  its  principal  causes,  consequently  it  is  more 
frequently  met  with  in  children  brought  up  on  the  bottle,  especially  in  asy- 
lums. In  adults  thrush  occurs  toward  the  end  of  any  long  exhausting 
disease,  such  as  cancer,  or  consumption. 

Symptoms. — In  children  the  mouth  becomes  hot  and  painful.  The  child 
will  not  allow  its  mouth  to  be  touched.  An  examination  shows  the  mu- 
cous membrane  to  be  drier  than  natural  ;  soon  after,  the  peculiar  thrush 
aphthae  appear,  and  there  is  salivation,  which  is  always  markedly  acid. 
The  lips  swell  and  become  everted.  Diarrhoea  is  frequent  and  the  passages 
are  often  green  and  smell  of  fatty  aci^s  ;  so  acid  are  they  at  times  that 
they  cause  an  erythema  about  the  anus.  If  this  condition  persists,  the  but- 
tocks and  parts  around  the  genitals  become  excoriated.  Besides  this  diar- 
rhoea, vomiting  and  purging  give  additional  evidence  of  gastro-intestinal 
disturbance.  In  adults  suffering  from  exhausting  disease,  the  mouth  be- 
comes hot,  dry  and  painful  before  the  thrush  appears,  and  there  is  diffi- 
culty in  swallowing,  after  which  the  mouth  and  tongue  soon  present  the 
characteristic  appearance  of  the  disease. 

Differential  Diagnosis. — The  presence  of  the  parasite  establishes  the  diag- 
nosis. 

Prognosis.— In  vigorous  children  the  average  duration  of  this  affection 
is  from  eight  to  ten  days,  but  in  feeble  infants  it  often  lasts  for  months. 
Its  only  serious  complication  is  gastro-intestinal  catarrh.  Death  may  result 
from  the  exhaustion  of  the  diarrhoea. 

Treatment. — The  most  important  thing  to  be  accomplished  in  the 
treatment  of  this  affection  is  to  arrest  or  counteract  the  acidity  of  the  se- 
cretions of  the  mouth.  After  each  feeding  the  mouth  must  be  thoroughly 
cleansed  with  borax  and  glycerine,  or  a  weak  solution  of  carbolic  acid,  and 
sulphate  of  soda.  The  diet  should  be  restricted  to  milk  with  lime-water  ; 
when  there  is  emaciation,  cod-liver  oil  and  the  lactophosphate  of  lime  will 
be  of  service.     The  bowels  must  be  regulated  as  in  follicular  stomatitis. 

GLOSSITIS. 

Glossitis  is  an  inflammation  of  the  parenchyma  of  the  tongue.  It  may 
be  acute  or  clironic,  and  when  chronic,  is  generally  circumscribed. 

Morbid  Anatomy. — There  is  first  intense  hypersemia,  causing  slight  swell- 
ing and  intense  redness  of  the  tongue.  This  is  soon  followed  by  so  great 
an  enlargement  of  the  organ  that  it  entirely  fills  the  mouth  and  protrudes 
beyond  the  teeth.  Its  surface  is  covered  by  a  thick  secretion,  and  its  sub- 
stance assumes  a  pale  or  grayish  color.  The  oedematous  condition  may 
rapidly  subside  and  leave  the  tongue  in  its  normal  state,  or  the  inflammac 


GLOSSITIS.  215 

tion  may  be  so  intense  that  small  abscesses  form  which  leave  deep  cica- 
tricial depressions,  giving  the  tongue  an  uneven  and  lobulated  appearance. 
In  some  instances  the  tongue  may  remain  enlarged  and  hardened  for  life. 
There  is  a  rare  variety  of  glossitis  which  does  not  invade  the  deeper  struct- 
ure of  the  tongue,  but  is  confined  to  its  mucous  and  sub-mucous  tissue, 
causing  thickening  and  sloughing  of  its  surface,  with  depressions  similar  to 
the  cicatricial  depressions  of  the  parenchymatous  variety. 

Chronic  glossitis  occurs  chiefly  in  patches  along  the  edges  of  the  tongue  ; 
the  thickening,  induration,  and  cicatricial  depressions  occur  in  circum- 
scribed spots.  When  chronic  glossitis  is  general,  the  tongue  is  uniformly 
enlarged  and  its  color  is  much  redder  than  normal,  some  spots  being 
darker  than  others  ;  its  movements  are  interfered  with,  and  its  surface  pre- 
sents the  appearance  of  eczema  of  the  skin. 

Etiology. — Acute  glossitis  may  develop  under  the  influence  of  mercurial 
poison,  or  as  a  consequence  of  direct  injury.  Croton  oil  and  other  acrid 
matters  taken  into  the  mouth  may  cause  it ;  burns,  blows,  and  the  poison 
of  insects  have  caused  it.  Chronic  glossitis  occurs  in  the  old  without  any 
apparent  cause.  It  may  be  produced  by  disease  of  the  teeth,  or  of  the  maxil- 
lary bones,  and  may,  in  some  instances,  result  from  the  action  of  the  mate- 
rials of  which  false  teeth  are  made. 

Symptoms. — With  the  enlargement  of  the  tongue  in  acute  glossitis,  there 
is  great  restlessness  and  anxiety,  accompanied  by  an  increase  of  the  pulse- 
rate,  and  an  elevation  of  the  temj)erature.  In  some  cases,  there  is  profuse 
salivation,  and  the  swollen  tongue  protrudes  between  the  lijDS.  There  is  a 
sensation  of  heat  in  the  mouth,  and  the  swelling  often  causes  severe  pain. 
The  glands  at  the  angle  of  the  jaw  are  enlarged  and  tender,  and  all  move- 
ments of  the  tongue  in  talking,  chewing  or  swallowing  become  exceedingly 
painful  and  frequently  impossible.  Dyspnoea  and  inability  to  lie  down  are 
sometimes  caused  by  the  obstniction  to  the  free  entrance  of  the  air  into  the 
lungs.  When  the  veins  in  the  neck  are  compressed,  cyanosis  of  the  face  is 
marked.  The  patient  is  anxious,  and  very  much  depressed,  and  may  show 
signs  of  asphyxia  ;  indeed  death  has  occurred  from  suffocation  in  extreme 
cases.  When  it  terminates  in  suppuration,  the  constitutional  symptoms  be- 
come severe,  and  all  the  oral  symptoms  are  intensified.  When  clefts  remain 
in  the  tongue  after  glossitis,  the  ulcers  in  them  are  painful,  but  otherwise 
there  is  no  inconvenience.  In  superficial  glossitis,  which  is  apt  to  be  pro- 
tracted, any  movement  of  the  tongue  is  painful,  and  there  is  constant  sali- 
vation. In  chronic  glossitis  patients  sometimes  complain  of  a  dull  aching 
in  the  tongue,  and  in  some  cases  movements  of  the  tongue  induce  pain  of 
a  burning  character. 

Differential  Diagnosis. — Chronic  circumscribed  glossitis  may  be  mistaken 
for  cancer.  Cancer  develops  rapidly,  and  chronic  circumscribed  glossitis  al- 
most imperceptibly.  Cancer  tends  to  speedy  ulceration,  and  hemorrhage  is 
frequent,  while  glossitis  passes  on  to  induration  and  there  is  no  hemorrhage. 
Fetor  of  the  breath  is  present  early  in  cancer,  while  it  is  slight  or  altogether 
absent  in  glossitis.  In  cancer  the  pain  is  sharp  and  lancinating,  running 
along  the  branches  of  the  fifth  nerve,  while  there  is  only  a  dull  pain  in 


216  DISEASES    OF   THE    DIGESTIVE    SYSTEM. 

glossitis.  In  cancer  the  adjacent  lympliatics  are  early  involved,  in  glossitia 
they  are  uninvolved.  In  cancer,  emaciation  and  cachexia  are  marked ; 
these  are  absent  in  glossitis.  A  microscopical  examination  of  a  portion  of 
the  diseased  tissue  will  establish  the  diagnosis. 

Prognosis. — In  acute  glossitis,  the  prognosis  is  uncertain,  for  suffocation 
may  occur  unexpectedly;  generally  it  subsides  in  from  three  to  seven  days. 
Of  the  modes  of  termination,  that  of  thickening  and  induration  is  the  most 
common,  and  is  rarely  entirely  recovered  from. 

Treatment. — In  acute  glossitis,  ice  should  be  freely  applied  to  the  tongue 
and  a  mild  cathartic  administered.  If  the  patient  is  not  able  to  swallow 
castor  oil,  a  turpentine  enema  may  be  given.  If  the  swelling  interferes  with 
respiration,  free  and  deep  incisions  on  the  upper  surface  must  be  at  once 
made,  and  if  abscesses  form  they  should  be  promptly  opened  and  washed 
out  with  some  disinfectant  fluid.  The  ulcerations  occurring  in  glossitis 
should  be  treated  in  the  same  way  as  those  of  ulcerative  stomatitis.  In  the 
chronic  form,  if  possible,  remove  the  cause.  In  superficial  glossitis,  the 
local  application  of  carbolic  acid  will  be  found  the  best  remedy.  If  suffo- 
cation becomes  imminent  in  either  variety,  tracheotomy  should  be  per- 
formed. 

CAlSrCER    OF    THE    TONGUE. 

The  most  common  variety  of  cancer  of  the  tongue  is  epithelioma. 

Morbid  Anatomy. — At  some  point  that  has  been  subjected  to  constant 
irritation,  or  in  some  ulcerative  cleft  in  the  tongue,  there  appears  a  small 
unhealthy  ulcer  or  a  small  deeply  seated  nodule.  When  appearing  on  an 
otherwise  healthy  tongue,  its  locality  is  usually  on  its  edge.  In  whatever 
way  it  may  begin,  an  ulcer  quickly  forms,  circular  in  shape  with  ragged 
everted  edges,  and  a  wide  indurated  base.  The  surface  of  the  tumor  has  a 
dirty  white  or  grayish-red  appearance,  is  papillated  and  friable,  and  com- 
monly of  a  firm  consistency.  As  the  disease  advances,  it  may  involve  the 
whole  tongue,  which  is  then  larger  than  normal,  unevenly  lobulated,  and 
covered  with  small  ulcerations.  The  mucous  membrane  on  the  floor  and 
sides  of  the  mouth  may  be  secondarily  invaded.  As  the  deeper  tissues  are 
encroached  upon,  hemorrhages  occur.  The  sub-maxillary  and  sub-lingual 
glands  early  take  part  in  the  cancerous  development,  and  the  oral  cavity 
may  be  filled  with  the  cancerous  mass.  On  scraping  the  surface  of  an  epi- 
thelial cancer,  a  grayish  granular  mass  is  found  beneath,  a  portion  of  which 
under  the  microscope  will  show  the  characteristics  of  an  epithelioma. 

Etiology. — Cancer  of  the  tongue  is  met  with  most  frequently  in  middle 
life,  between  the  ages  of  thirty-five  and  sixty,  and  occurs  in  men  more  often 
than  in  women.  Its  chief  exciting  cause  is  some  local  irritation,  as  from  a 
projecting  or  carious  tooth.  It  may  develop  in  syphilitic  fissures.  Oc- 
casionally it  appears  on  a  tongue  whose  mucous  membrane  has,  for  a  long 
time,  been  thickened  and  indurated.  Usually  there  is  an  hereditary  pre- 
disposition to  cancerous  develojDment.  It  may  develop  without  any  discov* 
erable  cause. 

Symptoms. — In  most  cases,  from  the  onset  there  is  a  sharp  pain  at  the  seat 


PAROTITIS.  217 

of  the  disease.  This  pain  is  aggravated  by  any  movement  of  the  tongue, 
and  generally  runs  along  the  branches  of  the  fifth  nerve.  Salivation  is  pro- 
fuse, and  swelling  of  the  lymphatics  in  the  neighborhood  is  present  early. 
Hemorrhages  not  infrequently  occur,  which  increase  the  anaemia  that  at- 
tends the  cancerous  cachexia.  The  disease  runs  a  very  rapid  course,  the 
pain  becomes  agonizing,  and  a  fatal  termination  may  at  anytime  occur  from 
hemorrhage  from  the  lingual  artery,  or  suffocation  may  result  from  me- 
chanical interference  with  respiration. 

Differential  Diagnosis.  —  This  disease  may  be  mistaken  for  syphilitic  ulcer- 
ation. A  syphilitic  ulcer  is  long  and  oval  or  irregular  in  shape,  while  can- 
cer is  circular.  A  syphilitic  ulcer  is  developed  slowly  and  with  little  or 
no  localized  pain,  but  cancer  spreads  rapidly  and  is  accompanied  by  severe 
pam.  The  constitutional  symptoms  of  syphilis  are  usually  well  marked, 
and  the  ulcer  improves  under  anti-syphilitic  treatment,  while  the  evidences 
of  syphilis  are  absent  in  cancer.  A  microscopical  examination  of  a  small 
portion  of  the  ulcerating  surface  removes  all  doubt  in  diagnosis. 

Prognosis. — The  disease  advances  rapidly;  its  average  duration  is  about 
fourteen  months.  I  have  known  cases  to  last  two  years.  Death  results 
from  the  cancer,  marasmus,  exhaustion  from  hemorrhage,  or  from  starva- 
tion, as  the  intense  pain  in  eating  causes  the  patient  to  refuse  food.  The 
constant  and  long-continued  pain  hastens  the  fatal  termination.  If,  after 
removal,  it  does  not  reappear,  death  may  result  from  cancerous  develop- 
ments in  other  parts  of  the  body. 

Treatment. — The  relief  of  pain  and  the  maintenance  of  the  vital  powers 
are  the  principal  indications.  The  hypodermic  use  of  morphia  is  the  best 
means  of  relieving  pain.  Antiseptic  gargles  are  grateful,  and  counteract 
the  offensive  odor  of  the  breath  and  the  unpleasant  taste.  The  checking 
of  hemorrhage,  removal  of  the  growth,  removal  of  the  tongue,  ligation  of 
the  lingual  artery  and  division  of  the  gustatory  nerve,  belong  to  the  surgical 
rather  than  to  the  medical  treatment  of  the  affection. 

PAEOTITIS. 

Parotitis,  or  "  mumps,"  is  a  catarrhal  inflammation  of  one  or  both  pa- 
rotid glands ;  rarely  are  the  other  salivary  glands  involved.  It  is  of  two 
varieties,  specific  and  non-specific.     The  latter  is  also  called  symptomatic. 

Morbid  Anatomy. — The  left  parotid  is  usually  first  affected.  The  disease 
commences  in  the  gland-ducts,  not,  as  was  formerly  supposed,  in  the 
intercellular  substance.  Both  varieties  begin  as  a  catarrh,  the  intense 
initial  hypersemia  of  the  parotid  being  followed  by  a  serous  exudation  and 
a  soft  swelling  of  the  gland.  From  the  few  cases  that  have  been  examined 
at  this  stage,  we  learn  that  there  is  oedema  of  the  acini,  and  that  the  gland 
is  reddened  and  injected,  presenting  a  fleshy  appearance.  The  connective- 
tissue  about  the  parotid  and  often  the  parts  beyond  it  are  involved.  The 
gland  which  is  so  enormously  swollen  may  decrease  to  its  normal  size  by 
the  absorption  of  the  exudation;  or,  when  the  process  is  very  severe,  the 
idiopathic  variety  may  end  in  abscess  ;  this  termination  is  much  less  fre- 


218  DISEASES    OF   THE    DIGESTIVE    SYSTEM. 

quent  than  in  metastatic  parotitis.  Occasionally,  the  gland  remains  per- 
manently  enlarged.     It  may  atrophy. 

Metastatic  parotitis  begins  with  a  catarrh  of  the  ducts  ;  there  is  first 
hypersemia,  followed  by  an  exudation  into  the  ducts,  which  is  semi-transpa- 
rent or  yellow.  The  acini  are  wholly  or  partly  filled  with  pus,  and  there 
result  numerous  little  spots  of  suppuration,  but  if  the  process  is  severe  and 
rapid  the  interstitial  tissue  becomes  involved,  and  the  whole  gland  may  be 
converted  into  an  abscess.  The  suppurating  process  may  extend  to  the 
neighboring  bones,  muscles,  connective-tissue,  or,  rarely,  to  the  cranial 
bones  and  meninges.  As  in  "cancrum  oris,"  if  the  adjacent  veins  are  in- 
volved, pyaemia  and  multiple  abscesses  are  the  result.  The  Eustachian 
tube  may  be  involved,  and  sometimes  pus  burrows  under  the  muscles  at 
the  back  of  the  neck. 

Etiology. — Specific  parotitis  seldom  occurs  except  as  the  result  of  conta- 
gion. It  is  contagious,  but  not  infectious,  and  seems  to  be  favored  in  its 
development  by  dampness.  Consequently,  it  is  common  in  autumn  and 
early  spring,  and  among  those  who  live  in  cold,  damp  cellars.  It  prevails 
most  in  crowded  localities,  such  as  asylums  and  foundling  hospitals.  It 
resembles  the  exanthemata,  in  that  it  attacks  the  same  gland  but  once. 
The  exact  cause  of  metastatic  parotitis  is  obscure.  The  reason  of  its  devel- 
opment in  small-pox,  typhus,  typhoid,  measles,  pyaemia,  septicaemia,  chol- 
era, and  rarely  in  pneumonia,  cannot  always  be  given.  The  period  of 
incubation  in  specific  parotitis  varies  from  seven  to  fourteen  days. 

Symptoms. — In  specific  parotitis  for  a  short  time  preceding  the  glandular 
enlargement  there  is  chilliness  followed  by  flashes  of  heat,  frequently  by 
dull  pains  in  the  limbs,  general  lassitude  and  loss  of  appetite.  In  nervous 
children  headache,  delirium,  and  often  convulsions  are  its  premonitory 
symptoms.  In  from  thirty-six  to  forty-eight  hours  after  these  phenomena, 
there  is  a  sensation  of  stiffness  about  the  angle  of  the  jaw,  followed  by  pain. 
and  swelling  in  the  parotid  region.  The  pain  is  increased  by  speaking, 
swallowing,  and  by  pressure.  Both  glands  may  be  simultaneously  affected 
but  usually  only  one  is  involved  at  a  time.  The  tumor  is  firmer  over  the 
centre  than  at  its  circumference,  the  outer  rim  being  slightly  cedematous 
and  pitting  on  pressure.  Moderate  salivation  occurs  in  a  few  instances. 
The  disease  reaches  its  height  in  from  three  to  five  days,  and  the  swell- 
ing of  the  gland  begins  to  subside  on  the  seventh  or  eighth  day. 

In  the  non-specific  variety,  if  abscess  form,  constitutional  symptoms  in- 
dicative of  the  formation  of  pus  are  developed,  and  the  adjoining  lymphat- 
ics become  enlarged.  These  abscesses  may  open  externally,  into  the  mouth, 
pharynx,  or  external  ear.  During  or  after  the  decline  of  specific  parotitis, 
metastasis  to  the  testicles,  mammae,  or  ovaries  may  occur.  Metastasis  to  the 
meninges  of  the  brain  (a  rare  occurrence)  is  indicated  by  delirium  and  active 
cerebral  symptoms,  which  terminate  in  coma  and  death.  Non-specific  paro- 
titis, developing  during  some  severe  constitutional  disease,  produces  few 
symptoms  of  its  own,  excepting  the  physical  evidences  of  the  tumor,  which 
shows  a  tendency  to  suppurate  from  its  beginning ;  very  soon  a  lobulated  red 
swelling  exhibiting  fluctuation  at  various  points  is  developed,  which  soon 


TONSILLITIS.  219 

discharges  laudable  pus.  In  this  variety,  but  one  gland  is  usually  in- 
volved. 

Diflferential  Diagnosis. — There  is  little  difficulty  in  recognizing  this  disease 
by  the  situation  of  the  swelling. 

Prognosis. — In  the  specific  variety  the  prognosis  is  favorable,  the  gland 
usually  returning  to  its  normal  si  e  and  consistence  in  from  ten  days  to  two 
weeks.  If  an  abscess  forms  and  implicates  the  ear  or  Eustachian  tube,  per- 
manent deafness  may  result ;  when  orchitis,  mammitis,  meningitis  and 
other  metastases  complicate  the  parotitis,  the  prognosis  is  more  or  less  un- 
favorable. Death  may  result  from  meningitis  with  active  brain  symptoms. 
Non-specific  parotitis,  occurring  in  the  course  of  any  acute  general  disease, 
must  be  regarded  as  a  very  unfavorable  symptom. 

Treatment. — Specific  parotitis  is  a  self-limiting  disease  ;  during  its  active 
period  the  patient  must  be  kept  in  an  even  temperature,  and  a  mild  saline 
cathartic  may  be  administered.  The  diet  should  be  non-stimulating.  If 
the  parts  are  painful,  warm  fomentations  may  be  applied.  If  the  patient 
suffers  severe  pain  or  is  restless,  the  bromide  of  potassium  or  hydrate  of 
chloral  may  be  given.  Inunctions  of  oil,  when  the  swelling  is  disappear- 
ing, are  said  to  aid  in  reducing  it.  When  orchitis  or  meningitis  occurs  it  is 
to  be  treated  as  a  complication.  During  convalescence  tonics  are  indicated. 
The  non-specific  variety  requires  no  treatment  except  the  use  of  means 
which  hasten  suppuration  and  support  the  patient. 

DISEASES   OF  THE   PHAEYNX. 

I.  Tonsillitis:— {a.)  Acute  ov  Quinsy ;  and  {h.)  Chronic— 11.  Inflam- 
mations:—{a.)  Catarrhal  which  is  either  Acute  or  Chronic;  and,  {h.) 
Memhranous,  which  is  either  Croupous  or  Diphtheritic. — III.  Retro- 
pharyngeal Abscess. 

TOl^SILLITIS. 

"  Quinsy  sore  throat,"  sometimes  called  phlegmonous  pharyngitis,  is  an 
inflammation  of  the  parenchyma  of  one  or  both  tonsils,  and  may  be  acute  or 
chronic. 

Morbid  Anatomy.— It  must  be  remembered  that  beneath  the  external  cov- 
ering of  the  tonsils  fibrous  trabecular  enclose  numerous  groups  of  lymph-fol- 
licles, and  that  this  interstitial  stroma  is  very  vascular.  In  acute  tonsillitis 
there  is  first  hypergemia  and  swelling  of  the  gland  and  of  the  parts  adjacent 
to  it.  The  angry,  red,  lobulated  surface  of  the  enlarged  gland  and  the 
back  part  of  the  tongue  are  covered  with  a  tough,  gelatinous  or  creamy 
secretion,  and  the  uvula  and  anterior  pillars  of  the  fauces  become  swollen 
and  oedematous.  When  suppuration  is  to  occur  a  point  on  the  surface  of 
the  inflamed  tonsil  becomes  prominent,  soft  and  fluctuating.  The  loose 
cellular  tissue  surrounding  the  tonsils  may  be  involved  in  the  suppurating 
processes.  If  chronic  tonsillitis  follows,  subsidence  of  the  acute  hypertrophy 
of  the  stroma  occurs,  accompanied  by  enlargement  of  the  supplying  ves- 
sels.    Chronic  enlargement  of  the  tonsils  may  also  be  developed  slowly 


220  DISEASES    OF   THE   DIGESTIVE    SYSTEM. 

without  being  preceded  by  the  acute,  and  then  the  glands  may  become  so 
large  that  they  touch  each  other  and  are  much  firmer  and  harder  than  the 
normal  gland.  Their  surface  presents  a  pitted  appearance,  the  mucous 
membrane  usually  being  paler  than  natural. 

Etiology. — Quinsy  is  rare  in  those  under  twelve  years  of  age,  but  it  is  more 
common  in  youth  than  in  adult  life.  Certain  atmospheric  influences  pre- 
dispose to  it.  There  is  a  strong  hereditary  predisposition  to  it  in  certain 
persons.  It  ^'runs  in  families."  Certain  diseases,  as  scrofula  and  syphilis, 
favor  its  development.  Exposure  of  the  surface  to  cold  almost  always  pre- 
cedes an  attack.  After  a  first  attack  it  is  liable  to  occur  at  stated  intervals 
each  year.  Tonsillitis  frequently  occurs  with  scarlatina,  measles,  typhoid 
fever,  and  with  inflammatory  conditions  of  the  mouth  or  tongue.  Chronic 
tonsillitis,  which  is  not  a  sequela  of  the  acute,  is  almost  always  hereditary. 

Symptoms. — Acute  tonsillitis  is  usually  ushered  in  by  a  distinct  chill  fol- 
lowed by  a  rapid  elevation  of  temperature  ranging  from  103°  F.  to  105°  F., 
with  a  corresponding  increase  in  the  frequency  of  the  pulse.  In  from 
twelve  to  thirty-six  hours  after  the  initial  fever  there  is  heat,  pain  and 
swelling  in  the  region  of  the  tonsils,  and  dryness  of  the  tongue  and  throat. 
The  attempts  which  the  patient  makes  to  swallow  an  imaginary  substance 
in  the  fauces  increase  the  pain.  Fluids  are  often  regurgitated  through  the 
nostrils.  The  respirations  become  difficult  on  account  of  the  obstruction  to 
the  ingress  and  egress  of  air.  The  tumor  produced  by  the  swollen  tonsil 
can  be  readily  felt  externally.  Thick  mucus  is  expectorated,  and  the 
tongue  becomes  swollen  and  covered  with  a  thick  pasty  coating.  The 
breath  is  offensive,  the  jaws  are  often  immovable,  any  attempts  to  move 
them  causing  darting  pains  along  the  Eustachian  tube  to  the  ear.  There 
is  a  peculiar  "nasal "  tone  to  the  voice,  and  if  the  throat  can  be  examined, 
the  passage  to  the  pharynx  is  found  obstructed  by  the  swollen  glands,  the 
cedematous  uvula,  and  the  oedematous  anterior  pillars  of  the  soft  palate. 

These  symptoms  steadily  increase  in  severity.  The  patient  is  unable  to 
sleep,  and  suffers  constantly  from  a  sense  of  impending  suffocation.  He  is 
sometimes  delirious.  The  constitutional  and  local  symptoms  increase  for 
several  days,  and  then  gradually  subside,  or  something  is  felt  to  give  way  in 
the  throat,  and  suddenly  the  patient  is  entirely  relieved  by  the  discharge  of 
fetid  yellow  pus.  Convalescence  is  rapid.  "When  a  chronic  enlargement  is 
the  result  of  quinsy,  violent  paroxysms  of  coughing  and  loud  snoring  dur- 
ing sleep  are  caused  by  the  enlarged  tonsils  and  elongated  uvula,  which  lat- 
ter, in  some  cases,  produces  an  inclination  to  vomit.  The  Eustachian  tube 
being  pressed  upon,  partial  or  permanent  deafness  results,  and  the  voice 
has  a  thick  and  often  husky  tone.  Chronic  catarrhal  stomatitis  frequently 
accompanies  this  form  of  tonsillitis  ;  acute  attacks  may  be  engrafted  upon 
the  chronic  condition.  Slight  dysphagia  and  impediment  to  full  and  deeji 
inspirations,  as  well  as  a  permanent  change  in  the  voice,  are  caused  b} 
chronic  tonsillitis. 

DifFerential  Diagnosis. — It  is  hardly  possible  to  mistake  quinsy  for  an} 
other  disease  if  a  proper  examination  of  the  throat  is  made. 

Prognosis. — The  prognosis  in  acute  tonsillitis  is  always  good.     The  onl}i 


CATARRHAL   PHARYKGITIS.  221 

thing  to  be  feared  is  that  chronic  enlargement  of  the  tonsils  may  result. 
The  duration  of  the  urgent  symptoms  is  from  four  to  five  days — the  entire 
duration  is  eight  days.  It  may  be  complicated  by  inflammatory  conditions 
of  the  tongue  and  mouth,  by  inflammation  of  the  Eustachian  tubes,  by 
pharyngitis  and  oedema  glottidis.  Death  in  rare  instances  may  result  from 
suffocation,  exhaustion,  or  cedema  glottidis. 

Treatment — When  seen  early,  astringent  gargles  and  the  carbolized  spray 
will  afliord  relief,  and  in  some  instances  seem  to  arrest  its  progress.  After 
the  chill,  suppuration  can  rarely  be  prevented.  Warm  poultices  of  linseed 
meal,  the  wet  pack,  or  external  applications  of  turpentine,  are  then  found 
most  efficacious  and  agreeable.  I  have  been  able  in  a  large  number  of 
cases  to  abort  a  quinsy  by  a  twenty-grain  dose  of  quinine  administered  at 
the  time  of  the  chill,  followed  by  a  large  dose  of  bromide  of  potassium. 
Mild  cathartics  should  be  administered  at  the  commencement  of  the  at- 
tack ;  a  combination  of  belladonna,  quinine  and  aconite  has  been  thought 
by  some  to  have  a  controlling  influence  over  this  disease.  Acetate  of  am- 
monia, chlorate  of  potash,  or  some  effervescing  draught  is  generally  grate- 
ful to  the  patient ;  the  diet  should  be  highly  nutritious ;  moderate  stimula- 
tion is  often  required.  As  soon  as  an  abscess  forms  it  should  be  opened. 
Warm  poultices  may  be  applied  over  the  region  of  the  glands  for  some  time 
thereafter.  If  suffocation  threaten  at  an  early  stage  of  the  disease,  free 
scarification  of  the  swollen  and  oedematous  parts,  or  excision  of  the  tonsils 
must  at  once  be  made.  In  chronic  tonsillitis,  tannin  and  glycerine,  or  a 
strong  solution  of  alum  or  iodine,  should  be  carefully  and  regularly  ap- 
plied ;  at  the  same  time  iodide  of  potash  or  iron  may  be  given.  It  may 
be  necessary  to  excise  a  part  or  all  of  the  gland,  and  part  of  the  uvula,  af- 
ter other  remedies  have  been  tried  and  found  unavailing. 

CATARRHAL     PHARYNGITIS. 

This  is  an  inflammation  of  the  mucous  membrane  of  the  tonsils,  uvula, 
soft  palate  and  pharynx.  It  may  be  acute  or  chronic,  and  may  affect  all  or 
only  portions  of  the  pharynx. 

Morbid  Anatomy. — The  morbid  changes  in  the  mucous  membrane  are  the 
same  as  in  catarrhal  laryngitis  and  stomatitis.  The  uvula  is  enlarged,  and 
the  calibre  of  the  pharynx  is  lessened.  In  chronic  catarrhal  pharyngitis 
the  mucous  membrane  is  either  generally  thickened  and  indurated,  or  the 
thickening  occurs  in  irregular  patches.  The  uvula  is  relaxed,  and  the  af- 
fected parts,  are  covered  with  a  viscid  mucus  of  a  slightly  offensive  odor. 
The  lymphatics  are  enlarged,  especially  at  the  back  part  of  the  pharynx, 
and  small  round  nodules  (often  aggregated  into  masses  of  considerable  size) 
present  the  appearance  called  "follicular  pharyngitis."  Tlie  escape  of  secre- 
tions from  the  glands  being  prevented,  the  latter  dilate  and  form  cysts 
whose  contents  undergo  cheesy  degeneration,  or,  after  forming  vesicles,  ul- 
cerate. The  cheesy  masses  in  the  cysts  may,  after  a  time,  become  calca- 
reous, or  undergo  purulent  change.  Follicular  pharyngitis  may  extend 
upward  and  involve  the  posterior  nares,  or  downward  and  involve  the  larynx. 


222  DISEASES   OF   THE   DIGESTIVE   SYSTEM. 

Etiology. — The  acute  form  occurs  most  frequently  in  children  and  in 
young  adults.  There  seems  to  be  a  predisposition  in  some  persons  to  this 
affection.  One  attack  predisposes  to  others.  The  causes  which  predispose 
to  quinsy  induce  acute  pharyngitis.  Chronic  follicular  pharyngitis  may  be 
produced  by  prolonged  use  of  the  voice  in  public  speaking  or  singing,  or 
by  the  excessive  use  of  tobacco  or  of  spirituous  liquors.  Weak,  scrofulous 
persons,  and  those  with  chronic  thoracic  disease  are  frequently  affected  with 
it.     Its  chief  cause  is  repeated  acute  attacks. 

Symptoms. — Slight  fever  may  usher  in  an  attack  of  acute  pharyngitis,  or 
precede  the  development  of  its  local  symptoms.  The  throat  first  becomes 
dry  and  redder  than  normal,  and  movement  of  the  parts  produces  pain  in 
the  direction  of  the  Eustachian  tubes,  so  that  swallowing  and  speaking  be- 
come painful.  The  elongated  uvula  may  induce  violent  fits  of  coughing. 
The  local  symptoms  are  very  severe  ;  there  will  be  more  or  less  regurgita- 
tion of  food  through  the  nose.  If  particles  of  food  do  not  readily  pass  into 
the  oesophagus  they  may  enter  the  larynx  and  cause  severe  fits  of  coughing. 
In  these  severe  cases  there  is  a  nasal  twang  to  the  voice,  and  any  movement 
of  the  throat,  tongue,  or  mouth  is  carefully  avoided  on  account  of  the  pain 
it  produces.  If  the  inflammation  invades  the  Eustachian  tube,  deafness 
may  result,  and  not  infrequently  the  tympanum  is  perforated  by  the  pus 
which  collects  in  the  middle  ear.  The  extension  is  more  often  forward,  so 
that  the  mucous  membrane  of  the  tongue  and  mouth  presents  the  same 
condition  as  that  of  the  pharynx.  These  symptoms  may  gradually  subside, 
after  a  few  days,  and  the  viscid  secretion  disappear  from  the  tongue, 
mouth  and  pharynx.  If  it  becomes  chronic,  the  voice  becomes  hoarse, 
and  there  is  a  stridulous  cough  accompanied  by  a  thick,  tough  mucous 
expectoration,  often  containing  small  firm,  yellow  masses.  There  is 
constant  irritation  of  the  throat,  which  is  variously  described  as  dry,  tick- 
ling or  tingling,  and  the  secretion  may  be  so  much  diminished  that  slight 
hemorrhage  may  occur  from  the  membrane  when  pressed  upon.  All  these 
symptoms  are  most  marked  in  the  morning.  The  symptoms  in  a  long 
standing  case  may  lead  to  anxiety  on  account  of  the  supposed  existence  of 
pulmonary  phthisis.  These  are  all  aggravated  by  ''  catching  cold,"  atmos- 
pheric changes,  and  the  prolonged  use  of  the  voice. 

Differential  Diagnosis. — Follicular  pharyngitis  may  be  mistaken  for  pul- 
monary  disease,  and  the  early  stage  of  mild  chronic  catarrh  often  excites 
suspicion  of  syphilis.  In  the  former  case  an  exploration  of  the  chest  and 
an  examination  of  the  throat  will  at  once  decide,  while  the  presence  or  ab- 
sence of  the  constitutional  signs  of  syphilitic  infection  will  establish  the 
diagnosis  in  the  latter  instance. 

Prognosis. — Acute  catarrhal  pharyngitis  is  a  very  mild  disease,  subsiding 
completely  in  most  cases  within  one  week  from  its  onset,  while  chronic  phar- 
ingitis  is  the  most  persistent  of  all  catarrhal  affections. 

Treatment. — In  acute  pharyngitis,  ice-cold  carbonated  water  affords  the 
greatest  relief  during  the  first  twenty  four  hours.  The  throat  and  mouth 
should  be  frequently  sprayed  with  a  solution  of  alum,  tannin,  or  sulphate 
of  zinc,  and  at  the  same  time  the  wet  pack  should  be  applied  to  the  throat 


MEMBKAjSTOUS   PHARTJS'GITIS. — EETRO-PHARYNGEAL   ABSCESS.         223 

either  hot  or  cold,  but  they  should  not  be  alternated.  In  chronic  pharyn- 
gitis, the  first  thing  to  be  done  is  to  remove  the  cause  and  live  an  out- 
door life.  Spraying  the  parts  two  or  three  times  a  day  with  the  astringent 
just  named,  or  a  mild  solution  of  nitrate  of  silver,  will  generally  afford 
temporary  relief.  In  some  cases  capsicum  or  guiacum  may  be  advan- 
tageously combined  with  the  astringents,  and  in  obstinate  cases  the  local 
use  of  iodine  or  a  twenty  per  cent,  solution  of  carbolic  acid  may  be  resorted 
to.  In  chronic  (follicular)  pharyngitis  a  nutritious  diet  is  especially  im- 
portant. German  physicians  recommend  very  highly  the  use  of  mineral 
waters,  but  alkaline  gargles  are  as  effective  as  a  residence  at  some  *' spring." 

MEMBRANOUS   PHARTISTGITIS. 

Under  this  head  are  included  both  croupous  and  diphtheritic  inflamma- 
tions of  the  pharynx.  Croupous  inflammation  may  be  primary,  but  diph- 
theritic inflammation  is  always  secondary.  This  form  of  pharyngitis  is 
considered  in  the  history  of  membranous  laryngitis  and  diphtheria. 

EETEO-PHAETNGEAL    ABSCESS. 

Suppuration  behind  the  pharynx,  in  the  areolar  tissue  between  it  and 
the  vertebrse,  is  known  as  retro-pharyngeal  abscess. 

Morbid  Anatomy. — This  is  a  cellulitis,  and  its  morbid  anatomy  is  the 
same  as  that  of  cellulitis  terminating  in  an  abscess  anywhere.  It  belongs 
properly  to  the  province  of  surgery. 

Etiology. — Eetro-pharyngeal  abscess  occurs  more  frequently  in  children 
than  in  adults.  It  is  developed  during  the  progress  of  caries  of  the  cervical 
vertebrge.  It  is  rarely  if  ever  due  to  the  extension  of  inflammation  from 
the  pharynx.  A  strumous  diathesis  predisposes  to  it.  Sometimes  it  appears 
late  in  pyaemia,  septicaemia,  typhoid,  typhus,  scarlet  fever  and  measles. 
Now  and  then  it  occurs  without  any  obvious  cause. 

Symptoms. — The  first  symptom  is  dysphagia.  With  this  there  is  stiffness 
of  the  neck,  slight  difficulty  in  articulation,  and  a  change  in  the  tone  of 
voice,  which  becomes  nasal  in  character.  On  examining  the  pharynx  its 
calibre  will  be  found  diminished  by  a  bulging  from  behind  and  perhaps  a 
little  to  one  side  ;  the  pharyngeal  mucous  membrane  is  redder  than  normal, 
and  there  may  be  a  slight  swelling  about  the  angle  of  the  jaw.  The  head 
is  thrown  backward,  and  any  attempt  at  flexion  causes  dyspnoea  ;  the  jaws 
seem  to  be  partially  locked.  There  is  regurgitation  of  food  through  the 
nose.  In  young  children  there  may  be  snuffling,  choking,  coughing  and 
great  dyspncsa,  with  a  certain  hoarse  tone  to  the  voice.  The  mouth  is 
filled  with  a  mucous  secretion. 

As  the  abscess  increases  in  size  the  tumor  may  be  seen  nearly  filling 
the  space  behind  the  soft  palate.  This  swelling  is  soft,  elastic  and 
fluctuating,  sometimes  rupturing  when  pressed  upon,  and  discharging 
an  offensive  pus.  If  it  opens  spontaneously  the  pus  is  vomited,  swal- 
lowed, discharged  through  the  nose,  or  is  inspired  into  the  trachea  and 
may  cause  suffocation.  Again,  the  abscess  filling  the  pharynx  may  press 
on  the  rima  glottidis  and  epiglottis  and  cause  oedema  glottidis.     In  rare 


224:  DISEASES   OF   THE    DIGESTIVE   SYSTEM. 

instances  the  pus  makes  its  way  around  to  the  opposite  wall  of  the 
pharynx,  and  then  breaks  into  the  oesophagus  or  trachea,  or  burrows  into 
the  pleural  cavity  or  even  the  pericardium.  It  may  burrow  between  the 
tracheal  muscles  and  appear  at  the  anterior  part  of  the  neck. 

Differential  Diagnosis. — When  fully  developed,  a  careful  examination  of 
the  pharynx  will  detect  at  once  the  existence  of  a  retro-pharyngeal  abscess. 

Prognosis. — The  prognosis  is  bad  whenever  caries  of  the  spine  has  caused 
the  abscess.  The  complications  which  may  cause  death  are  oedema  glot- 
tidis,  pleurisy,  pneumonia,  and  pericarditis.  Death  may  result  from  suffo- 
cation from  pressure. 

Treatment. — Open  the  abscess  early,  and  never  wait  for  its  spontaneous 
rupture.  The  position  of  the  child  when  the  bistoury  is  used  should  be 
such  that  the  escape  of  pus  through  the  mouth  is  facilitated. 

DISEASES  OF  THE  (ESOPHAGUS. 
The  following  diseases  of  the  oesophagus  will  be  considered  : 

I.  Inflammation,  either  catarrhal  or  membranous,  including  Stricture 
of  the  (Esophagus  ;  and,  II.  (Esophageal  Cancer. 

OESOPHAGITIS. 

QEsophagitis,  or  inflammatory  dysphagia,  is  a  catarrhal  inflammation  of 
the  mucous  membrane  of  the  whole  or  a  part  of  the  oesophagus.  It  is  an 
exceedingly  rare  disease. 

Morbid  Anatomy. ^ — In  the  acute  variety  the  mucous  membrane  is  red, 
swollen,  softened  and  covered  with  a  layer  of  mucus  containing  epithelium 
and  pus.  In  the  chronic  variety  the  mucous  surface  is  of  a  dull  pink  or 
slaty  blue  color.  The  sub-mucous  tissue  is  thickened,  and  a  thick  viscid 
mucus  or  pus  covers  its  surface.  It  may  cause  dilatation  of  the  oesopha- 
gus, which  may  affect  the  whole  tube  uniformly  or  form  a  pouch  at  its  lower 
portion,  or  it  may  give  rise  to  a  hernial  protrusion  of  the  mucous  mem- 
brane through  the  muscular  coat.  In  all  cases  of  oesophageal  dilatation  due 
to  chronic  catarrh,  there  is  more  or  less  thickening  of  the  oesophageal  walls. 
In  some  cases  the  thickening  may  diminish  the  calibre  of  the  tube.  Ulcer- 
ation of  the  mucous  membrane  at  the  seat  of  the  catarrh  sometimes  occurs. 
The  ulcer  may  be  superficial,  or  extend  through  the  walls  of  the  tube. 

Membranous  Inflammation  of  the  oesopliagus  may  be  either  croupous  or 
diphtheritic.  In  either  case  the  morbid  changes  are  the  same  as  in  croup- 
ous or  diphtheritic  inflammation  of  other  mucous  surfaces. 

Etiology. — Acute  oesophagitis  has  its  most  common  cause  in  the  irritation 
produced  by  acrid  fluids  or  solids  in  their  passage  to  the  stomach.  Irritat- 
ing drugs  and  corrosive  poisons  may  excite  it.  Too  frequent  introduction 
of  instruments  into  the  stomach  may  cause  it,  and  it  may  arise  from  the 
excessive  use  of  alcohol.  Extension  of  inflammation  from  the  parts  above 
or  below  it  often  induces  acute  oesophagitis.  Chronic  oesophageal  catarrh 
may  occur  as  part  of  a  similar  process  affecting  the  whole  alimentary  tract. 
It  may  develop  as  the  result  of  a  strumous  or  phthisical  diathesis,  or  follow 


CESOPHAGITIS.  235 

an  acute  attack.  Membranous  oesophagitis  is  always  secondary  and  results 
from,  or  occurs  with  similar  processes  in  the  respiratory  or  other  portions 
of  the  digestive  tract.  It  also  may  appear  after  some  of  the  eruptiye  fevers, 
cholera,  pyaemia  and  septicsemia. 

Symptoms. — Varying  with  the  intensity  of  the  inflammation,  an  aching 
or  severe  burning  pain  is  felt  at  the  back,  between  the  shoulders,  or  deep 
behind  the  sternum.  Even  the  ingestion  of  fluids  causes  dysphagia,  the 
pain  being  greatest  as  the  fluids  pass  through  the  upper  portion  of  the 
oesophagus.  More  or  less  febrile  excitement  and  great  depression  and  anxi- 
ety accompany  the  disease,  and  throughout  its  course  the  thirst  is  torment- 
ing. In  severe  cases  there  are  paroxysms  of  coughing,  and  perhaps  slight 
dyspnoea  with  hoarseness.  Vomiting  sometimes  follows  attempts  at  swal- 
lowing. All  these  symptoms  gradually  increase  in  severity.  If  extensive 
ulceration  is  present,  sudden  rupture  of  the  oesophagus  may  occur  during  the 
act  of  deglutition.  In  chronic  oesophagitis  there  is  dysphagia  and  pain  only 
on  swallowing  solids.  If  ulcers  exist,  there  may  be  vomiting  of  viscid  mucus 
tinged  with  blood,  accompanied  by  the  symptoms  of  oesophageal  stricture. 

Stricture  of  tlie  cesophagus  is  accompanied  by  gradually  increasing 
dysphagia,  emaciation  and  debility,  which  finally  terminate  in  death  from 
inanition.  The  most  frequent  seat  of  stricture  of  the  oesophagus  is  at  its 
cardiac  extremity.  It  may  be  caused  by  structural  changes  in  its  wall,  as 
in  oesophagitis  with  or  without  ulceration,  and  cancer,  or  by  compression 
from  mediastinal  and  other  tumors.  As  oesophageal  strictures  develop 
slowly,  for  a  long  time  the  only  symptom 
is  slight  difficulty  in  swallowing  solids,  the 
patient  usually  referring  the  difficulty  to  a  point 
behind  the  manubrium  sterni.  As  the  constric- 
tion increases  there  is  difficulty  in  swallowing 
liquids.  Food  and  drink  collect  in  the  oesopha- 
gus, and  after  a  longer  or  shorter  delay  are  re- 
gurgitated with  the  saliva  through  the  mouth  and 
nose.  With  oesophageal  stricture  there  are  usually 
painful  eructations.  Sometimes  the  pain  is  lan- 
cinating in  character,  shooting  from  the  region  of  ^'^''^^i  showing  stricture  of  the 

°  '  o  o  CEsopnaguB  near  cardiac  extrem- 

the  oesophagus  back  to  the  spinal  column.     The     ity- 

introduction  of  a  bougie  will  determine  the  seat,   ±  E^:^':ZZl%''o/sf^T.^- 

extent,  and  form  of  the  stricture. '  _  ^;  ^7^^  ,^^  ^,^^.^^^^^_ 

Uniform  dilatation  cannot  be  recognized  dur- 
ing life.  When  dilatation  is  partial,  or  when  pouches  exist,  there  may  be 
vomiting  of  undigested  offensive  food  some  hours  after  eating.  In  all  cases 
of  alteration  in  the  calibre  of  the  oesophagus,  the  oesophageal  bougie  will 
determine  the  amount  of  narrowing  and  the  locality  of  the  pouches. 
Membranous  inflammations  of  the  oesophagus  cannot  readily  be  determined 
during  life.  A  portion  of  membrane  may  be  vomited,  but  it  cannot  be 
determined  whether  it  comes  from  the  oesophagus,  or  has  been  swallowed 
and  regurgitated. 

>  The  treatment  of  stricture  of  the  CESophagus  belongs  to  surgery. 
15 


326  DISEASES    OF   THE   DIGESTIVE   SYSTEM. 

Differential  Diagnosis. — This  disease  may  be  mistaken  for  cancer  of  the 
oesophagus ;  the  diagnostic  points  will  be  considered  in  the  history  of 
oesophageal  cancer.  At  the  onset  it  may  also  be  mistaken  for  hydropholia, 
but  the  diagnosis  is  soon  established  by  the  development  of  the  character- 
istic nervous  phenomena  of  the  latter  disease. 

Prognosis. — The  immediate  prognosis  in  acute  oesophagitis  caused  by 
chemicals  or  mechanical  irritants  depends  more  on  the  changes  which  have 
occurred  around  the  larynx  and  in  the  stomach,  than  upon,  the  oesophagitis. 
The  prognosis  in  croupous  and  dijjhtheritic  inflammations  of  the  oesophagus 
is  also  determined  by  the  conditions  of  the  primary  disease.  In  chronic 
oesophageal  catarrh  without  stricture  the  prognosis  is  good. 

Treatment. — In  acute  oesophagitis,  if  the  inflammation  has  been  excited 
by  foreign  bodies  lodged  in  the  oesophagus,  they  must  at  once  be  removed  ; 
if  corrosive  chemicals  have  been  swallowed,  the  proper  antidote  must  be  ad- 
ministered. In  severe  cases,  all  movement  of  the  parts  must  be  prevented. 
Ice  in  the  mouth  is  grateful  and  does  no  harm.  Nutrient  enemata  may  be 
given,  and,  if  the  pain  is  severe,  hypodermics  of  morphine  must  be  given 
in  sufficient  quantities  to  afford  relief.  Hot  anodyne  fomentations  applied 
locally  are  usually  of  service.  In  chronic  oesophageal  catarrh,  if  ulcers  ex- 
ist, spray  the  parts  with  astringent  fluids,  such  as  a  solution  of  nitrate  of 
silver.  Surgery  directs  that  if  starvation  seems  imminent  a  gastric  fistula 
should  be  made.  In  oesophageal  stricture,  bougies  must  be  daily  intro- 
duced for  a  long  time,  with  the  hope  of  dilating  the  stricture.  No  treat- 
ment is  required  in  oesophageal  dilatation. 

CANCER    OF   THE    (ESOPHAGUS. 

The  most  frequent  variety  of  oesophageal  cancer  is  epithelioma,  but 
scirrhus  and  medullary  cancer  are  not  unknown.  It  occupies  the  upper  and 
middle  third  of  the  oesophagus  more  often  than  the  cardiac  portion  ;  in  the 
former,  it  is  associated  with  pharyngeal  and  laryngeal  cancer,  and  in  the 
latter  with  cancer  of  the  cardiac  extremity  of  the  stomach. 

Morbid  Anatomy. — Epithelioma  begins  in  the  mucous  tissue,  and  pursues 
ihe  same  course  as  cancer  of  the  tongue.  The  ulceration  may  be  limited 
io  a  circular  patch  an  inch  in  diameter,  or  may  involve  the  whole  circum- 
ference of  the  oesophagus.  The  growth  after  a  time  invades  all  the  tissues 
of  the  oesophagus,  and  causes  stricture  of  its  calibre.  Above  the  stricture 
there  is  either  uniform  dilatation  or  a  pouch,  sometimes  as  large  as  an 
orange.  If  the  cancerous  mass  involves  the  entire  oesophageal  wall,  it  may 
press  upon  and  destroy  one  or  both  pneumogastrics,  and  lead  to  the  devel- 
opment of  pneumonia  or  pulmonary  gangrene.  If  the  oesophagus  is  rupt- 
ured, openings  may  be  made  into  the  trachea,  through  the  diaphragm  into 
Ihe  peritoneal  cavity,  or  into  the  posterior  mediastinum.  Cancer  has  some- 
times ulcerated  into  the  aorta,  pulmonary  artery,  and  even  into  the  right 
subclavian  artery. 

Etiology. — Two-thirds  of  the  cases  of  cancer  of  the  oesophagus  occur  in 
males  between  the  ages  of  forty  and  sixty.     It  is  generally  primary ;  it 


CANCER   OF  THE   CESOPHAGUS.  227 

may  be  secondary  to  cancer  of  the  mouth,   pharynx,   mediastinum,    or 
stomach. 

Symptoms. — The  first  thing  noticed  in  cancer  of  the  oesophagus  is  difficult 
deglutition  ;  soon  well-marked  dysphagia  occurs.  Pain  is  present  early, 
and  may  be  dull,  burning,  or  lancinating  in  character ;  it  is  located  about 
the  centre  of  the  sternum,  in  the  throat,  or  in  the  interscapular  space.  It 
varies  greatly  in  kind  and  degree,  but  it  is  greatly  aggravated  when  food 
reaches  that  portion  of  the  oesophagus  which  is  the  seat  of  the  cancer.  As 
the  stricture  grows  narrower,  flatulence,  regurgitation  of  food  and  vomiting, 
with  steadily  increasing  emaciation,  become  prominent  symptoms,  and  a 
well-marked  cachexia  is  developed.  Cough,  dyspnoea,  and  hoarseness  some- 
times result  from  pressure  of  the  cancerous  tumor.  As  the  disease  advances, 
the  pain  becomes  more  constant,  the  cachexia  is  better  marked,  and  hem- 
orrhages are  frequent  ;  the  bloody  fluid  vomited  often  contains  shreddy 
masses  which  contain  cancer  elements  and  show  the  character  of  the  dis- 
ease. The  neighboring  lymphatic  glands  may  also  be  implicated,  and,  by 
pressure  on  a  main  bronchus,  cause  feeble  respiration  in  the  lung  to  which 
the  bronchus  is  distributed.  If  rupture  occurs,  it  is  followed  by  a  sudden 
sharp  pain  in  the  chest,  fainting,  and  coldness  of  the  extremities,  followed 
almost  immediately  by  death. 

Differential  Diagnosis. — (Esophageal  cancer  may  be  mistaken  for  stricture 
of  the  cesophagus  from  chronic  catarrhal  inflammation.  In  cancer,  pain  is 
constant  and  greatly  aggravated  by  taking  food,  while  in  non-cancerous 
oesophageal  stricture  pain  is  absent,  or  is  only  present  on  swallowing.  The 
glands  about  the  neck  are  early  involved  in  cancer,  but  are  normal  with 
chronic  catarrh.  Chronic  pulmonary  disease  is  rarely  absent  when  oeso- 
phageal cancer  is  present,  but  is  never  induced  by  non-malignant  stricture. 
Hemorrhage  is  frequent  in  cancer,  and  does  not  often  occur  with  stricture 
from  chronic  catarrh.  The  bougie  may  bring  up  shreddy  masses,  with  evi- 
dences of  cancer  in  the  one  case,  but  merely  meets  with  obstruction  in  the 
other. 

Prognosis. — This  is  always  a  fatal  disease.  Its  average  duration  is  one 
year,  but  death  may  occur  in  a  few  weeks.  The  prognosis  as  to  time  varies 
with  the  presence  or  absence  of  complications.  Death  may  result  from  any 
of  the  complications,  from  hemorrhage  or  septicsemia. 

Treatment. — Early  in  cancer  let  the  food  be  finely  chopped  and  taken  in  a 
semi-fluid  state ;  later,  it  should  be  entirely  fluid,  and  when  the  patient 
cannot  swallow,  nutrient  enemata  must  be  given.  The  diet  in  all  cases 
must  be  nourishing  in  the  highest  possible  degree,  and  stimulants  can  usu- 
ally be  given  with  benefit.  When  the  pain  is  intense  morphia  per  rectum 
or  hypodermically  should  be  administered  in  doses  sufficient  to  relieve  it. 
Bougies  should  be  used  with  great  care  ;  early,  they  should  only  be  used  to 
locate  and  diagnosticate  the  disease  ;  later,  tubes  must  only  be  used  for  the 
purpose  of  introducing  food  into  the  stomach,  as  fatal  hemorrhage  or  rupt- 
ure has  followed  their  use.  The  subject  of  gastrotomy  comes  within  the 
domain  of  surgery. 


i2ii  DISEASES    OF   THE   DIGESTIVE   SYSTEM. 


DISEASES  OF  THE  STOMACH. 

I.  Inflammations  of  its  mucous  membrane  and  its  submucous  or  areolae 
tissue. 

a.  Acute  or  Toxic  Gastritis. 

b.  Sub-acute  Gastritis,  or  Acute  Gastric  Catarrh. 

c.  Chronic  Gastritis,  or  Chronic  Gastric  Catarrh. 

d.  Phlegmonous  Gastritis. 

II.  Dyspepsia.  IV.  Neuroses  or  Gastralgia. 

III.   Cancer  and  Ulcer.  V.  Hcematemesis. 

VI.  Dilatation. 


ACUTE    GASTEITIS. 

Acute  or  toxic  gastritis  is  a  general  inflammation  of  the  mucous  and  sub- 
mucous tissue  of  the  stomach.  It  is  of  rare  occurrence,  unless  the  result  of 
the  introduction  into  the  stomach  of  irritating  poisons. 

Morbid  Anatomy. — On  opening  a  stomach  which  is  the  seat  of  toxic  gas- 
tritis a  thick  layer  of  tough,  viscid  mucus  will  be  found  spread  over  its 
mucous  surface.  Beneath  this  there  will  be  found  an  intense  redness  of  the 
membrane,  which  is  most  marked  along  the  edge  of  the  rugse,  near  the  car- 
diac orifice.  The  mucous  and  submucous  tissues  will  be  soft  and  oedema- 
tous.  In  some  rare  instances  the  whole  or  a  portion  of  the  mucous  mem- 
brane will  be  found  to  present  the  appearance  of  a  detached  brown  or  black 
slough  ;  it  may  be  entirely  eroded.  Fibro-plastic  exudation  may  cause  com- 
plete occlusion  of  its  cardiac  or  pyloric  orifices.  When  the  muscular  tissue 
is  involved  it  becomes  soft,  easily  torn,  often  gelatinous.  In  severe  cases 
perforations  may  exist. 

Etiology. — Acute  gastritis  is  almost  always  caused  by  the  entrance  into 
the  stomach  of  irritant  poisons,  such  as  sulphuric,  nitric,  and  oxalic 
acids,  arsenic,  the  chloride  of  zinc,  and  large  quantities  of  concentrated 
alcohol.  Mechanical  irritation,  such  as  results  from  the  introduction  into 
the  stomach  of  knives,  pins,  false  teeth,  etc.,  may  produce  a  local  acute  gas- 
tritis. Introduction  into  the  stomach  of  boiling  water,  hot  lead,  or  steam 
may  cause  a  most  intense  gastric  inflammation,  with  extensive  sloughing  of 
its  mucous  surface. 

Symptoms. — Soon  after  the  introduction  of  corrosive  substances  into  the 
stomach,  there  will  be  a  dull,  uneasy  feeling,  sometimes  one  of  warmth, 
over  the  epigastrium.  This  is  rapidly  followed  by  an  intense  burning  pain 
shooting  through  to  the  back.  The  epigastric  region  becomes  extremely  ten- 
der. With,  or  preceding  these  symptoms,  there  is  nausea,  and  vomiting  of 
tenacious  macus  ;  the  vomiting  is  very  distressing ;  the  ejected  mucus  often 
contains  blood,  and,  at  first,  portions  or  traces  of  the  substance  which  has 
caused  the  gastritis.  As  the  pain  becomes  more  severe  the  vomiting  is  more 
distressing  ;  there  is  intense  thirst,  and  frequent  spasms  of  the  abdominal 
muscles.     The  temperature  rapidly  rises,  sometimes  to  105°  F.;  the  pulse 


SUB-ACUTE    GASTRITIS.  229 

reaches  120  or  140  per  minute  and  is  feeble  and  irregular.  If  the  oesophagus 
is  implicated,  there  is  dysphagia.  The  urine  becomes  scanty  and  high 
colored,  and  is  sometimes  suppressed.  These  violent  symptoms  soon  give 
place  to  a  condition  of  general  prostration,  in  which  there  is  almost  con- 
stant hiccough.  The  surface  becomes  cold  and  clammy,  the  radial  pulse 
grows  feeble  and  finally  imperceptible,  while  the  respirations  are  hurried, 
short  and  irregular,  the  mind  remaining  clear  to  the  last.  There  are  cases 
on  record  of  poisoning  by  chloride  of  zinc  and  sulphuric  acid,  in  which 
there  was  no  pain  in  the  epigastrium  during  the  whole  course  of  the  disease. 

Differential  Diagnosis.— The  diagnosis  is  not  difficult.  The  history  of 
its  cause  and  the  character  of  the  vomiting  establish  it. 

Prognosis. — The  prognosis  depends  upon  the  cause.  The  more  intense 
the  pain,  the  more  extensive  the  gastric  inflammation.  Death  may  occur 
in  a  few  hours,  or  it  may  be  delayed  two  or  three  weeks.  Acute  gastritis 
may  be  complicated  by  analogous  conditions  of  the  mouth,  pharynx,  or 
oesophagus,  by  enteritis,  laryngitis,  or  oedema  glottidis,  and  as  sequelae  there 
may  remain  constrictions  at  the  cardiac  or  pyloric  orifices.  Death  may 
result  directly  from  the  shock  of  the  gastritis,  from  the  constitutional  effects 
of  the  poison  which  produces  it,  or  from  resulting  peritonitis. 

Treatment. — The  fia^st  thing  is  to  administer  the  proper  antidote  to  the 
poison  which  has  caused  the  gastritis,  and  thoroughly  wash  out  the  stom- 
ach, after  which  the  gastritis  should  be  treated  as  a  local  inflammation.  Four 
or  five  leeches  may  be  applied  over  the  epigastrium,  followed  by  warm  poul- 
tices or  fomentations.  Some  prefer  the  application  of  ice  to  the  epigas- 
trium. Unless  contra-indicated  by  the  chemical  constitution  of  the  poison, 
the  intense  pain  should  be  relieved  by  hypodermic  injections  of  morphia. 
During  the  whole  period  the  patient  should  be  kept  absolutely  at  rest  in 
the  horizontal  position. 

SUB- ACUTE    GASTRITIS. 

Suh-acute  gastritis,  or  acute  gastric  catarrh,  is  always  a  secondary  affec- 
tion. 

Morbid  Anatomy. — The  parts  principally  involved  in  this  form  of  gas- 
tritis are  the  ridges  between  the  depressions,  the  vessels  which  lie  in  imme- 
diate proximity  to  them,  and  the  apertures  of  the  tubules.  The  mucous 
membrane  is  mottled  by  red  spots  scattered  over  it  in  irregular  patches ; 
sometimes  there  are  extensive  ecchymoses  and  blood  extravasations.  The 
gastric  Juice  is  much  diminished  in  quantity,  and  being  mixed  with  much 
mucus  loses  its  acidity  and  to  a  great  extent  its  digestive  power.  The  sur- 
face of  the  mucous  membrane  is  covered  with  an  abundant,  tenacious  mu- 
cus ;  there  is  also  a  moderate  production  of  pus  cells  on  the  surface  of  the 
mucous  membrane.  The  gastric  tubules  become  filled  with  granular  mat- 
ter. Late  in  the  disease  the  solitary  and  lenticular  glands,  especially 
about  the  pylorus,  increase  in  size  and  stud  the  surface  as  small  white 
specks.  The  inflammatory  processes  are  superficial  and  do  not  involve 
the  deeper  tissue  of  the  mucous  membrane.     Superficial  sloughs  are  some- 


330 


DISEASES    OF    THE    DIGESTIVE    SYSTEM. 


times  formed  varying  in  size  from  a  pea  to  that  of  a  three-cent  piece  ;  they 


rarely  involve  the  submucous  tissue. 


Fig.  51. 

A  Vertical  Section  of  the  Stomacii  walls  in  Sub-acute 
Gastritis. 

A.  Mvscular  fibres  in  longitudinal  section. 

B.  The  same  cut  tranfwehely . 

C.  Submucous  tissue,  in  which  are  seen  at 

J),  D.  Blood-vessels  enlarged  and  filled  with  blood. 

E.  Mucous  coat.     The  gastric  follicles  are  shown  Jillei 

with  granular  detritus  and  covered  with  pus— G. 

F.  Small  vessels  betioeen  the  follicles,     x  40. 


Its  most  prominent  lesion  is  the 
coating  of  the  gastric  mucous 
surface  with  tenacious  mucus. 

Etiology. — No  period  of  life  is 
exempt  from  this  form  of  gastri- 
tis. It  occurs  most  frequently 
under  two  conditions  : — first,  with 
acute  alcoholismus ;  secondly, 
with  those  diseases  in  which  there 
is  extensive  blood-poisoning,  as  in 
scarlet  fever,  small-pox,  measles, 
typhoid  and  typhus  fevers,  diph- 
theria, pneumonia,  pysemia  and 
septicgemia.  It  sometimes  com- 
plicates pulmonary  phthisis,  and 
may  follow  the  disappearance  of 
gout,  rheumatism,  or  affections 
of  the  Joints. 

Symptoms.  —  Vomiting  is  its 
first  and  most  prominent  symp- 
tom. The  matter  vomited  con- 
sists of  the  substances  which  have 
been  taken  into  the  stomach, 
mingled  with  a  grayish,  stringy  mucus,  and  sometimes  streaks  of  blood. 
"When  the  vomiting  is  severe  and  prolonged,  bright  green,  bitter  fluid 
is  often  ejected.  The  fermentation  which  takes  place  in  the  fluid  con- 
tained in  the  stomach  sometimes  develops  gases  which  cause  distention 
of  the  stomach  and  a  prominence  of  the  epigastrium.  The  patient  has  no 
desire  for  food,  but  constantly  craves  ice  and  cooling  drinks.  The  thirst  is 
intense.  The  smallest  quantity  of  food  taken  into  the  stomach  causes  nausea 
and  vomiting,  which  may  be  so  severe  as  to  induce  extreme  exhaustion  or 
collapse.  Accompanying  the  nausea  and  vomiting  there  is  more  or  less 
pain  at  the  epigastrium.  This  pain  is  sometimes  intense,  and  shoots  back- 
ward between  the  shoulders,  but  usually  it  is  not  severe  unless  firm  pressure 
is  made  over  the  stomach.  The  tongue  is  coated  with  a  yellow  or  ash-col- 
ored material,  and  becomes  dry  and  red  at  the  tip.  The  papillae  are  prom- 
inent. The  breath  has  an  offensive  odor.  Late  in  the  disease,  herpetic 
eruptions  make  their  appearance  about  the  lips  and  in  the  mouth.  Often 
during  its  course  there  will  be  flashes  of  heat,  with  a  burning  sensation  in 
the  palms  of  the  hands  and  the  soles  of  the  feet.  The  thermometer  may 
indicate  an  axillary  temperature  of  103°,  or  even  105°  P.  The  patient  be- 
comes restless  and  irritable  and  often  has  attacks  of  syncope.  In  alcoholic 
cases  the  anorexia  is  absolute,  and  vomiting  occurs  mostly  in  the  morning. 
Delirium  tremens  is  often  a  complication.  Its  symptohas  are  always  more 
or  less  varied  by  the  diseases  with  which  it  occurs.  In  rare  instances  I  have 
seen  an  icteric  and  sometimes  a  bronzed  hue  of  the  skin  come  on  during  a 


CHRONIC    GASTRITIS.  231 

prolonged  attack  of  acute  gastric  catarrh.  Diarrhoea  is  usually  present,  the 
stools  having  a  very  offensive  odor.  Obstinate  constipation  is  rare.  The 
urine  is  scanty  and  high  colored,  and  in  severe  cases  presents  slight  traces 
of  albumen.  Nitric  acid  gives  a  deep  red  color  to  it,  or  there  is  a  copious 
deposit  of  lithates. 

Differential  Diagnosis. — The  diagnosis  is  easily  made,  and  it  is  not  likely 
to  be  confounded  with  any  other  affection,  if  its  etiology  and  symptoms  are 
carefully  analyzed. 

Prognosis. — The  prognosis  is  decided  by  the  disease  which  it  complicates. 
Unless  associated  with  acute  alcoholismus,  it  rarely  becomes  chronic.  Its 
duration  is  from  ten  days  to  two  or  three  weeks.  It  may  be  complicated  by 
catarrhal  conditions  of  the  oral  and  pharyngeal  mucous  membranes,  and  in 
very  rare  instances  by  implication  of  the  intestines  (gastro-enteritis).  It  only 
causes  death  when  it  is  extensive  and  complicates  some  grave  acute  general 
disease,  as  septicsemia,  pyaemia,  typhoid  or  puerperal  fever. 

Treatment. — The  most  important  thing  in  the  treatment  of  this  affection 
is  rest  to  the  stomach.  In  mild  cases,  entire  abstinence  from  food  for  twenty- 
four  hours,  and  then  milk  with  lime-water  in  small  quantities  at  stated  in- 
tervals, is  all  that  is  required.  In  severe  cases,  and  in  all  cases  occurring 
in  children,  nourishment  must  be  given  jiger  rectum  as  long  as  the  gastric 
symptoms  are  urgent.  One  or  two  leeches  applied  over  the  epigastrium, 
followed  by  warm  fomentations,  usually  afford  marked  relief.  In  adults, 
if  the  pain  is  so  severe  as  to  prevent  sleep,  or  if  there  is  great  restlessness, 
small  hypodermics  of  morphia  may  be  administered.  After  the  patient  has 
passed  twenty-four  hours  without  vomiting,  milk  and  lime-water  may  be 
given  in  small  quantities.  In  those  cases  in  which  vomiting  is  persistent, 
and  there  are  symptoms  of  collapse,  stimulants  must  be  freely  administered 
by  the  rectum.  None  of  the  remedies  which  are  so  often  employed  for  the 
relief  of  vomiting  are  serviceable  in  the  treatment  of  this  affection.  Dur- 
ing convalescence,  if  the  stomach  is  in  an  atonic  condition,  mineral  acids 
and  the  vegetable  bitters  will  be  found  of  service  ;  great  care  must  be  exer- 
cised in  the  diet  during  the  whole  period  of  convalescence.  The  improve- 
ment of  the  diet  must  be  gradual,  and  those  who  have  been  spirit  drinkers 
should  be  warned  of  their  danger,  and  the  use  of  stimulants  prohibited. 

CHRONIC    GASTRITIS. 

Chronic  gastritis  is  known  under  the  names  of  simple  gastritis,  chronic 
catarrh  of  the  stomach,  morbid  sensihility  of  the  stomach,  and  chronic  in- 
flammatory dyspepsia. 

Morbid  Anatomy. — The  morbid  appearances  in  chronic  gastritis  vary 
with  its  character  and  duration,  and  are  usually  best  marked  around  the  py- 
loric extremity  of  the  stomach.  Over  all,  or  part  of  the  mucous  surface, 
there  is  a  layer  of  gray  mucus,  varying  in  thickness  and  tenacity  with  the 
duration  and  character  of  the  disease.  On  its  removal  the  mucous  mem.- 
brane  is  seen  studded  with  ecchymotic  and  pigmented  spots,  the  result  of 
small  extravasations.     In  some  cases  the  mucous  tissue  is  oedematous  and 


233  DISEASES   OP   THE   DIGESTIVE   SYSTEM. 

presents  a  well-marked  granular  appearance.  The  walls  of  the  stomach  are 
usually  thickened  and  more  or  less  indurated,  especially  about  the  pyloric 
orifice,  which  gives  rise  to  more  or  less  constriction,  or  ^'pyloric  stenosis.'^ 
The  thickened  membrane  is  often  "leathery"  to  the  feel,  and  the  indura- 
tion may  be  so  great  that  it  tears  with  difficulty  and  can  be  stripped 
off  the  submucous  tissue.  The  submucous  tissue  may  also  be  thickened 
and  congested,  the  color  varying  from  an  inflammatory  blush  to  a  livid,  al- 
most purple  red.  When  the  submucous  tissue  is  involved,  there  is  an  infil- 
tration of  cells  into  it ;  and  upon  their  organization  into  new  connective- 
tissue,  and  the  subsequent  contraction  of  this  tissue,  there  will  be  more  or 
less  interference  with  the  peristaltic  motion  of  the  stomach.  Besides  this 
there  will  be  hypertrophy  and  distention  of  the  gastric  tubules,  for  their 
secretion  is  retained  by  the  tissue-increase  in  the  intertubular  structure, 
which  will  cause  them  to  stand  out  as  small  granulations  in  the  atrophied 
tissue,  presenting  an  appearance  denominated  " mammilla t ion."  This  condi- 
tion may  also  be  the  result  of  hypertrophy  of  the  glandular  layer,  which  thus 
becoming  too  large  for  the  basement  muscular  layer  is  corrugated  and  gives 
rise  to  another  form  of  mammillation.  It  is  only  in  rare  instances  that 
there  is  any  mammillation  about  the  cardia. 

In  long-continued  chronic  catarrh  of  the  stomach  the  muscular  coat  of 
the  organ  may  become  involved,  and  then  the  peristaltic  movements 
will  be  still  more  impaired  ;  finally,  the  peritoneum  may  become  thickened 
and  adhesions  take  place  between  it  and  the  adjacent  parts. 

A  microscopic  examination  of  tlie  gastric  tubules  in  chronic  gastritis  will 
sometimes  show  that  their  epithelium  has  undergone  granular  degeneration, 
and  in  others  there  is  a  complete  loss  of  epithelium,  the  tubules  being  filled 
with    a    granular    detritus.     Occasionally   there    will    be    found  on  the 

mucous  membrane  dirty  white  spots  in 
irregular  patches,  which  appear  like  de- 
pressions on  the  mucous  surface.  Under 
the  microscope,  there  will  be  found  in 
those  spots  some  tubules  completely  filled 
with  discrete  fat  spherules,  and  others 
whose  epithelium  has  undergone  fatty  de- 
generation. If  the  tubules  are  constricted 
near  their  openings,  cysts  are  formed  from 
distention  of  the  portion  near  the  base  by 

A  Vertical  Section  of  Mucous  Membrane  Of    , ,  , .  i  •   ^  ,  t 

the  Stomach,  showing  changes  in  the  Tu-    the    SCCrctlOn    WhlCh    CanUOt    CSCapC.        in 

buiesin  Chronic  Gastritis.  ^^^^  ^^^^^  ^j^^  ^^^.    degeneration  will  in- 

A.  Mn  ocularis  mucogce.  ,  ,        .,        i-.-ii-  n        tj» 

B.  Small  blood-vessels  armmd  the.  follicles.  VOlve    the    interstitial    tlSSUe    aS    Well.       il 

C.  Tiibide  with  qrannlar  epithelimn  and  filled   ■,  ^        •  l  j.-  •    j.     j-1,„ 

with  ammdar  detritm.  hemorrhagic  extravasation  occurs  into  the 

^•i':f^?/;;;*;;f^A%r^/»t/.f'''''^'^''''"^'  gastric  mucous  membrane,  the  tubules 
f:  fS^'c^t&SZS^t^nun.th  Will   have  their  epithelium   stained  and 

t^Xat'f^zC^'-^'''''^'"'''''^^''''^''  ■t^eir  base  blackened  as  a  result  of  the 

sanguineous  infiltration.  Sometimes  there 
is  an  increase  in  the  intertubular  lymphatic  elements,  with  hyperplasia  of 
the  nuclei  in  the  sheath  of  the  vessels. 


CHEOKIC   GASTETTI8.  333 

In  long-standing  chronic  gastritis  there  may  be  abrasions  of  the  mu- 
cous surface  and  formation  of  ulcers  (chiefly  about  the  lesser  curvature 
and  the  pylorus),  circular  in  shape,  varying  in  diameter  from  half  an  inch 
to  an  inch.  These  ulcers  are  very  superficial,  rarely  extending  beyond  the 
mucous  coat.  They  are  pale  in  color,  and  their  surface  is  covered  with 
mucous  cells,  nuclei,  and  epithelium  ;  between  the  ulcers  the  rugae  are  con- 
gested. The  intervening  tissue  is  rarely  normal.  There  may  also  be  small 
follicular  or  punctate  ulcerations,  originating,  it  is  supposed,  in  the  enlarged 
solitary  and  lenticular  glands.  The  base  of  these  ulcers  is  infiltrated  with 
lymph-cells  and  granular  detritus  ;  they  are  never  present  except  in  the  ad- 
vanced stage  of  chronic  gastric  catarrh.  Chronic  gastric  catarrh  may 
involve  a  large  portion  of  the  mucous  surface  of  the  stomach,  and  is  gen- 
erally associated  with  a  like  condition  of  the  intestinal  mucous  membrane. 
Waxy  degeneration  may  be  associated  with  these  morbid  changes,  but  in 
such  cases  other  organs,  as  the  liver  and  spleen,  will  have  been  primarily 
affected  by  the  amyloid  infiltration.  The  size  of  the  stomach  varies  :  some- 
times it  is  smaller  than  normal ;  at  others  it  is  dilated. 

Etiology. — Chronic  gastric  catarrh  is  essentially  a  secondary  affection  ;  it 
is  rarely  the  sequela  of  sub-acute,  much  less  of  acute,  gastritis,  unless  the 
former  has  been  caused  by  an  abuse  of  alcoholic  stimulants.  In  many  persons 
there  is  an  hereditary  tendency,  after  middle  life,  to  chronic  gastric  catarrh. 
The  principal  general  cause  of  this  affection  is  ancBinia.  The  most  common 
local  cause  is  the  daily  use  of  alcoholic  stimulants. 

Mechanical  obstruction  to  the  capillary  circulation  of  the  stomach,  induc- 
ing continued  passive  hyperemia  (congestion)  will  cause  it,  and  hence  we  find 
it  associated  with  cirrhosis  of  the  liver  and  other  chronic  hepatic  affections 
where  the  blood  is  dammed  back  in  the  formative  branches  of  the  vena 
portEe.  In  the  same  way,  valvular  and  other  cardiac  lesions,  and  pulmon- 
ary diseases,  such  as  emphysema,  chronic  bronchitis,  and  phthisis,  which 
offer  an  obstacle  to  the  venous  return,  will  induce  chronic  gastric  catarrh. 
Pressure  on  the  walls  of  the  stomach  by  tumors  produces  first  congestion, 
and  then  chronic  catarrh.  Degeneration  of  the  capillaries — '' arterio- 
capillary  filrosis" — occurring  in  the  cirrhotic  form  of  Bright's  disease, 
causes  it,  and  it  often  accompanies  ulcer  and  cancer  of  the  stomach. 

Those  causes  which  may  be  denominated  recent  are  rapid  ingestion  of 
food,  improper  quality  of  food,  or  food  which  is  known  *Ho  disagree  with 
the  stomach,"  and  the  sudden  arrest  of  the  digestive  process  after  hearty 
meals.  The  prolonged  use  of  arsenic,  mercury,  cubebs,  and  purgatives 
often  causes  it.  Finally,  scrofula,  syphilis,  and  gout  seem  to  predispose 
to  it,  and  I  am  inclined  to  regard  the  chronic  gastritis  which  is  so  often 
found  associated  with  these  diseases  as  the  result  of  some  degeneration  of, 
or  alteration  in,  the  hlood-vesseh  of  the  stomach. 

Symptoms. — The  early  symptoms  of  chronic  gastric  catarrh  are  chiefly 
those  of  indigestion.  There  is  at  first  a  sense  of  weight  and  fulness  in  the 
epigastrium,  sometimes  amounting  to  constriction,  which  comes  on  from 
half  an  hour  to  an  hour  after  meals.  Later  there  is  actual  pain  and 
heat  in  the  epigastrium  (*'  heart-burn  ").     Pressure  increases  the  pain  and 


234  DISEASES   OF   THE    DIGESTIVE   SYSTEM. 

causes  it  to  shoot  backward  and  upward  toward  the  scapulae.  Following, 
or  with  the  advent  of,  these  symptoms  there  is  loss  of  appetite,  first  for 
solids  such  as  meats ;  later  there  is  complete  anorexia.  Nausea  and  eruc- 
tations accompany  the  anorexia  ;  the  stomach,  and  often  the  intestines 
become  distended  with  gas,  but  vomiting  is  not  usually  present  unless 
pyloric  stenosis  exists.  The  most  important  of  the  dyspeptic  symptoms  are 
the  acid  risings  after  meals,  and  the  vomiting  or  regurgitation  of  acid 
mucus  in  the  morning,  which  may  be  regarded  as  characteristic,  and  with- 
out which  the  diagnosis  is  uncertain.  It  is  this  acid  material  belched  up  intO' 
the  oesophagus  that  causes  "  heart-burn."  If  there  is  actual  vomiting  of 
food,  traces  of  butyric  acid  are  present,  with  the  sarcinm  ventricuU,  cuboid 
cells  averaging  1-2500  inch  in  diameter,  each  being  divided  into- 
four  equal  parts  containing  nuclei,  usually  heaped  into  large 
cubes. 

As  the  disease  progresses,  the  feeling  of  malaise  and  un- 
easiness following  meals  changes  to  one  of  languor  or  ex- 
Fig.  53.  haustion,  and  there  is  a  sensation  of  heat  in  the  epigastrium  r 
mii.  X  750.  thirst  becomes  a  promment  symptom,  one  person  craving 
cold,  another  hot  drinks.  The  thirst  is  greatest  in  the  evening,  but 
the  taking  of  fluids  is  usually  followed  by  a  sense  of  weight  in  the 
epigastrium,  and  by  acidity  and  flatulence.  The  appearance  of  the  tongue 
varies  :  it  may  be  normal,  paler  than  normal,  florid  and  "beefy,"  or  may 
be  covered  with  a  white  or  brown  coating.  The  general  symptoms  which 
accompany  the  ansemic  condition  which  attends  this  diwsease  are  headache, 
vertigo,  cardiac  palpitation,  a  gradual  loss  of  strength  and  emaciation. 
Constipation  and  hemorrhoids  are  usually  present,  and  the  stools  are  often 
coated  with  mucus.  In  the  chronic  gastric  catarrh  of  phthisis,  diarrhoea  is 
present.  In  cases  of  long  standing,  the  hair  becomes  harsh  and  loses  its 
lustre  or  turns  gray ;  the  skin  is  dry,  sallow,  and  shrivelled,  sometimes 
covered  with  an  eczematous  eruption  ;  the  nails  are  corrugated  and  exhibit 
a  tendency  to  split,  while  in  some  there  is  premature  caries  of  the  teeth. 
Hypochondriasis,  despondency,  and  irritability  of  temper  are  generally 
more  or  less  marked.  Hseraatemesis  often  occurs  in  that  form  of  gastritis 
which  accompanies  cirrhosis  of  the  liver,  and  the  bleeding  may  for  a  time 
relieve  the  unpleasant  gastric  symptoms.  Vomiting  in  the  morning  al- 
ways accompanies  the  gastritis  of  Bright's  disease. 

The  urine  in  chronic  gastritis  is  cloudy,  usually  alkaline  in  reaction, 
depositing  urates,  phosphates  and  oxalates.  Its  specific  gravity  is  highest 
at  evening.  The  alkalinity  is  due  either  to  imperfect  gastric  digestion  or  im- 
paired function  of  the  liver  and  pancreas.  The  greater  the  mental  depres- 
siion  the  more  of  earthy  phosphates  will  be  found  in  the  urine. 

If  hemorrhagic  erosion  exist  in  a  stomach  which  is  the  seat  of  chronic 
catarrh,  the  pain  in  the  epigastric  region  is  constant,  frequently  shoot- 
ing back  to  the  scapulae.  Vomiting  occurs  not  only  in  the  morning,  on 
rising  and  after  meals,  but  also  in  the  intervals.  The  vomited  matter  con- 
tains traces  of  blood,  and  bile  mixed  with  mucus  ;  all  of  the  gastric  symp- 
toms are  augmented  in  hemorrhagic  erosion.     Punctate  ov  follicular  vlcer- 


CHKONIC    GASTRITIS.  335 

ation  presents  few,  if  any,  symptoms  differing  from  those  of  ordinary  chronic 
catarrh.  In  most  instances  where  a  post-mortem  has  revealed  this  patho- 
logical state,  there  was  vomiting  of  coffee-ground  material  during  life. 

Differential  Diagnosis. — Chronic  catarrh  of  the  stomach  is  to  be  differ- 
entiated from  atonic  dyspepsia,  from  cancer,  and  ulcer  of  the  stomach. 

Atonic  dyspepsia  is  associated  with  anaemic  conditions  dependent  uj)on 
habits  of  life  and  an  unhealthy  occupation  ;  while  chronic  catarrh  is 
associated  with  the  immoderate  use  of  alcoholic  stimulants,  or  is  secondary 
to  chronic  thoracic,  renal  or  hepatic  disease.  In  atonic  dyspepsia  there  is 
little  or  no  pain  or  tenderness  in  the  epigastric  region,  which  is  always 
present  in  chronic  gastritis.  In  atonic  dyspepsia  the  tongue  does  not 
present  the  coated  appearance  so  constant  in  chronic  gastritis,  but  is 
broad,  pale,  and  flabby.  In  atonic  dyspepsia  there  is  loss  of  appetite,  but 
never  the  complete  anorexia  and  constant  thirst  which  are  present  in 
chronic  gastritis.  Spices  and  stimulating  ingesta  often  relieve  the  gastric 
symptoms  of  atonic  dyspepsia,  while  in  chronic  gastritis  they  aggravate  the 
gastric  symptoms.  The  constitutional  symptoms  in  atonic  dyspepsia  are 
slight,  while  in  chronic  gastritis  they  are  marked  and  severe.  The  urine  is 
unaltered  in  atonic  dyspepsia,  while  it  is  cloudy  and  alkaline,  and  deposits 
urates,  oxalates  and  phosphates  in  chronic  gastritis.  Nausea  and  vomiting 
are  more  apt  to  occur  in  chronic  gastritis  than  in  dyspepsia,  and  eructations 
are  never  present  in  simple  dyspepsia. 

The  points  in  the  differential  diagnosis  between  chronic  gastritis  and 
ulcer  of  the  stomach  are  given  under  the  latter  heading. 

Prognosis. — The  duration  of  chronic  gastric  catarrh  is  variable;  it  may 
last  for  months  or  years  and  may  terminate  in  ulcer  or  stenosis  of  the 
pyloric  orifice.  It  is  amenable  to  treatment  except  when  associated  with 
advanced  hepatic,  renal,  or  pulmonary  diseases,  or  where  stricture  at  the 
pyloric  orifice  exists.  A  not  infrequent  complication  is  disease  of  the  supra- 
renal capsules,  and  the  connection  between  the  two  diseases  has  by  some 
been  supposed  to  be  a  "sympathetic"  one,  but  no  rational  explanation  has 
yet  been  offered.  Sub-acute  gastric  catarrh  sometimes  complicates  chronic 
gastric  catarrh  and  renders  the  prognosis  unfavorable.  G-astro-enteritis  is 
a  very  rare  complication.  Death  may  result  from  heematemesis  or  from 
stricture  of  the  pylorus.  The  general  feebleness  which  results  from  long 
standing  gastritis  predisposes  to  acute  disease. 

Treatment. — The  most  important  thing  to  be  accomplished  in  the  treat- 
ment of  chronic  gastritis  is  the  removal  of  its  cause.  Each  case  requires  a 
special  treatment  suited  to  its  special  indications  and  to  its  complicating 
causes.  When  alcohol  is  the  cause,  all  stimulants  must  at  once  be  pro- 
hibited, and  the  patient  placed  on  a  diet  in  which  there  are  few  fats  or 
carbo-hydrates.  The  food  should  be  taken  slowly  in  small  qiiantities,  at 
shorter  intervals  than  in  health,  and  thoroughly  masticated.  I  have  found 
"  underdone  beef  "  and  milk  to  be  especially  adapted  to  this  class  of  cases. 
In  catarrh  induced  by  dram-drinking  the  best  drug  to  allay  morbid 
sensibility  of  the  stomach  and  the  morning  sickness  is  opium,  which  also,  by 
inducing  sleep,  relieves  the  nervous  symptoms,  which  are  always  prominent 


236  DISEASES    OF   THE    DIGESTIVE   SYSTEM. 

in  this  variety.  Strychnia  and  zinc  in  combination  with  mineral  acids  have 
a  wide  reputation  in  this  class  of  cases,  acting  favorably  on  both  the  nervous 
and  digestive  disturbances.  The  vegetable  bitters  as  tonics  are  often 
serviceable  when  the  craving  for  alcoliol  is  excessive.' 

When  there  is  marked  anaemia,  j)reparations  of  iron  and  pepsin  may  be 
given.  When  chronic  catarrh  is  associated  with  cardiac  disease,  granules 
of  digitaline,  1-50  of  a  grain  each,  may  be  given  twice  a  day  with  advan- 
tage. When  associated  with  pulmonary  diseases,  an  out-of-door  life  in  a 
suitable  climate  not  infrequently  effects  a  cure.  In  phthisical  gastritis,  a 
form  that  is  very  obstinate,  hydrocyanic  acid  with  the  alkaline  carbonates 
combined  with  bismuth  is  often  of  service.  If  hepatic  disease  exists  tho 
portal  congestion  may  be  relieved  by  ^leeches  about  the  anus,  and  an 
occa^onal  brisk  mercurial  purge ;  a  course  of  mineral  waters  will  in  a 
large  proportion  of  cases  give  temporary  relief.  The  daily  use  of  cold  water 
enemata  will  in  these  cases  preclude  the  necessity  of  resorting  to  cathartics. 

Scrofulous  subjects  should  be  treated  with  iodine  and  cod-liver  oil.  The 
Vichy  waters  in  combination  with  colchicum  are  indicated  in  gouty 
patients.  Free  purgation  and  warm  alkaline  baths  are  also  serviceable  in  this 
class  of  cases.  There  is,  perhaps,  no  remedy  which  will  for  a  time  relieve 
the  irritability,  pain,  and  acidity  after  meals  as  certainly  as  bismuth. 
When  it  fails  in  cases  of  long  standing,  zinc,  alum,  tannin,  or  nitrate  of 
silver  may  be  tried.  The  habitual  constipation  which  often  complicates 
these  cases  will  be  relieved  by  daily  use  of  aloes  and  strychnia,  or  rhubarb 
and  soda.  When  there  is  evident  deficiency  of  gastric  juice,  five  or  six 
drops  of  hydrochloric  acid  in  a  wine-glass  of  water  and  ten  or  fifteen  grains 
of  saccharated  pepsin  will  greatly  assist  the  digestive  process.  If  there  is 
an  excess  of  gastric  juice,  alkaline  waters  should  be  freely  used  during,  and 
after  meals.  When  fermentation  is  very  active  and  flatulence  is  annoying, 
sulphite  of  soda  or  creosote  given  after  meals  is  serviceable.  If  the  stomach 
rejects  food  as  soon  as  it  is  taken,  rest  is  essential,  and  the  patient  must  be 
nourished  for  a  time  by  the  rectum  and  then  placed  on  a  milk  diet.  Mi- 
nute doses  of  arsenic  and  of  belladonna  have  been  recommended  as  curative 
agents,  but  there  is  no  evidence  that  they  have  any  such  power.  Blisters, 
moxae  and  issues  over  the  stomach  are  sometimes  of  service  in  very  chronic 
cases. 

PHLEGMOXOIJS  GASTEITIS. 

Phlegmonous  gastritis  is  a  suppurative  inflammation  of  the  areolar  (sub- 
mucous) tissue  of  the  stomach ;  it  has  also  been  called  "  suppurative 
Unit  is.''' 

Morbid  Anatomy. — The  suppurative  process  may  be  circumscribed  oi 
diffused.     On  removal  of  the  stomach  its  wall  is  found  thicker  than  normal, 

J  I  have  found  the  following  to  allay  this  craving  : 

3    Tr.  cinchonae  comp 5  iv. 

Tr.  capsici 3  ss. 

Tr.  nuc.  vomicae 3  ij. 

M.    A  teaspoonful  every  two  or  three  hours. 


PHLEGMONOUS    GASTKITIS.  237 

and  its  substance  oedematous  and  very  friable.  Tiie  submucous  tissue  is 
distended  by,  and  infiltrated  with  fibrin  and  pus,  which  not  infrequently 
accumulate  in  large  quantities  in  the  muscular  tissue  as  well.  The  entire 
mucous  coat  is,  in  rare  instances,  very  much  thinned  and  undermined  by 
the  purulent  accumulation  which  perforates  it  at  different  points  ;  the 
small  openings  thus  formed  give  exit  to  the  pus  from  the  spongy,  irregular 
shaped  cavities,  or  "abscesses,''  lying  beneath.  The  mucous  surface  is 
reddened  in  patches,  or  is  of  a  deep  purple  color  ;  sometimes  it  is  gangren- 
ous. If  the  peritoneal  coat  is  involved  it  presents  the  usual  appearance  of 
acute  peritonitis.  The  abscesses  in  the  sab-mucous  tissue  tend  to  open 
into  the  cavity  of  the  stomach,  although  they  may  perforate  externally  and 
be  discharged  into  the  peritoneal  cavity.  In  circumscribed  phlegmonous 
gastritis  these  pus  cavities  may  be  the  starting-point  of  ulcers  of  the 
stomach. 

Etiology. — Phlegmonous  gastritis  is  a  very  rare  disease,  usually  occurring 
between  the  ages  of  twenty  and  forty  years.  It  may  occur  idiopathically  in 
previously  healthy  persons,  without  any  assignable  cause,  or  it  may  be 
secondary  to  pysemia,  septicaemia,  puerperal  fever,  typhus  fever,  and 
diphtheria. 

Symptoms. — Phlegmonous  gastritis  is  ushered  in  by  a  distinct  chill,  fol- 
lowed or  accompanied  by  intense  pain  and  tenderness  over  the  region  of 
the  stomach.  Complete  anorexia  is  an  early  symptom,  and  is  accompanied 
by  intense  and  constant  thirst ;  there  is  persistent  vomiting,  which  increases 
in  severity  with  the  advance  of  the  disease  ;  the  ejected  matters  are  some- 
times purulent,  but  usually  consist  of  a  dark  colored,  bitter  fluid.  The 
pain  increases  in  severity  until  it  becomes  as  severe  as  in  peritonitis.  The 
temperature  may  reach  104°  or  106°  ¥.  When  the  disease  has  reached 
its  climax  there  is  great  depression  and  exhaustion  ;  the  patient  is  anxious 
and  fretful,  not  infrequently  passing  into  active  delirium,  but,  whether 
the  latter  is  present  or  not,  typhoid  symptoms  with  low  muttering  delirium, 
jaundice,  stupor,  and  collapse  are  rapidly  developed,  and  the  patient  passes 
into  a  state  of  coma  and  dies. 

Differential  Diagnosis. — The  diagnosis  of  phlegmonous  gastritis  is  only 
made  by  exclusion  ;  it  often  passes  unrecognized  during  life. 

Prognosis. — The  prognosis  is  always  unfavorable.  The  majority  die  dur- 
ing the  first  week.  When  it  is  circumscribed  its  duration  may  be  pro- 
longed to  two  or  three  weeks.  Its  only  complications  are  secondary 
abscesses  in  other  organs  (as  the  liver)  and  peritonitis.  When  primary, 
the  disease  reaches  a  fatal  termination  either  from  peritonitis  or  from 
exhaustion  with  typhoid  symptoms. 

Treatment. — When  phlegmonous  gastritis  is  secondary  the  primary  dis- 
ease will  demand  attention;  in  all  cases  the  treatment  is  merely  palliative ; 
stimulants  are  indicated  very  early,  and  the  sufferings  of  the  patient  must 
be  relieved  by  morphia  hypodermically. 


238  DISEASES   OF   THE   DIGESTIVE    SYSTEM. 


aASTEIC    DYSPEPSIA. 

Dyspepsia  and  indigestion  are  terms  used  to  indicate  a  train  of  symp- 
toms caused  by  a  functional  derangement  of  the  digestive  processes.  When 
these  derangements  are  confined  to  the  stomach  they  constitute  gastric 
dyspepsia. 

Morbid  Anatomy. — Strictly  speaking,  gastric  dyspepsia  has  no  morbid 
anatomy.  If  it  has  continued  for  a  long  time  the  walls  of  the  stomach 
may  be  found  thinned,  the  mucous  membrane  atrophied,  and  many  of  the 
gastric  tubules  shrunken  and  in  a  state  of  fatty  degeneration.  Not  infre- 
quently the  tubular  structure  of  the  stomach  is  replaced  by  a  fibro-nucle- 
ated  tissue.  After  death  the  power  of  self-digestion  in  such  a  stomach  is 
markedly  diminished  or  entirely  lost.  It  is  often  met  with  as  a  part  of 
senile  decay. 

Etiology. — Dyspepsia-  is  often  an  inherited  condition  and  accompanies 
the  changes  of  advancing  age.  There  is  no  affection  in  which  individual 
idiosyncrasies  are  so  strongly  marked.  Its  etiology  can  best  be  considered 
under  the  following  heads  : — 

First : — A  class  of  cases  in  which  there  is  a  deficiency  in  the  quantity  of 
gastric  Juice  secreted.  Such  deficiency  often  occurs  in  those  disordered 
states  of  the  blood  which  precede  the  onset  of  acute  diseases.  It  occurs  in 
enfeebled  conditions,  as  the  result  of  exhausting  discharges,  venereal 
excesses,  masturbation,  leucorrhcea  and  phthisis,  and  from  the  excessive 
use  of  narcotics,  the  tannin  of  tea,  and  the  nicotine  of  tobacco. 

Second : — There  is  a  class  of  cases  in  which  there  is  an  excess  in  the  gas- 
tric secretion.  This  is  most  apt  to  occur  in  those  suffering  with  chronic 
hepatic  and  cerebral  diseases  and  in  gouty  subjects.  It  is  sometimes 
changed  in  quality  and  in  quantity  in  young  persons  who  have  grown 
rapidly,  and  in  females  at  the  menopause. 

Third: — There  is  a  class  of  cases  in  which  the  gastric  secretion  is 
changed  in  quality.  This  occurs  with  ulcer  and  cancer  of  the  stomach, 
gout,  rheumatism,  disease  of  the  kidneys,  uterus,  and  gall  bladder.  A 
lithic-acid  diathesis  is  said  to  cause  a  change  in  the  quality  of  the  gas- 
tric juice. 

Fowtli : — There  is  a  form  of  gastric  dyspepsia  due  to  impaired  motion 
of  the  stomach,  which  may  be  the  result  of  its  adhesion  to  neighbor- 
ing parts,  to  an  omental  hernia  dragging  it  out  of  its  normal  position, 
to  cicatrices  and  new  growths  at  its  pyloric  extremity,  to  thickening  of  its 
walls,  or  to  a  weak,  flabby,  enfeebled  condition  of  its  muscular  coat, 
and  to  pressure  on  the  stomach  from  tight  lacing  and  from  positions 
assumed  by  shoemakers,  needlewomen,  writers,  etc. 

Fifth  .'—Mental  emotion,  prolonged  mental  labor,  and  anxiety  rather 
than  continuous  and  regular  brain  work,  cause  dyspepsia ;  in  such  cases  it 
is  the  sudden  arrest  of  the  digestive  functions,  especially  after  eating  too 
much,  which  is  the  main  etiological  factor.     Organic  cerebral  disease  and 


GASTRIC   DYSPEPSIA.  239 

pressure  on,  or  disease  of  one  or  both  pneumogastrics  act  in  the  same 
way. 

Sixth : — Deficient  or  excessive  physical  labor  may  be  a  cause  of  dyspepsia. 
"Walking  immediately  after  a  full  meal  is  a  prolific  cause  of  this  variety,  ex- 
amples of  which  are  frequently  met  with  in  letter-carriers. 

Seventh: — Improper  diet  is  a  common  cause  of  dyspepsia.  It  may  arise  from 
an  excess  of  starchy  materials,  as  potatoes  ;  or  from  deficiency  of  meats.  Un- 
der improper  diet  may  be  included  decomposing  food,  impure  water,  badly 
cooked  food,  too  rapid  eating,  the  food  not  being  sufficiently  masticated,  or 
taken  at  too  short  intervals  and  irregularly.  Articles  of  food  that  may  be 
suited  to  one  climate,  season,  or  age  may  in  another  be  wholly  indigestible 
and  cause  dyspepsia. 

Symptoms. — The  symptoms  of  dyspepsia  are  a  series  of  phenomena  which 
vary  not  only  in  different  individuals,  but  in  the  same  individual  at  differ- 
ent times  ;  the  most  constant  is  an  abnormal  appetite  :  it  may  be  lost,  in- 
creased, or  perverted.  There  is  a  weight,  dull  pain,  and  a  sense  of  burning 
in  the  epigastrium  after  ingestion  of  food,  accompanied  by  flatulence,  heart- 
burn, gastralgia,  constipation  or  diarrhoea,  a  dull  headache,  languor,  de- 
pression of  spirits  and  irritability  of  temper.  Indiscretion  in  eating  or  drink- 
ing, and  exercise  or  exposure  in  dyspeptic  subjects  are  apt  to  bring  on  an  at- 
tack of  sick  headache.  There  is  frequently  a  bitter  taste  in  the  mouth, 
bilious  vomiting  and  sluggish  bowels  ;  this  is  called  a  bilious  attack.  If 
these  symptoms  immediately  follow  the  taking  of  food,  it  is  called  "inges- 
tive  dyspepsia,"  or  "  morbid  sensibility  of  the  stomach."  In  some  dyspep- 
tics the  breath  and  faeces  have  a  very  offensive  odor. 

Pyrosis,  which  is  the  chief  symptom  in  another  class  of  cases,  is  the 
regurgitation  into  the  mouth  of  a  large  amount  of  thin,  watery,  saline  fluid, 
preceded  by  a  sense  of  constriction  and  pain  in  the  epigastrium.  This  fluid 
consists  mainly  of  saliva.  Sometimes  there  is  not  only  a  feeling  of  oppres- 
sion in  the  thorax,  but  a  severe  pain  is  referred  to  the  heart,  accompanied 
by  palpitation  and  dyspnoea.  In  such  cases  the  patient  is  very  apt  to  im- 
agine he  has  heart-disease. 

Accompanying  some  cases  there  is  vertigo,  ringing  in  the  ears,  spots 
before  the  eyes,  and  other  sensations  which  together  have  been  called 
"stomachic  vertigo."  These  patients  hear  a  buzzing  sound  and  feel  as  if  a 
vapor  were  enveloping  them;  they  grow  pale,  and  grasp  for  support  through 
fear  of  falling.  When  in  any  case  the  "indigestion"  has  lasted  a  long 
time,  chronic  gastric  catarrh  will  almost  always  be  developed,  and  evidences 
of  mal-nutrition  show  themselves  by  anaemia,  premature  old  age,  corruga- 
tion of  the  nails,  caries  of  the  teeth,  etc.  At  other  times,  the  patient  will 
suffer  from  dyspnoea,  with  a  short,  dry  cough  and  occasional  paroxysms  of 
an  asthmatic  character.  The  skin  becomes  sallow,  dry  and  rough,  while 
various  eruptions  appear  on  it,  and  the  abnormal  contents  of  the  urine  show 
that  the  functions  of  the  kidneys  are  disturbed.  Often  in  long  standing 
dyspepsia  in  females  there  will  be  a  feeble  pulse,  leucorrhoea,  and  irregu- 
larities in  the  menstrual  functions.  There  is  no  characteristic  change  in  the 
appearance  of  the  tongue  ;    in  one  case  it  is  white  and  heavily  coated,  in 


;^40  DISEASES    OF   THE    DIGESTIVE   SYSTEM. 

another  it  is  clean,  large  and  indented.  The  urine  often  contains  oxalate 
of  lime  C'oxaluria").  After  the  oxalates  disappear,  lithates  may  appear 
for  a  time,  soon  to  be  followed  by  normal  urine. 

Differential  Diagnosis. — The  phenomena  of  dyspepsia  closely  resemble  those 
of  chronic  gastric  catarrh.  Their  differential  diagnosis  has  already  been  con- 
sidered. Acidity  from  hypersecretion  may  be  confounded  with  acidity  from 
fermentation,  and  stomachal  may  be  confounded  with  cerebral  vertigo. 

The  following  are  the  principal  points  in  their  differential  diagnosis  :  pain 
in  acidity  irora.  hypersecretion,  either  immediately  follows  the  taking  of  food, 
and  is  accompanied  by  "  heartburn,"  or,  quite  as  often,  it  is  felt  most  when 
the  stomach  is  empty,  and  is  relieved  by  taking  food  ;  but  the  pain  from 
fermentation  due  to  obstruction  to  movements  of,  or  to  chronic  inflammatory 
processes  in,  the  stomach  comes  on  some  time  after  eating,  and  is  more  a 
sense  of  weight  or  fulness  in  the  epigastrium  than  pain.  It  is  never  pres- 
ent during  the  intervals  between  taking  food.  Vomiting  is  rare  in  acidity 
from  fermentation,  but  if  it  does  occur  the  ejected  materials  will  contain 
organic  acids,  torulae  and  sarcinae  ;  while  with  hypersecretion,  vomiting  is 
a  common  symptom,  and  very  frequently  there  is  an  excess  of  hydrochloric 
acid  in  the  matter  vomited.  The  constitutional  symptoms,  mental  depres- 
sion, and  emaciation,  the  sallow  skin,  etc.,  are  much  more  marked  in  dys- 
pepsia with  fermentation  than  in  dyspepsia  with  hypersecretion.  In  case  of 
acid  stomach  from  fermentation,  flatulence  is  very  common,  while  it  rarely 
occurs  with  acidity  from  hypersecretion.  The  urine  is  alkaline  or  neutral 
in  acidity  from  fermentation,  while  it  is  always  acid  with  hypersecretion. 
Lastly,  acidity  from  fermentation  has  a  history  of  some  cause  or  causes 
which  interfere  with  digestion ;  while  hypersecretion  is  usually  a  reflex 
symptom,  or  occurs  with  cancer  or  ulcer  of  the  stomach. 

With  vertigo  or  dizziness  from  stomachal  causes  there  is  a  history  of  indi- 
gestion, and  it  usually  occurs  in  middle  life  ;  while  in  cerebral  vertigo,  the 
individual  is  beyond  middle  life,  and  there  will  be  no  history  of  difficult  or 
impaired  digestion.  Vertigo  from  stomachal  causes  occurs  during  an  attack 
of  indigestion,  or  after  some  particular  kind  of  food  has  been  taken.  Cer- 
ebral vertigo  occurs  wholly  independent  of  the  state  of  the  stomach.  Con- 
sciousness is  never  lost,  nor  are  the  special  senses, — sight  alone  excepted, — 
involved  in  stomachal  vertigo  ;  while  ringing  in  the  ears,  temporary  deaf- 
ness, and  often  complete  loss  of  consciousness  occur  in  an  attack  of  cerebral 
vertigo.  A  person  suffering  with  stomach  vertigo  knows  that  the  apparent 
motion  of  the  surrounding  objects  is  unreal  ; — while  a  patient  with  cerebral 
vertigo  believes  the  apparent  movement  of  the  objects  to  be  real. 

Prognosis. — The  prognosis  varies  with  the  etiology.  Dyspepsia  in  most 
cases  can  be  cured,  but  the  cure  depends  for  the  most  part  on  the  will  of 
the  patient.  The  only  danger  is  that  the  conditions  induced  by  dyspepsia 
may  predispose  to  organic  diseases  in  other  organs,  as  the  lungs  or  kidneys, 
and  that  it  may  lead  to  a  condition  of  melancholia. 

Treatment— First,  if  possible,  remove  the  cause.  When  the  gastric  juice 
is  deficient  in  quantity,  hydrochloric  acid  and  pepsin  are  indicated.  In 
these  cases,  also,  the  vegetable  bitters  are  especially  beneficial  ;  indeed,  in 


CANCEE    OF   THE   STOMACH.  241 

most  cases  of  dyspepsia  they  are  valuable  adjuvants  to  the  other  remedies. 
Tea  and  tobacco  are  always  to  be  avoided  ;  alcoholic  stimulants  in  moderate 
quantities  may  sometimes  be  combined  with  the  vegetable  bitters  with  ad- 
vantage. When  acid  risings  occur  after  ingestion  of  food,  and  there  are 
actual  evidences  of  active  fermentation,  the  sulphite  of  soda,  creosote  and 
the  alkalies,  after  meals,  are  of  service.  A  course  of  saline  waters  will  be 
found,  in  such  instances,  to  aid  the  other  remedies. 

When  there  is  great  irritahility  of  the  stomach  bismuth  acts  almost  as  a 
specific,  and  should  be  given  in  twenty-grain  doses  before  eating.  If  there 
is  pain  in  the  epigastrium  the  local  application  of  heat  by  means  of  the 
hot-water  bag  will  relieve.  Dyspeptics  should  never  wear  corsets  or  belts 
about  the  abdomen  ;  they  should  retire  and  rise  early,  and  eat  slowly, 
masticating  their  food  thoroughly.  The  meals  should  be  small  and  taken 
at  stated  intervals,  and  should  be  free  from  hydrocarbons.  No  mental  or 
physical  work  should  be  performed  directly  after  or  before  eating.  Horse- 
back-riding and  walking  in  the  open  air  should  be  insisted  upon.  A 
change  of  scene  and  climate  works  rapid  cures  in  many  instances.  Dyspep- 
tics should  take  plenty  of  rest,  have  their  sleeping-rooms  well  ventilated, 
and  take  a  cold  sponge-bath  morning  and  evening.  The  general  princi- 
ples of  treatment  in  gastric  dyspepsia  are  similar  to  those  given  in  chronic 
gastric  catarrh. 

CANCER    OF    THE    STOMACH. 

The  stomach,  next  to  the  liver,  is  the  most  frequent  seat  of  internal  can- 
cerous developments  ;  one-third  of  all  the  cases  of  primary  cancer  have 
their  seat  in  the  stomach.  The  varieties  of  cancer  of  the  stomach  in  the 
order  of  their  frequency  are  as  follows  : 

First,  scirrJius ;  second,  medullary  j  third,  colloid ;  fourth,  villous  ; 
fifth,  melanotic  J  and  lastly  epithelial.  The  last  three  varieties  are  exceed- 
ingly rare. 

Morbid  Anatomy. — Cancer  has  its  seat  at  the  pyloric  extremity  of  the 
stomach  in  about  three-fifths  of  the  cases.  The  next  favorite  seat  is  the 
cardia  and  the  lesser  curvature.  When  it  is  developed  at  the  pylorus,  it 
sometimes  extends  an  inch  or  two  into  the  duodenum  ;  cancer  at  the 
cardia  usually  involves  the  lower  part  of  the  oesophagus. 

Scirrhus  of  the  stomach  first  appears  as  a  small,  grayish  white,  opaque 
nodule  in  the  submucous  tissue,  the  normal  structures  of  which  are  en- 
closed by  the  new  growth.  The  fibrous  stroma  is  far  in  excess  of  the  cell- 
element  ;  it  develops  rapidly  at  the  exterior  of  the  mass,  causing  in- 
duration and  contraction  of  the  surrounding  structures.  The  mass 
sometimes  extends  inward  toward  the  cavity  of  the  stomach,  causing 
flattened  tumors  which  project  into  it.  The  contraction  of  these  nodules 
puckers  the  mucous  surface,  which  becomes  immovably  fixed  upon  them,, 
and  fibrous  lines  radiating  from  the  growth  penetrate  the  mucous  mem- 
brane, which  first  undergoes  a  slight  increase  in  thickness,  and  then  be- 
comes pale  from  compression  of  its  vessels.  The  solitary  glands  are  en- 
16 


243 


DISEASES    OF   THE    DIGESTIVE    SYSTEM. 


Pig.  54. 
Cancer  of  the  Pyloric  Extremity  of  the  Stomach. 

A.  Mucous  membram  of  the  stomach  beyond  the  seat  of  the  cancerous  in- 

filtration. 

B.  Pylorus. 

C.  Commencement  of  the  Duodenum. 

D,  B.  Vertical  sectiort  of  the  cancerous  mass. 

E,  E.  Internal  surface  of  the  cancerous  infiltration  encroaching  on  th£  py- 

loric orifice. 
F.  Small  opening  in,  the  cancerous  growth  at  the  pyloric  extremity. 


larged  and  the  gastric  tubules  are  matted  together  in  an  indistinguishable 
bundle.  A  dark  slough  sometimes  forms  upon  its  surface  and  exposes 
the  cancerous  growth,  which  then  ulcerates.     The  ulceration  may  extend 

so  deeply  as  to  destroy 
^  ^.^^ff^X^l  (  J/  the  new  growth  and 
invade  the  wall  of 
the  stomach  under- 
neath it,  causing  ir- 
regular  cavities, 
bounded  by  a  raised 
and  indurated  band 
of  connective-tissue, 
and  sometimes  open- 
ing into  the  stom- 
ach. These  poly- 
p  o  i  d  tumors  are 
sometimes  as  large  as 
a  hen's  egg  and  de- 
velop upon  the  can- 
cerous mass.  The 
glands  and  villi  are 
the  longest  to  resist 
this  encroachment  of 
the  cancerous  development,  the  first  change  in  them  being  an  increase  in 
the  number  of  their  epithelial  cells.  After  a  time  the  muscular  coat  be- 
comes fused  with  the  areolar,  so  that  at  the  seat  of  the  neoplasm  they  can- 
not be  distinguished  from  each  other  on  section  of  the  mass.  At  other 
times  the  parts  affected  are  hard  and  fibrous,  the  stomach  walls  being  so 
thickened  that  the  disease  is  only  differentiated  from  hypertrophy  of  its 
coats,  by  the  glistening,  pearly  look,  and  cartilaginous  texture  of  the  mass. 
After  involving  the  muscular  coat,  the  growth  may  involve  the  peritoneal 
covering  ;  local  peritonitis  establishes  adhesions  between  it  and  the  dia- 
phragm, liver,  pancreas  and  spleen. 

The  lesions  which  follow  the  development  of  scirrhus  in  the  stomach  are 
as  follows  : 

Dilatation  of  the  stomach  is  a  frequent  result  of  the  obstruction  at 
the  pylorus  caused  by  the  cancerous  development.  Less  common  than 
dilatation  of  the  stomach  is  the  gizzard  appearance  caused  by  the  same  con- 
traction that  shrivelled  the  mucous  membrane,  inducing  a  shrinking  of 
the  whole  stomach  wall,  which  sometimes  becomes  an  inch  thick,  the 
cardia  and  pylorus  not  infrequently  being  closely  approximated,  and  the 
anterior  and  posterior  stomach  walls  being  almost  in  juxtaposition. 

Chronic  gastritis  is  developed  when  the  new  growth  attains  sufficient 
size  to  cause  pressure,  and  in  such  cases  the  mucous  membrane  presents 
the  characteristic  appearances  of  that  affection. 

Perforation  of  the  stomach  sometimes  occurs,  causing  a  fatal  peritonitis  ; 
a  secondary  opening  may  penetrate  into  the  duodenum,  liver.  Jejunum,  or  ile- 


CANCER   OF   THE    STOMACH.  243 

Tim,  or  through  the  anterior  wall  of  the  abdomen,  and  thus  form  an  external 
opening.  In  rare  instances  openings  are  made  into  the  lungs,  pleural  cavity, 
bronchi,  or  pericardium.  Large  branches  of  the  pneumogastric  may  be 
destroyed  by  the  new  growths.  In  five  per  cent,  of  the  cases  of  cancer  of 
the  stomach,  secondary  cancer  is  developed  in  other  organs.  The  organ 
which  is  the  most  frequent  seat  of  this  secondary  development  is  the  livery 
and  after  the  liver  the  lymphatic  glands  in  the  immediate  vicinity  of  the 
peritoneum,  and  various  segments  of  tlie  intestine,  especially  the  rectum. 
The  kidneys,  bladder,  spleen,  pancreas  and  ovaries  may  also  be  the  seat 
of  these  secondary  developments.  The  position  of  the  stomach  is  some- 
times changed,  the  weight  of  the  tumor  dragging  it  into  the  lower  portion 
of  the  abdomen,  and  there  it  may  be  bound  to  the  intestines,  bladder, 
uterus  or  ovaries  by  firm  adhesions. 

Medullary,  or  acute  cancer  of  the  stomach,  commences  in  the  same  tis- 
sues as  scirrhus,  in  the  form  of  nodules  much  softer  than  those  of  scirrhus. 

On  section,  cancer-juice  can  be  readily  expressed  from  the  cut  surface 
of  the  cancerous  mass  ;  the  proportion  of  the  stroma  being  much  less,  and 
the  cells  more  abundant.  The  growth  is  more  vascular,  and  not  infrequently 
contains  small  blood  extravasations.  It  is  much  more  rapid  in  its  de- 
velopment than  scirrhus,  and  while  proliferation  of  the  epithelial  struct- 
ure occurs  at  the  periphery,  fatty  degeneration  breaks  down  the  centre, 
and  it  sometimes  becomes  diffluent.  The  mucous  tissue  is  rapidly  invaded. 
Large,  spongy,  ''  fleshy  "  excrescences  project  into  the  cavity  of  the  stomach. 
Around  the  growth,  which  varies  in  size  from  that  of  a  pigeon's  ^g^,  to  that 
of  an  orange,  is  a  transparent  ring  of  tissue  infiltrated  with  cancer,  beyond 
which  the  solitary  glands  are  enlarged,  and  the  stomach-follicles  degen- 
erated. ''Villous"  cancer  of  the  stomach  is  a  modification  or  variety  of 
medullary  cancer.  If  medullary  cancer  ulcerates,  the  slough  is  thrown 
off,  and  an  excavated  ulcer  is  exposed,  surrounded  by  an  elevated  rim, 
from  which  projects  the. cauliflower-like  growth,  very  friable  and  vascular. 
The  surface  exposed  by  such  ulceration  is  often  very  large,  even  six  or 
seven  inches  in  diameter. 

Colloid  or  alveolar  cancer  has  the  same  structure  as  colloid  cancer 
occurring  in  other  parts  of  the  body.  It  appears  oftener  in  the  stomach 
than  elsewhere,  but  even  here  \t  is  rare.  There  are  different  opinions  as 
to  its  starting  point  ;  some  state  that  it  begins  in  the  sub-serous,  others  in 
the  submucous  tissue.  •  Eecently  a  glandular  origin  has  been  ascribed  to 
it,  similar  to  epithelioma  of  the  skin.  Wherever  commencing,  it  rarely 
appears  as  nodules,  but  commonly  as  an  irregular  mass  of  "  gum-like " 
glistening  material,  contained  in  large  and  distinctly  marked  alveoli,  in 
which  are  embedded  polygonal  nucleated  cells.  The  walls  of  the  stomach, 
the  seat  of  colloid  degeneration,  are  very  much  thicker  than  normal.  Its 
tendency  is  to  spread  rapidly  over  a  large  surface.  The  contents  of  some  of 
the  alveoli  are  discharged  into  the  stomach,  thus  giving  to  its  inner  sur- 
face an  irregular,  '' honey-comb"  appearance. 

Etiology. — Cancer  of  the  stomach  occurs  most  frequently  between  the 
ages  of  forty-five  and  sixty-five.     It  is  more  frequent  in  males  than  females. 


^'44  DISEASES   OF   THE    DIGESTIVE   SYSTEM. 

Hereditary  predisposition  is  undoubtedly  its  most  important  etiological 
factor.     Beyond  this  its  etiology  is  obscure. 

Symptoms. — The  earliest  and  most  prominent  symptom  of  cancer  of  the 
stomach  is  anorexia,  accompanied  by  a  sense  of  uneasiness  or  distention  in 
the  epigastrium,  with  nausea  and  vomiting.  Pyrosis  is  often  present  quite 
early.  Patients  describe  the  pain  as  dull,  gnawing,  or  as  a  tightness  or  ''  sore- 
ness "  over  the  stomach  ;  after  a  time  it  becomes  lancinating,  fixed  and 
constant ;  the  locality  of  the  pain  does  not  correspond  to  the  seat  of  the 
cancer  ;  when  the  growth  has  its  seat  in  the  lesser  curvature,  the  pain  is 
referred  to  the  interscapular  region  ;  it  is  not  usually  increased  by  ingestion 
of  food,  and  if  it  is  it  does  not  cease  at  the  end  of  the  digestive  process  ;  it 
may  become  constant  and  severe.  These  symptoms  usually  exist  before  the 
appearance  of  a  tumor.  During  the  period  of  its  growth  vomiting  becomes 
frequent.  There  are  three  prominent  causes  of  the  vomiting  :  first,  from 
olstruction.  Vomiting  from  this  cause  comes  on  comparatively  late  ; 
when  the  obstruction  is  at  the  cardia  it  occurs  immediately  after  eating. 
If  it  is  situated  at  or  about  the  pylorus,  the  food  is  retained  for  one  or  two 
hours.  Secondly,  from  irritation.  This  occurs  independent  of  taking  food 
and  the  time  of  its  digestion.  Thirdly,  from  fermentation.  This  occurs 
after  a  large  accumulation  of  food  in  the  stomach  ;  and  the  matters  vom- 
ited are  dark  and  yeasty,  not  infrequently  containing  sarcince  ventriculi. 

Hiccough,  flatulence  and  constipation  are  often  very  annoying,  some- 
times very  distressing  symptoms,  and  emaciation,  debility,  and  the  haggard 
"cancer  countenance,"  are  often  present.  There  is  mental  depression,  anxi- 
ety, and  the  patient  is  morose  or  apathetic. 

When  ulceration  of  the  free  surface  of  the  cancerous  mass  occurs  the 
most  constant  symptom  is  hemorrhage.  This  may  be  copious  and  bright 
red  in  color,  but  usually  the  blood  is  so  altered  by  the  gastric  Juice,  and  so 
mixed  with  food,  that  it  is  rusty,  brown  or  blackish  in  color  {"coffee 
ground"  vomit).  In  the  later  and  larger  hemorrhages,  the  blood  may 
in  part  escape  by  the  bowels,  and  then  diarrhoea  occurs  caused  by  the 
decomposing  blood  ;  the  stools  have  a  dark  tarry  appearance  with  a  very 
offensive  odor  ("melsena").  The  yellowish  green  color  of  the  skin, 
usually  present,  may  change  to  a  jaundiced  hue,  due  to  pressure  of  th& 
cancerous  mass  upon  the  bile  ducts. 

One  may  be  deceived  or  puzzled  during  the  course  of  cancer  of  the  stom» 
ach,  by  a  remission  of  the  anorexia,  pain,  hemorrhage,  and  vomiting, 
so  that  improvement  seems  to  be  taking  place  and  the  patient  believes 
he  is  recovering ;  but  in  a  short  time  all  these  symptoms  will  return 
with  increased  severity  and  the  disease  will  progress  more  rapidly  than 
before. 

Again,  there  is  sometimes  a  febrile  reaction — not  a  definite  hectic,  but  a 
symptomatic  fever — which  appears  irregularly  during  the  progress  of  the 
cancer,  and  which  often  misleads  on  account  of  the  belief  that  the  temper- 
ature in  malignant  disease  is  normal  or  sub-normal.  During  the  advanced 
stage  in  many  cases  the  tongue  becomes  covered  with  aphtha,  typhoid 
symptoms  develop,  and  death  is  often  preceded  by  delirium  which  is  fol- 


CASrCER   OF   THE   STOMACH.  245 

lowed  by  coma.  The  urine  is  scanty,  high  colored,  and  of  a  high  specific 
gravity.  It  is  loaded  with  urates,  and  deposits  a  pink  sediment  regarded 
by  some  as  a  diagnostic  symptom. 

Physical  Signs. — By  palpation  a  tumor  is  discovered — sometimes  large, 
hard,  irregular  and  nodulated ;  sometimes  small,  deep-seated  and  elastic. 
In  the  former  case  it  is  easy,  in  the  latter  very  difficult  of  recognition. 
If  the  cancer  is  situated  at  the  cardiac  extremity  of  the  stomach,  no 
tumor  will  be  felt.  The  tumor  is  usually  movable,  except  when  ad- 
hesions have  formed  between  it  and  the  adjacent  tissues.  If  the  can- 
cer is  at  the  pyloric  extremity  of  the  stomach  the  tumor  is  usually 
situated  in  the  median  line  ;  it  may,  however,  be  felt  at  the  lower  part  of 
the  epigastric  region,  in  the  right  hypochondrium,  at,  or  just  above  the 
line  of  the  umbilicus,  or  it  may  be  far  over  on  the  left  side.  It  may  receive 
and  transmit  the  impulse  of  the  aorta,  that  is,  become  a  pulsating  tumor. 
The  epigastric  region  is  prominent,  hard,  resisting  and  tender.  It  is  im- 
portant during  the  examination  to  have  the  patient  distend  his  stomach  by 
drinking  one  or  two  tumblers  of  carbonated  water. 

Percussion  over  the  tumor  elicits  circumscribed  dulness  with  a  tympa- 
nitic, or  a  peculiar  hollow  quality  ;  light  percussion  may  give  absolute 
flatness,  when  forcible  percussion  gives  a  tympanitic  resonance. 

Auscultation  gives  negative,  results. 

Differential  Diagnosis. — Cancer  of  the  stomach  may  be  mistaken  for  gas- 
tric ulcer,  abdominal  aneurism,  cancer  of  the  left  lobe  of  the  liver,  and  for 
chronic  gastric  catarrh  toith  licBmatemesis  ;  the  latter  is  considered  under 
Chronic  Gastritis.  It  is  hardly  possible  after  a  careful  study  of  a  case  to 
mistake  cancer  of  the  stomach  for  gastric  dyspepsia,  or  to  confound  a  can- 
cerous tumor  at  the  pylorus  with  an  ovarian  tumor. 

Ulcer  of  the  stomach  occurs  most  in  young  adults,  especially  females, 
while  cancer  is  seldom  met  with  in  persons  under  forty.  In  cancer  there 
is  usually  a  history  of  hereditary  cancer;  while  ulcer  of  the  stomach  is 
usually  associated  with  anaemia,  chlorosis,  prolonged  lactation,  or  pro- 
longed compression  of  the  stomach,  as  in  the  case  of  shoemakers  and  sew- 
ing-girls. The  pain  in  cancer  is  continuous,  and  described  as  lancinating  ; 
while  in  ulcer  the  pain  is  intermittent,  greatly  increased  by  taking  food, 
often  referred  to  the  lower  dorsal  vertebrae,  and  described  as  "gnawing" 
or  burning.  Hcematemesis,  in  cancer,  has  a  sooty  or  ^'  coffee-ground^^ 
appearance,  is  small  in  amount  and  appears  late  in  the  disease ;  while  in 
ulcer  it  is  bright  red  arterial  blood,  is  profuse,  and  appears  as  an  early  symp- 
tom. Vomiting  in  cancer  does  not  relieve  the  pain,  is  not  very  severe 
and  comes  on  late ;  but  in  ulcer  it  is  severe,  comes  on  early,  and  affords 
temporary  relief  from  the  pain.  The  cancerous  cachexia  and  debility  are 
present  early  and  steadily  progress  in  cancer  ;  while  in  ulcer  there  may  be 
pallor,  but  no  characteristic  cachexia.  The  presence  of  an  epigastric  tumor 
establishes  the  diagnosis  of  cancer. 

An  anenrismal  tumor  is  smooth  and  ovoid  ;  a  cancerous  tumor  is  hard 
and  irregular.  An  expansive,  dilating  impulse  is  given  to  the  hand  on 
palpating  an  aneurismal  tumor ;  but  in  cancer  this  impulse  is  lifting  in 


346  DISEASES  OE  THE  DIGESTIVE  SYSTEM. 

character.  In  aneurism  there  is  constant  pain  in  the  back  corresponding 
to  the  position  of  the  tumor,  which  is  absent  in  cancer.  There  is  a  change 
in  the  femoral  pulse  in  aneurism,  which  is  not  present  in  cancer.  The  gas- 
tric symptoms,  the  cachexia  and  the  debility  of  cancer  are  not  present  in 
aneurism. 

Prognosis. — The  prognosis  in  cancer  is  always  unfavorable.  Its  shortest 
duration  is  seven  weeks,  and  its  longest  three  and  one-half  years,  the  aver- 
age duration  being  one  year.  Early  vomiting,  with  hsematemesis,  great 
and  sudden  emaciation,  and  complete  anorexia,  are  especially  unfavorable 
symptoms.  The  important  complications  of  cancer  of  the  stomach  are  the 
development  of  secondary  cancer  in  other  organs,  peritonitis, — independent 
of,  or  with  perforation, — pleurisy  and  pneumonia,  pericarditis,  endocardi- 
tis and  fatty  heart,  tuberculosis,  coagula  in  the  sinuses  of  tbe  dura  ma- 
ter, phlegmasia  dolens,  non-cancerous  ulcerations  in  the  rectum  and 
colon,  ascites  and  general  anasarca.  Death  may  occur  from  hemorrhage, 
peritonitis,  exhaustion,  marasmus,  and  from  complications. 

Treatment. ^The  treatment  is  altogether  palliative.  The  indications  are 
to  make  the  patient  comfortable  by  relieving  pain  and  vomiting.  The  diet 
may  be  determined  by  the  experience  of  each  patient.  In  the  majority  of 
cases  alcoholic  stimulants  in  moderation  are  beneficial.  When  the  pain  be- 
comes severe,  morphia  may  be  administered  hypodermically.  If  at  any 
time  the  stomach  becomes  overloaded,  its  contents  may  be  carefully  re- 
moved by  means  of  a  stomach  pump.  The  constipation,  which  is  often  ob- 
stinate, is  best  overcome  by  aloes  ;  the  flatulence  and  painful  eructations  by 
sulphite  of  soda  or  oil  of  cajeput.  During  the  whole  course  of  cancer, 
subnitrate  of  bismuth  may  be  administered,  its  combination  with  soda, 
conium,  and  stramonium  being  highly  recommended  by  English  physicians. 
Some  assert  that  arsenic  is  efjfective  in  retarding  the  cancerous  growth,  and 
that  its  administration  with  iodine  and  carbolic  acid  may  arrest  its  devel- 
opment. My  experience  does  not  confirm  this  statement.  If  the  stomach 
entirely  rejects  food,  rectal  alimentation  may  be  resorted  to. 


ULCER    OF    THE    STOMACH. 

Statistics  show  that  gastric  ulcers,  or  cicatrices  caused  by  ulcers,  are  found 
in  three  out  of  every  hundred  cases  of  diseases  of  the  stomach.  They  may 
be  classed  as  follows  : 

I.  Superficial  Ulcer,  or  Hemorrhagic  V.  The  Typhoid  Ulcer. 

Erosion.  YI.  The  Variolous  Ulcer. 

II.  Follicular  Ulcer.  Yli.  The  DijjMlieritic  Ulcer. 

III.  The  Chronic,  Round,  or  Perfora-  VIII.  The  Syphilitic  Ulcer. 

ting  Ulcer.  IX.  The  Tutercular  Ulcer. 

IV.  The  Typhus  Ulcer.  X.  The  Cancerous  Ulcer. 

The  first  two  have  already  been  considered. 

The  specific  ulcers  Vi^hich  receive  their  names  from  the  diseases  in  which 


ULCER   OF   THE    STOMACH. 


247 


they  occur  as  occasional  patliological  lesions,  will  be  considered  in  connec- 
tion with  the  history  of  those  diseases. 

The  chronic,  round,  perforating  ulcer  is  l^y  far  the  most  frequent  form 
of  gastric  ulcer,  and  is  the  one  indicated  when  the  unqualified  term,  ulcer 
of  the  stomach,  is  used. 

Morbid  Anatomy. — Chronic  perforating  ulcers  most  frequently  occupy 
the  posterior  wall  of  the  stomach  near  its  pyloric  extremity.  They  var}^ 
in  size  from  half  an  inch  to  two  or  three  inches  in  diameter ;  an  ulcer 
one-half  inch  in  diameter  may  exhibit  all  the  clinical  characteristics  of 
one  of  large  size.  These  ulcers  are  at  first  circular  or  elliptical  in  form  ; 
occasionally  they  become  irregular  when  two  or  more  are  fused  together. 
When  oblong  they  have  their  axis  either  parallel  with,  or  transverse  to 
the  axis  of  the  stomach  ;  sometimes  they  form  a  zone  about  the  pyloric 
end  of  the  stomach.  The  large  ulcers  are  formed  by  the  fusion  of  several 
small  ones.  They  begin  in  the  mucous  membrane  of  the  stomach ;  their 
boundary  is  nearly  vertical,  smooth  and  sharp,  so  that  now  and  then  at  a 
post-mortem  the  mucous  membrane  will  present  an  appearance  as  if  a  cir- 
cular piece  had  been  "  punched  out "  with  a  sharp  instrument.  There  is 
no  evidence  of  an  inflammatory  process. 
The  loss  of  substance  may  involve  only  the 
mucous  layer,  or  it  may  extend  to  the  sub- 
mucous tissue,  or  penetrate  deeper  and  in- 
volve the  muscular  and  peritoneal  coats ; 
as  it  extends,  smaller  and  less  regular  cir- 
cles are  formed,  gradually  diminishing  in 
diameter,  a  small  opening  in  the  muscular 
coat,  or  a  mere  point  upon  the  peritoneum, 
being  the  apex  of  the  conical  or  "funnel- 
shaped"  excavation.  As  the  ulcer  spreads 
transversely  in  the  course  of  the  vessels,  this  ^^^ 

"step-like,"   bevelled  appearance  becomes        pejorating  uicei  of  "the  stomach. 
more  and  more  marked.  The  tissues  around  ^  mvcovk  surface 
the  ulcer  are  sometimes  normal,  especially  ^- ^^^^g'&^lLS^-^c'^^^"'  "" 
when  the  mucous  membrane  alone  is  in- 
volved ;  at  other  times  the  mucous  layer  encircling  the  base  of  the  ulcer  is 
thickened  and  indurated.     The  mucous  membrane  in  the  vicinity  of  an 
ulcer  is  sometimes  the  seat  of  a  circumscribed  chronic  catarrh  ;  but  more 
often  chronic  catarrh  involves  the  whole  gastric  mucous  membrane. 

The  variations  from  these  usual  pathological  appearances  consist, /rs^f,  in  a 
mass  of  black  blood  adh.ering  to  the  base  of  the  ulcer  ;  secondly,  in  petechial 
extravasations  around  the  injected  margin  of  the  ulcer  ;  thirdly,  in  the  villous 
or  "polypoid"  vegetations  springing  up  from  the  mucous  membrane  sur- 
rounding the  base  of  the  ulcer  ;  a.ndfotirtI/ly,  in  suppuration  in  the  coats  of 
the  stomach  with  subsequent  suppurative  pylephlebitis.  The  progressive  in- 
crease in  the  depth  of  the  ulcer,  which  is  part  of  its  natural  history,  would 
alwaj'^s  lead  to  perforation  and  discharge  of  the  contents  of  the  stomach  into 
the  peritoneal  cavity, were  it  not  for  the  establishment  of  a  local  jierifonitis 


248  DISEASES    OF   THE    DIGESTIVE    SYSTEM. 

which  causes  the  corresponding  portion  of  the  stomach  to  hecome  adherent 
to  the  adjacent  parts.  These  adhesions  may  join  it  to  the  pancreas,  liver,  me' 
sentery  or  spleen. 

The  number  of  ulcers  which  may  be  found  in  a  stomach  varies  from  one 
to  six  ;  as  a  rule  there  is  but  one.  Gastric  ulcers,  if  not  large  or  deep, 
may  heal  without  producing  deformity  of  the  stomach.  If  they  are  large 
or  deep,  the  resulting  cicatrix,  by  its  contraction,  causes  deformity  of  the 
stomach.  When  the  mucous  and  submucous  tissues  are  alone  involved, 
the  loss  of  substance  is  replaced  by  new  connective-tissue,  which  does  not 
contract ;  the  resulting  cicatrix  is  merely  a  white  spot,  with  little  or  no 
puckering.  The  usual  process  of  repair  in  deep  ulcers  is  that  of  a  local  in- 
flammation with  lymph  exudation.  The  connective-tissue  formed  at  the 
base  and  around  the  ulcer  contracts,  and  there  remains  a  central,  hard 
mass  from  which  radiate  bands  of  connective-tissue  into  the  adjacent 
mucous  membrane.  The  contraction  of  this  cicatricial  tissue  may  cause  a 
stricture  at  the  pylorus,  or,  if  the  ulcer  extends  around  the  central  portion 
of  the  stomach,  may  give  it  an  "  hour-glass  "  shape.  When  there  is  steno- 
sis at  the  pyloric  orifice,  the  stomach  is  dilated  and  the  walls  are  thickened 
in  one  subject  and  thinned  in  another. 

Ulcers  may  extend  by  degeneration  of  the  newly-formed  tissue.  With 
the  extension  of  the  ulcers,  some  of  the  larger  vessels  (as  the  superior  py- 
loric) may  become  involved,  and  extensive  hemorrhage  result ;  usually,  a 
"protective  thrombosis  "  prevents  this  accident.  Hemorrhages,  the  result 
of  intense  passive  hyperaemia,  or  of  erosion  of  small  vessels,  are  of  little  con- 
sequence compared  with  those  which  result  from  the  opening  of  vessels  of 
large  size  or  of  the  organs  with  which  the  stomach  becomes  adherent.  In 
this  way  the  portal  vein,  and  the  splenic,  pancreatic  and  hepatic  arteries 
have  been  pierced.  Perforation  of  the  stomach  in  gastric  ulcer  occurs 
only  in  about  one-eighth  of  all  the  cases.  Though  the  posterior  surface 
of  the  stomach  is  the  more  frequent  seat  of  these  ulcers,  the  liability  to 
perforation  is  greatest  when  the  ulcers  are  situated  in  its  anterior  wall. 
If  perforation  and  escape  of  the  contents  of  the  stomach  take  place  into 
the  peritoneal  cavity  a  general,  rapidly  fatal  peritonitis  immediately  fol- 
lows ;  when  adhesions  prevent  the  contents  of  the  stomach  from  escaping 
into  the  peritoneal  cavity,  a  local  peritonitis  is  developed  and  an  abscess 
may  be  formed  in  the  neighborhood  of  the  ulcer,  which  abscess  may  com- 
municate with  the  pleural  cavity,  duodenum,  colon,  or  gall-bladder.' 

'  Etiology. — Ulcer  of  the  stomach  occurs  in  females  oftener  than  in  males, 
the  proportion  being  more  than  two  to  one.  The  liability  to  it  is  greatest 
between  the  ages  of  fourteen  and  thirty,  although  no  age  is  exempt ;  it  has 
been  found  in  the  new-born  babe  and  in  the  octogenarian.     Angemia  an^ 

I  Many  theories  have  been  advanced  in  regard  to  the  pathogenesis  of  gastric  ulcers  ;  the  following  are 
the  principal  ones  :  perf orating  ulcers  may  be  the  result  of  an  inflammatory  process,  a  sequel,  oftentimes, 
of  chronic  gastritis.  Eokitansky  attributes  them  to  congestion,  extravasation,  and  subsequent  necrosis  of 
the  tissue.  Virchow  maintains  that  embolism  or  a  venous  stasis  deprives  ai  portion  of  the  stomach  of  its 
vascular  supply,  and  that  the  stomach-tissue  thus  deprived  of  its  nutrition,  is  acted  upon  by  the  gastric 
juice  as  dead  tissue  ;  as  a  result,  there  is  a  loss  of  substance  and  the  formation  of  ulcers.  He  compares  the 
funnel  or  cone-shaped  appearance  of  the  ulcer  to  embolic  infarctions  elsewhere,  the  capillaries  always  ram^ 
jfying  outwards  from  the  main  trunk. 


ULCER   OF  THE   STOMACH.  249 

cUorosis  are  the  two  great  predisposing  causes.  Chronic  and  phlegmonous 
gastritis,  cirrhosis  of  the  liver,  and  obstruction  of  the  gall-ducts  may  lead 
to  ulcer  of  the  stomach  by  inducing  obstruction  in  the  vessels  of  the  walls 
of  the  stomach.  Ulcer  may  resalt  from  an  habitual  stooping  position,  as  in 
milliners,  seamstresses,  and  shoemakers,  or  may  come  from  the  constant 
striking  of  the  shuttle  of  the  weaver  against  the  epigastrium.  Miliary 
aneurisms  in  the  gastric  walls  may  cause  gastric  ulcers.  Such  ulcers  are 
most  frequently  met  with  in  connection  with  a  cirrhotic  kidney.  It  may 
occur  without  any  recognized  cause. 

Symptoms, — The  symptoms  of  gastric  ulcer  are  sometimes  obscure,  at 
others  well  marked. 

Pain  is  one  of  its  constant  symptoms  :  at  first  it  is  dull  and  heavy ; 
then  it  becomes  burning  and  gnawing,  causing  a  sickening  sensation  quite 
distinct  from  nausea.  It  usually  comes  on  soon  after  the  ingestion  of 
food,  and  lasts  during  the  entire  period  of  stomach  digestion  ;  occasionally 
it  is  not  present  until  an  hour  or  so  after  eating.  It  is  circumscribed  to  a 
spot  rarely  larger  than  a  silver  dollar,  is  accompanied  by  tenderness  on 
dee]p  pressure,  and  its  intensity  is  usually  greatest  just  above  the  umbili- 
cus. The  "dorsal"  pain  of  gastric  ulcer  was  first  recognized  by  Cruveil- 
hier.  It  comes  on  some  weeks  or  months  after  the  pain  in  the  epigas- 
trium ;  it  is  located  at  the  eighth  or  ninth  dorsal  vertebra,  and  is  constant, 
although  it  may  sometimes  alternate  with  the  epigastric  pain.  In  a  few 
cases  the  pain  is  paroxysmal ;  there  are  intervals  of  freedom  from  pain,  fol- 
lowed by  severe  attacks,  resembling  those  of  neuralgia.  Eelief  from  the 
pain  of  gastric  ulcer  is  frequently  obtained  by  a  recumbent  posture  ;  this 
happens  when  the  ulcer  has  its  seat  on  the  anterior  wall  of  the  stomach. 

Nausea,  vomiting  or  regurgitation  of  food  may  accompany  the  pain  ; 
in  some  instances  there  is  pyrosis,  or  "  water  brash  ;  *'  usually  the  vomit- 
ing occurs  when  the  pain  is  most  severe.  The  matter  vomited  consists, 
first,  of  the  food  taken  into  the  stomach,  which  has  a  strong  acid  re- 
action ;  later  it  is  mingled  with  bile.  The  vomiting  temporarily  relieves 
the  pain.  After  a  time  these  dyspeptic  symptoms  are  complicated  by 
haematemesis,  which  may  be  regarded  as  essential  to  its  diagnosis.  In  a 
few  cases  there  is  no  vomiting.  Some  will  vomit  several  times  in  the 
twenty-four  hours,  others  once  a  day,  and  others  every  two  or  three  days. 
As  small  bleedings  do  not  cause  vomiting,  and  as  attention  is  rarely 
paid  to  the  stools  at  this  period,  the  exact  date  of  the  first  hemorrhage 
is  usually  unknown.  The  symptoms  which  attend  the  haematemesis  are 
a  sense  of  unusual  fulness  in  the  stomach,  accompanied  by  a  feeling  of 
faintness ;  the  face  is  blanched,  nausea  exists  for  a  varying  period,  and  this 
is  followed  by  vomiting  of  partially  coagulated  blood,  which  is  so  bright 
as  to  leave  no  doubt  of  its  arterial  origin.  In  rare  instances  the  first  hem- 
orrhage causes  distention  of  the  stomach,  s3Ticope  and  painless  collapse, 
followed  by  death.  Sometimes  the  blood  vomited  has  a  dark,  grumous 
appearance,  looking  like  coffee-grounds.  In  young  females  the  hemor- 
rhage is  usually  preceded  by  a  diminution   or  stoppage  of  the  menses. 

Preceding  and  accompanying  the  hsematemesis  there  are  usually  dyspeptic 


250  DISEASES    OF   THE   DIGESTIVE    SYSTEM. 

symptoms  similar  to  those  of  gastric  dyspepsia.  Cachexia  is  a  late  symp- 
tom, the  appetite  is  rarely  impaired,  sometimes  it  is  even  increased  ;  great 
debility  and  extreme  anaemia  result  from  the  recurring  hemorrhages.  The 
face  assumes  an  earthy  pallor  ;  when  the  pain  is  intense  it  is  '^  drawn  " 
and  haggard,  which  by  some  is  regarded  as  characteristic  of  ulcer  of  the 
stomach.  Perforation  of  the  stomach  is  attended  by  the  symptoms  of 
rapidly  developed  and  extensive  peritonitis.  Pain  in  the  right  shoulder  is 
a  prominent  symptom  if  an  ulcer  of  the  stomach  involves  the  under  sur- 
face of  the  liver.  If  cicatrization  of  a  gastric  ulcer  takes  place  without 
adhesions  or  stricture  all  the  above  symj)toms  remit  and  complete  recovery 
follows;  if  adhesions  or  stricture  remain  dyspepsia  and  cardialgia  may  con- 
tinue for  the  remainder  of  the  patient's  life.  Obstinate  constipation  is  the 
rule  in  ulcer  of  the  stomach,  but  hemorrhage  may  cause  diarrhoea. 
The  blood  gives  to  the  dejections  a  dark  color  and  a  "tarry"  consist- 
ence, a  condition  called  '^melsena."  The  ovl\j  physical  sign  oi  gdL&tvia 
ulcer  is  extreme  tenderness  on  firm  pressure  over  the  epigastric  and 
dorsal  regions. 

Differential  Diagnosis. — The  diagnosis  in  a  typical  case  of  ulcer  of  the 
stomach  is  not  difficult ;  in  the  more  obscure  cases  it  may  be  mistaken 
for  cancer  of  the  stomach,  hepatic  colic,  the  second  stage  of  cirrhosis, 
cardialgia,  and  chronic  gastric  catarrh  with  hcematemesis.  The  diag- 
nosis of  cancer  of  the  stomach,  hepatic  colic,  and  the  second  stage  of 
cirrhosis  are  considered  under  these  headings  (q.  v.). 

In  neuroses  causing  cardialgia,  there  will  be  a  history  of  neuralgia  in 
other  parts  of  the  body  or  a  well-marked  history  of  hysteria.  The 
pain  of  cardialgia  is  not  excited  or  increased  by  the  introduction  of 
food  into  the  stomach,  but  often  comes  on  when,  the  stomach  is  empty  ; 
while  in  ulcer  the  pain  is  associated  with  ingestion  of  food.  In  cardialgia 
pressure  over  the  epigastrium  and  the  ingestion  of  food  relieve  the 
pain ;  the  reverse  is  the  case  in  ulcer.  Again,  cardialgia  is  relieved  by 
the  constant  current  and  Faradization,  which  increase  rather  than 
relieve  the  pain  of  gastric  ulcer.  Dyspeptic  and  gastric  disturbances 
are  constantly  present  in  ulcer ;  while  these  are  absent  in  the  intervals 
between  the  paroxysms  of  neurotic  cardialgia.  Haematemesis  never  occurs 
in  cardialgia. 

In  chronic  gastritis  with  hemorrhage  there  is  the  history  of  disease 
of  the  liver,  heart,  lungs  or  kidneys ;  while  in  gastric  ulcer  there  is 
usually  no  such  history.  The  pain  in  gastritis  is  not  so  intense  or 
of  the  same  character  as  in  ulcer  of  the  stomach.  A  coated  tongue, 
great  thirst,  malaise,  and  pyrexia  are  prominent  in  cases  of  chronic 
gastritis,  and  absent  in  ulcer.  The  vomiting  in  chronic  gastritis  comes 
on  in  the  morning,  and  the  matter  vomited  is  stringy  mucus,  some- 
times streaked  with  blood  ;  while  in  ulcer  the  attacks  of  vomiting  usually 
follow  the  taking  of  fluids  or  solids,  and  the  blood  is  vomited  in  consider- 
able quantities. 

Prognosis. — More  than  one  half  of  the  cases  of  ulcer  of  the  stomach  re- 
cover.    The  average  duration  cannot   be   determined.     Some   terminate 


ULCER   OF   THE   STOMACH.  251 

fatally  in  a  few  weeks,  otliers  continue  for  a  long  period.  In  the  pro- 
tracted cases,  the  symptoms  are  probably  due  to  the  existence  of  more 
than  one  ulcer.  Most  of  the  cases  that  recover  continue  for  more  than  a 
year.  The  prognosis  is  bad  where  ulcer  occurs  in  the  aged  and  in  feeble 
women. 

The  complications  of  gastric  ulcer  are  chlorosis  and  hysteria ;  thoracic 
complications,  such  as  pneumonia,  bronchitis,  pulmonary  tubercle,  acute 
pleurisy,  and  empyema  ;  abdominal,  such  as  suppurative  pylephlebitis  and 
peritonitis.  Death  occurs  from  hemorrhage  four  times  as  often  in  the 
male  as  in  the  female.  Exhaustion,  either  from  pain  or  from  vomiting 
or  from  starvation,  causes  death  in  5  per  cent,  of  the  cases.  Perforation, 
with  peritonitis  or  without  it,  occurs  in  about  13  per  cent,  of  all  the  cases. 
The  liability  to  perforation  is  greatest  in  the  female  between  the  ages  of 
fifteen  and  thirty ;  while  in  the  male  the  liability  is  greatest  about  the 
fortieth  year.  Cicatrization  of  an  ulcer  at  the  pyloric  extremity  of  the 
stomach  is  usually  followed  by  dilatation  of  the  stomach. 

Treatment. — The  most  important  thing  to  be  accomplished  in  the  treat- 
ment of  gastric  ulcer  is  to  give  rest  to  the  stomach.  To  this  end  the  patient 
must  be  kept  in  led,  and  if  possible  should  be  restricted  to  a  milk  diet. 
From  a  tablespoonful  to  a  teacupful  may  be  given  at  intervals  of  two  hours 
during  the  day  and  night.  When  milk  is  refused,  digested  beef-juice  may 
be  given  in  its  stead  ;  all  vegetables,  tea,  coffee,  starchy  food  and  fruits 
must  be  prohibited.  If  all  kinds  of  food  are  rejected,  rectal  alimentation 
must  be  practised,  four  ounces  of  defibrinized  blood  (containing  four  grains 
of  chloral  to  prevent  its  decomposition)  may  be  thrown  into  the  rectum 
every  six  hours. 

The  remedial  agents  which  have  been  found  most  useful  in  gastric 
"ulcers  are  the  sub-nitrate  of  bismuth,  in  twenty-grain  doses,  four  times 
a  day,  sulphite  of  soda,  oxalate  of  cerium,  and  hydrocyanic  acid. 
Half  a  grain  of  nitrate  of  silver,  three  times  a  day,  seems  to  exert  a  bene- 
ficial effect  on  gastric  ulcers  of  long  standing,  as  well  as  on  the  accompany- 
ing gastric  cntarrh.  Several  observers  claim  that  arsenic  retards  the  spread 
of  gastric  ulcers  ;  my  experience  does  not  confirm  this  observation.  If  the 
pain  is  severe,  and  there  is  no  hemorrhage,  warm  poultices  may  be  applied 
to  the  epigastrium  ;  but  morphia  hypodermically  is  far  more  reliable  for 
the  relief  of  pain,  and  may  be  used  at  regular  intervals  with  benefit.  Hypo- 
dermic injections  of  ergotin,  and  ice-bags  to  the  epigastrium,  will  usually 
check  the  hemorrhages.  The  flatulence,  which  is  often  very  distress- 
ing, may  be  mitigated  by  sulphite  of  soda,  carbolic  acid,  or  the  alka- 
lies. Constipation  when  present  is  relieved  by  ox-gall  enemata,  or  saline 
mineral  waters,  the  latter  being  especially  useful  when  there  are  acid  eruc- 
tations. When  the  patient  will  bear  it,  castor-oil  is  a  safe  and  efficient 
laxative.  Stimulants  must  never  be  given  by  the  stomach.  They  may  be 
given  by  enemata  in  emergencies. 

Eest  in  bed  and  a  restricted  diet  should  be  enforced  for  at  least  three 
months.  Then,  if  the  symptoms  indicate  that  cicatrization  is  well  es- 
tablished, maccaroni,  potatoes,  stale  bread  and  cocoa  may  be  allowed ;  still 


252  DISEASES   OE   THE   DIGESTIYE   SYSTEM. 

later  oysters,  soft  eggs,  and  sago.  The  patient  must  not  return  to  an 
ordinary  mixed  diet  for  at  least  six  months.  The  anaemia  which  follows 
gastric  ulcer  must  be  overcome  by  fresh  air,  moderate  exercise,  iron,  and 
quinine.  It  must  be  remembered  that  the  higher  the  nutrition  is  carried, 
the  more  rapid  and  complete  will  be  the  repair  of  the  ulcer.  This  end 
must  be  had  constantly  in  view  in  the  management  of  these  cases.  The 
establishment  of  nitric  acid  issues,  and  the  employment  of  moxcB  over 
the  abdomen  or  epigastrium,  as  recommended  by  some,  are  of  doubtful 
service,  either  for  the  relief  of  pain,  or  to  hasten  the  healing  of  the  ulcer. 

JSTEUROSES    OF    THE    STOMACH. 

These  are  comparatively  rare  independent  of  a  well-marked  neuralgic 
diathesis.  They  are  known  as  nervous  gastralgia,  or  cardialgia,  and  as 
erytliism  of  the  stomach.     They  have  no  distinct  pathological  lesions. 

Etiology. — Neuroses  of  the  stomach  are  met  with  most  frequently  in 
females,  and  occur  especially  in  those  with  an  hereditary  neurotic  predis- 
position. Exhaustion,  anaemia,  and  chlorosis,  especially  when  accompanied 
by  depressing  influences,  as  grief,  fear,  anxiety,  or  great  intellectual  effort, 
play  a  most  important  part  in  its  etiology.  In  the  same  way  exhaustion 
from  hemorrhage,  insufficient  food,  venereal  excess  and  masturbation  will 
induce  it.  Central  nervous  diseases  and  disease  of  the  pneumogastrics  or 
sympathetic  will  sometimes  cause  it.  The  excessive  use  of  tea  or  coffee  has 
been  cited  as  a  cause,  but  those  cases  where  some  particular  article  of  diet, 
as  milk,  brings  on  attacks  of  pain  in  the  stomach,  are  not  true  neuroses. 
Reflex  irritation  caused  by  painful  affections  of  the  teeth,  ear,  kidneys, 
testicles,  ovaries  and  disturbances  in  the  alimentary  canal,  as  hemorrhoids, 
constipation,  worms  and  hernia,  has  been  regarded  as  a  cause  of  gastralgia. 
Diseases  and  displacement  of  the  uterus,  accompanied  by  disturbance  of  its 
functions,  will  very  frequently  give  rise  to  attacks  of  cardialgia. 

Hysteria  and  hypochondriasis  are  its  two  most  frequent  causes  ;  statistics 
show  that  of  360  cases  of  these  two  diseases  only  30  were  free  from  gas- 
tralgia. Malarial  gastralgia  is  accompanied  by  othei^  forms  of  malarial 
neuralgiae. 

Symptoms. — Gastralgia  usually  begins  with  a  sense  of  distention  and 
tightness  in  the  epigastrium,  followed  by  a  severe  and  agonizing  pain, 
which  will  be  described  differently  by  different  patients.  In  many  in- 
stances the  pain  shoots  through  to  the  back.  During  an  attack  the  abdomen 
is  sometimes  distended  and  rigid,  sometim.es  flattened  and  retracted.  The 
pain  is  often  so  severe  that  the  heart's  action  becomes  irregular,  the  ex- 
tremities cold,  the  face  pinched,  and  there  is  a  tendency  to  syncope  ;  in 
rare  instances  convulsions  occur.  The  pain  is  relieved  by  firm  pressure 
over  the  epigastrium,  by  the  constant  current,  and  by  Faradization  ;  the 
duration  of  these  attacks  is  not  at  all  regular,  sometimes  lasting  only  a  few 
minutes,  at  other  times  an  hour  or  two,  generally  terminating  with  gaseous 
eructations,  or  the  ejection  of  an  acid  or  an  alkaline  fluid.  Sometimes  be- 
fore the  first  attack  there  will  be  complete  anorexia.     Vomiting,  preceded 


HiEMATEMESIS.  253 

by  nausea,  may  be  a  part  of  an  attack,  and,  though  very  severe,  it  does  not 
depress  the  patient.  Between  the  attacks,  which  occur  at  intervals  of  days 
or  weeks,  regularly  or  irregularly,  the  digestive  functions  are  normal. 

Differential  Diagnosis. — Neurotic  cardialgia  may  be  mistaken  for  ulcer  of 
the  stomach,  which  has  already  been  considered. 

Prognosis. — This  depends  upon  the  cause  ;  cardialgia  may  continue  for 
years  and  not  endanger  or  shorten  life. 

Treatment. — In  the  treatment  of  this  affection,  tonics  are  always  indi- 
cated. Iron,  arsenic,  nitrate  of  silver,  and  oxide  of  zinc  maybe  tried  alter- 
nately. For  relief  when  pain  is  intense,  morphia  may  be  given  hypoder- 
matically.  Great  care  must  be  exercised  not  to  repeat  the  hypodermatic  too 
frequently,  for  this  class  of  patients  readily  become  addicted  to  the  use  of 
opium.  Obstinate  and  pi'otracted  cases  sometimes  yield  quickly  to  the 
constant  current  or  to  Faradization. 

HJEMATEMESIS. 

Hasmatemesis,  or  hlood  vomiting,  is  a  symjotom  in  a  variety  of  diseases ; 
it  varies  in  amount  and  frequency  with  the  morbid  conditions  which  in- 
duce it.     Eupture  of  a  blood-vessel  is  one  of  its  essential  conditions. 

Etiology. — I.  Injury  to  the  mucous  tissue  of  the  stomach  by  traumatism 
or  poisons. 

II.  Diseases  of  the  wall  of  the  stomach,  associated  with  diseased  condi- 
tions of  the  blood-vessels. 

III.  Obstruction  to  the  portal  circulation,  as  in  cirrhosis,  acute  yellow 
atrophy,  aneurism  of  the  hepatic  artery  and  tumors  compressing  the  vena 
portae  ;  gastric  hemorrhage  may  remotely  be  produced  by  obstruction  in 
the  portal  tissue,  the  result  of  cardiac  and  pulmonary  diseases  ("nut- 
meg liver  "). 

IV.  Blood  poisoning  may  cause  hfematemesis,  as  scurvy,  yellow,  ty|)hus, 
and  relapsing  fevers,  snake-bites,  and  cholera.  It  also  occurs  in  patients 
with  the  '*  hemorrhagic  diathesis,"  and  in  "  bleeders,"  or  those  affected 
■with  limmophila. 

V.  Cancer  and  ulcer  of  the  stomach  cause  it. 

VI.  Passive  hyperemia,  stoppage  of  menses  in  the  female,  and  the  sud- 
den arrest  of  hemorrhoidal  discharges,  are  supposed  to  cause  ha3matemesis 
by  suddenly  raising  the  blood-pressure  in  the  portal  system. 

VII.  Finally,  this  symptom  appears  nearly  three  times  as  often  in  females 
as  in  males,  and  usually  between  the  ages  of  twenty  and  forty  years. 

Symptoms.— In  hsematemesis,  if  the  hemorrhage  is  profuse,  the  patient 
experiences  a  sense  of  heat  and  distention  in  the  epigastrium,  with  nausea 
and  vomiting  ;  he  becomes  pallid,  and  the  surface  cold  and  clammy,  as 
the  blood  rushes  up  in  a  full  stream  through  the  mouth  and  nose,  or  is 
thrown  up  by  successive  acts  of  vomiting.  When  the  blood  comes  up  with 
a  sudden  gush,  some  portion  of  it  may  enter  the  larynx  and  excite  cough- 
ing, and  then  it  may  appear  to  be  coughed  up.  The  appearance  of  the 
blood  differs  according  to  the  length  of  time  it  has  been  acted  upon  by 


254  DISEASES    OF   THE    DIGESTIVE    SYSTEM. 

the  gastric  jaice.  If  it  is  vomited  in  large  quantities  immediately  after  the 
bleeding  has  occurred,  it  will  be  partly  fluid  and  partly  coagulated  ;  but 
if  it  has  been  retained  in  the  stomach  for  a  considerable  time,  it  will  be 
fluid  and  have  a  black,  or  brownish-black  appearance,  with  an  acid  reac- 
tion. 

Differential  Diagnosis. — Hsematemesis  may  be  confounded  with  hcBmopty- 
5i5  or  "blood-spitting." 

Hcemoptysis  is  preceded  by  bronchial  or  pulmonary  symptoms,  and 
hsematemesis  by  gastric  symptoms.  Haemoptysis  is  preceded  or  accom- 
panied by  a  sense  of  constriction  across  the  chest,  by  dyspnoea  and  cough ; 
while  before  hsematemesis,  there  is  nausea,  with  oppression  and  distention 
felt  in  the  epigastrium.  If  cough  is  associated,  it  follows  the  expulsion 
of  blood.  Blood  is  coughed  up  in  mouthfuls,  bright  red,  frothy,  alkaline 
and  mingled  with  sputa  in  haemoptysis  ;  while  it  is  vomited  more  or  less 
profusely,  is  dark  colored,  mixed  with  food,  coagulated,  and  often  acid  in 
hsematemesis.  In  haemoptysis  there  is  a  sense  of  "  trickling  "  behind  the 
sternum,  and  for  a  few  days  after  the  hemorrhage,  small  blood-spittings ; 
and  a  physical  examination  of  the  chest  readily  determines  the  origin  of 
the  hemorrhage  and  establishes  a  diagnosis. 

Prognosis. — Haematemesis,  though  a  grave  symptom,  does  not  often 
directly  cause  death  ;  the  prognosis  is  determined  by  the  diseased  condi- 
tions with  which  it  occurs.  Hsematemesis  from  cirrhosis  of  the  liver  or 
ulcers  is  always  more  dangerous  than  from  any  other  conditions. 

Treatment. — During  the  hemorrhage  the  patient  must  be  kept  absolutely 
quiet,  in  a  horizontal  position.  Ice  should  be  taken  freely,  and  ice-bags 
applied  to  the  epigastrium.  Morphine  and  ergotin  may  be  hypodermically 
administered,  and  the  patient  sustained  by  rectal  alimentation.  Astrin- 
gents given  by  the  stomach  usually  do  more  harm  than  good,  and  should 
not  be  employed.  In  severe  cases  the  head  must  be  kept  low  and  brandy 
may  be  given  by  the  rectum.  If  there  is  evidence  of  heart-failure,  brandy 
and  digitaline  may  be  given  hypodermically.  After  the  hemorrhage  ceases 
great  care  must  be  exercised  in  the  diet  of  the  patient ;  milk  is  the  only 
nutritive  article  that  should  be  allowed  for  the  first  week.  The  conditions 
which  cause  the  hemorrhage  must  receive  their  appropriate  treatment. 

DILATATION    OF    THE    STOMACH. 

Morbid  Anatomy. — A  dilated  stomach  is  much  larger  than  normal ;  in 
one  instance  it  was  found  capable  of  containing  ninety  pounds  of  fluid  ;  it 
may  be  either  uniformly  dilated,  or  there  may  be  dilated,  circumscribed 
pouches  corresponding  to  ulceration  or  erosion  of  its  walls.  When  stenosis 
at  the  pylorus  exists,  the  walls  of  the  stomach  are  first  hypertrophied,  and 
then  a  muscular  paralysis  is  followed  by  atrophy,  thinning  of  its  walls, 
and  dilatation  of  its  cavity,  which  is  usually  to  the  left  and  upwards. 
The  muscular  coat  may  be  so  stretched  and  thinned  as  sometimes  to  be 
scarcely  traceable  ;  this  is  more  frequently  the  case  when  the  dilatation  is 
independent  of  stenosis.     In  some  few  instances  fatty  degeneration  of  the 


DILATATION"    OF   THE   STOMACH.  255 

muscular  coat  has  been  found,  and  with  it  the  rugse  of  the  mucous  coat 
have  disappeared,  and  the  mucous  membrane  has  become  j)ale  and  thin. 

Etiology. — Dilatation  results^rs^ 
from  pyloric  stenosis,  and  this  may  .      ^ 

be    caused  by   cancerous  or  non-  \      \-- — ^""""^^v 

malignant  ulceration,  by  the  effects  j  \  \ 

of   corrosire    poisons    (acute    gas-    y — ^-^c        ^  \  \ 

tritis),  by  thickening  from  chronic         j^^^N^— k-^Vj  1  t,     \ 

and    phlegmonous    gastritis,    and       '\\  j  1 

from    fibroid    indurations   of    the  \^  .       y 

pylorus.       Whether   spasm    of  the  ^"v^  \^r  y 

pylorus  is  sufficient  to  cause  dila-  ^^-,  ■     ""^  ^--'' 

tatiou  or  not,  is  as  yet  undecided.  "     ~ ■"' 

Secondly,  dilatation  of  the  stomach  '^'^'  ^^' 

,  T,         7    ,  ,.  „  ji  Diagram  Illustrating  Dilatation  of  the  stomach. 

may  becaused  by  oc»,sfrz<cno?i  01  the   ,   ^    , 

•^  ■'  T     I         1       -^-  (^I'd'^i'  curvature. 

pylorus  by  tumors  external    to    the  -B.  Lesser  curvature. 
■^  ~  -      •'  -        ^  C.  Pylorus,  the  dotted  line  indicates  the  point  of  sten- 

stomach  and  duodenum,  as  cancer  osis. 

»  ,  1       T  n   1  1     T  1  D.  Lineshmvinq  the  usual  direction  of  the  dilatation,  to 

of  the  liver,  pancreas,  gall-bladder,  the  le/t  and  upward. 

and  lymphatics  of  the  lesser  omen- 
tum. Thirdly,  paralysis  and  consequent  impaired  peristalsis  will  cause 
dilatation  of  the  stomach.  It  may  be  the  result  of  parenchymatous  degen- 
eration occurring  in  fevers  and  severe  constitutional  diseases.  Suppurations 
about  the  stomach,  as  empyema  and  purulent  pericarditis,  may  induce 
dilatation  by  diminishing  its  nerve  supply.  Fourthly,  habitual  over-disten- 
tion  of  the  stomach  results  from  drinking  inordinately  and  eating  im- 
moderately, especially  of  food  which  will  ferment,  and  by  accumulated  gases, 
which  still  more  distend  an  overloaded  stomach.  Fifthly,  hernia,  by 
dragging  down  the  stomach,  and  fibrous  bands  binding  it  to  other  organs, 
may  lead  to  dilatation. 

Symptoms. — Dilatation  of  the  stomach  may  be  acute  or  chronic.  Acute 
dilatation  usually  occurs  after  exhausting  diseases,  though  in  some  instances 
there  is  no  discoverable  cause.  It  begins  with  sharp  pain  in  the  epigastric 
region,  with  tympanitic  distention  and  sometimes  with  tenderness  on  press- 
ure. These  symptoms  rapidly  subside,  and  the  subsequent  dilatation  is 
revealed  by  a  physical  examination  of  the  abdomen. 

In  chronic  or  slow  dilatation,  vomiting  is  the  first  important  symptom. 
This  sometimes  occurs  only  after  eating,  but  usually  every  two  or  three 
days  there  is  ejected  the  accumulation  of  a  portion  of  the  previous 
day's  food  :  the  quantity  vomited  varies  in  amount  from  one  to  three  gal- 
lons, and  has  a  fetid  odor,  a  black,  ''yeasty"  aiDpearance,  and  an  intensely 
acid  reaction.  On  a  microscopic  examination  of  the  matter  vomited,  sar- 
cinse  and  torulse  are  found  in  abundance.  The  eructations  are  offensive, 
consisting  of  sulphuretted  and  phosphuretted  hydrogen,  the  results  of  the 
fermentation  and  putrefaction  accompanying  this  condition  ;  pyrosis  is  a 
very  annoying  and  often  painful  symptom.  There  is  progressive  emacia- 
tion, with  pain,  a  sense  of  weight,  and  distention  in  the  epigastrium. 
Muscular  cram])  in  the  calves  of  the  legs  is  often  a  painful  attendant. 


356  DISEASES    OF   THE    DIGESTIVE    SYSTEM. 

The  pulse  is  compressible  ;  the  appetite  remains  good,  often  amounting  to 
*'  iulimia."  In  some  cases  where  there  is  complete  paresis,  there  is  no 
vomiting,  but  rapid  emaciation,  and  anorexia  from  the  commencement. 
The  howels  are  constipated  and  the  fsecal  discharges  hard  and  dry. 

Physical  ^i'gias,—Inspectio7i  reveals  a  prominent  rounding  just  above  the 
umbilical  region.  In  some  cases  there  is  a  peculiar  depression  just  at  the 
epigastrium.  When  the  patient  takes  an  effervescing  draught  the  stomach 
is  visibly  enlarged  and  the  epigastrium  becomes  prominent. 

PaJjjation  shows  slight  resistance  at,  or  below,  the  epigastrium,  the  walls 
of  the  stomach  being  tense  and  elastic  ;  sometimes  the  motions  of  the 
stomach  and  a  prominence  at  the  pylorus  can  be  detected. 

Percussion, — If  the  stomach  is  empty,  percussion  reveals  an  increased 
tympanitic  area,  by  which  the  position  and  shape  of  the  stomach  can  be 
quite  accurately  mapped  out ;  or,  on  filling  the  stomach  with  fluid,  an  ab- 
normal area  of  dulness  indicates  the  enlarged  stomach  area. 

On  auscultation,  a  splash  or  "  succussio7i  sound  "  is  heard  on  shaking 
the  patient ;  and  when  fluid  is  swallowed,  it  can  be  heard  dropping  into 
the  enlarged  cavity. 

DiiFerential  Diagnosis. — This  condition  may  be  mistaken  for  ascites,  dis- 
tended uri7iary  Madder,  or  for  hydatids  of  the  liver,  hi  ascites  the  fluid 
distends  the  lower  and  not  the  upper  portion  of  the  abdomen  ;  the  area  of 
the  abdomen  broadens  and  flattens  when  the  patient  assumes  the  supine 
posture,  and  there  is  fluctuation  on  palpation. 

An  hydatid  tumor  does  not  change  its  shape  or  position  when  fluids 
are  taken  into  the  stomach  ;  it  is  fixed  in  its  position  and  it  is  not  accom- 
panied by  gastric  symptoms. 

Prognosis. — The  prognosis  is  determined  by  the  conditions  which  cause 
the  dilatation.     In  all  cases  it  is  incurable. 

Treatment. — The  most  important  thing  to  be  remembered  in  the  treat- 
ment of  this  affection  is,  to  adapt  the  diet  to  the  condition  of  the  patient ; 
food  must  be  taken  in  small  quantities ;  as  small  a  quantity  of  fluid  as 
possible  should  be  allowed.  When  the  stomach  is  overloaded,  its  contents 
may  be  withdrawn  by  the  stomach-pump,  and  thoroughly  washed  out 
with  warm  water.  The  daily  use  of  the  siphon  in  washing  out  the  viscus 
in  these  cases  has  not  proved  to  be  as  useful  a  therapeutic  measure  as  was 
claimed  for  it  when  it  was  first  employed.  To  overcome  the  paresis  of 
the  muscular  coat  strychnine  has  been  very  extensively  employed.  Benefit 
may  be  obtained  in  some  cases  by  the  use  of  galvanism.  To  prevent 
fermentation,  the  sulphites  or  carbolic  acid  may  be  used.  All  saccharine 
and  starchy  foods  must  be  abstained  from,  and  a  diet  suited  to  each  case 
must  be  persisted  in. 


ENTERITIS   OR   i:S^TESTIlirAL   CATARRH. 


257 


DISEASES  OF  THE  INTESTINES. 

I  shall  consider  Intestinal  Diseases  under  the  following  heads  : — 
I.  Enteritis  or  Intestinal  Catarrh.     IX.  Intestinal  Obstruction. 


II.  Diarrlicea. 

III.  Cholera  Morbus. 

IV.  Cholera  Infantum. 
Y.  Dysentery. 

VI.   Typhlitis  and  Perityphlitis. 
VII.  Intestinal  Ulcers. 
VIII.  Intestinal  Hemorrhage. 


X. 


Waxy  Degeneration   of  the- 

Intestine. 
Cancer  of  the  Intestine. 
XII.  Rectitis  or  Proctitis. 
XIII.  Ditestinal  Parasites. 
Intestinal  Colic. 
Constipation. 


XI. 


XIV. 
XV. 


EITTERITIS    OR   ESTTESTINAL    CATARRH. 

Enteritis  is  a  general  term  applied  to  a  catarrhal  inflammation  of  the  in- 
testinal mucous  membrane.  It  may  be  acute  or  chronic,  circumscribed  or 
diifused.  The  name  "  muco-enteritis "  has  been  applied  to  it,  when  the 
mucous  coat  of  the  intestine  only  is  involved  ;  when  the  inflammation  in- 
volves the  muscular  and  peritoneal  coats,  it  is  termed  ''phlegmonous  en- 
teritis." When  situated  in  the  colo7i,  it  has  been  called  "inflammatory 
diarrhoea. " 

Morbid  Anatomy. — At  its  onset  acute  enteritis  is  characterized  by  conges- 
tion, tumefaction  and  dryness  of  the  mucous  surface  of  the  intestines  ;  this 
is  soon  followed  by  an  abundant  secretion  of  mucus  and  pus,  which  covers 
the  inflamed  surface.  Peyer's  patches  and  the  solitary  glands  are  congested 
and  swollen,  and  stand  out  over  the  inflamed 
surface,  causing  it  to  present  an  appearance 
as  if  it  were  sprinkled  with  sand.  After  a 
time,  a  thin  serous  fluid  is  copiously  exuded 
into  the  intestinal  canal.  This  inflamma- 
tory exudation,  with  the  active  peristalsis, 
causes  liquid  discharges  from  the  bowels. 
The  layer  of  mucus  and  pus  which  covers 
the  mucous  membrane  is  either  loosely 
attached  or  firmly  adherent ;  in  the  latter 
case  it  resembles  in  appearance  a  diph- 
theritic exudation ;  when  portions  of  the 
mnco-j^urulent  layer  are  removed,  the  mu- 
cous surface  underneath  is  found  eroded. 
This  is  the  severest  form  of  muco-enteritis. 

Simple  or  erythematous  intestinal  catarrh 

begins  in  the  small  intestine,   and  may  rap- Acute  Enteritis,.     Smalllntestine,  near  mid- 
°  .  .  "^  die  of  Ileum,  showing  iiyperoemia. 

idly  spread  over  the  entire  alimentary  tract.  ^^  ^  ^^^^^^^^^^^^  ^^^.^^^^,,^^  ^^^^^^^ 

The  membranous  variety  is  usually  confined  b,  b.  Congestea  Peyefs  paiches,  presenting 

•'  -l  .  the     shaven  beard "  appeai'ance. 

to  the  ]avgeintesttne  and  rectum,  the  portion 

near  the  ileo-coecal  valve  being  most  extensively  implicated.    In  severe  cases 
17 


Fig.  57. 


258 


DISEASES   OF   THE   DIGESTIVE   SYSTEM. 


Fig.  58. 


the  mucous  membrane  is  often  dotted  with  ecchj'motic  spots.  These  changes 
in  the  intestinal  mucous  membrane  are  not  infrequently  accompanied  by- 
changes  in  its  lymphatic  structures.  The  lymph  follicles  become  greatly 
enlarged,  and  are  surrounded  by  an  inflammatory  areola.  Their  contents 
soften,  undergo  necrosis,  and  a  small,  round,  funnel-shaped  ulcer  is  formed, 
called  a"  follicular  ulcer."     This  ulcerative  process  may  extend  beyond  the 

follicles  and  involve  the  submucous  and 
muscular  tissues.  A  dull  pink  floccu- 
lent  substance,  of  a  "porridge-like" 
consistence,  is  often  found  in  the  intes- 
tine at  the  seat  of  numerous  follicular 
ulcers.  In  nearly  every  case  of  acute 
intestinal  catarrh,  the  mesenteric  glands 
are  congested. 

In  2)lilegmO'nous  enteritis  all  the  coats 
of  the  intestine  are  involved.  It  is  usually 
limited  to  a  small  portion  of  the  intestine, 
varying  in  length  from  two  or  three 
inches  to  one  or  two  feet.  The  affected 
portion  is  excessively  dilated ;  the  mu- 
cous and  submucous  tissues  correspond- 
ing to  its  seat  are  thickened,  softened 
,    ,  ^  ,,.    ,    ^  ,   . .    ^  „  ,     ,  .,  and  congested,  and  are  either  of  a  dark 

Acute  Follicular  Enteritis.  Transverse  Colon  laid  ®  ' 

open,  showing  enlarged  follicles,  which  have    color  from  blood   CxtravasatlOUS,   Or  pale 
ulcerated  at  their  apices.  •  t       ,  •     r- 1 1       i  ■  mi  i 

irom  purulent  mfaltration.  The  muscular 
coat  is  thick,  soft  and  cedematous.  Upon  the  peritoneal  coat  are  irregular 
patches  of  submucous  extravasations,  and  the  free  peritoneal  surface  is 
covered  with  a  thin  plastic  exudation.  The  intestine  below  the  seat  of  the 
phlegmonous  inflammation  is  contracted,  empty,  and  its  mucous  membrane 
healthy,  while  above,  its  seat  the  intestine  is  dilated  and  filled  with  faecal 
matter,  its  mucous  membrane  remaining  normal ;  sometimes  at  the  seat  of 
the  inflammation  numerous  ulcers  appear,  extending  in  rings  transversely 
about  the  intestine.   It  may  be  confined  to  the  cgecum  and  ascending  colon. 

In  chronic  intestinal  catarrh  the  mucous  membrane  has  a  slaty,  blue  or  gray 
color  ;  sometimes  black  pigment  deposits  are  found  in  the  villi,  and  between 
the  follicles,  '(.''he  membrane  is  thicker  than  normal,  and,  as  a  result,  the 
peristaltic  motion  of  the  intestine  is  impeded.  Hyperplasia  of  the  connective- 
tissue  immediately  beneath  the  epithelium,  and  perhaps  of  the  solitary 
and  agminated  glands,  occurs.  The  epithelium  itself,  in  most  cases,  un- 
dergoes fatty  or  granular  degeneration.  The  lymphatics  are  enlarged,  and 
project  from  the  mucous  surface,  as  numerous  distinct  white  nodules,  cov- 
ered with  viscid  gray  mucus,  which  is  sometimes  purulent.  The  veins  un- 
derneath the  mucous  membrane  are  enlarged  and  tortuous.  If  acute  intes- 
tinal catarrh  passes  into  chronic,  the  intestinal  coats  become  thinned  and 
pale,  or  hypertrophied,  causing  stricture  of  the  intestinal  canal ;  such  ste- 
nosis occurs  most  frequently  at  the  sigmoid  flexure  and  in  the  rectum. 

Follicular  ulcerations  occur  more  frequently  in  chronic  than  in  acute 


ENTERITIS   Oil   INTESTIN"AL   CATARRH.  259 

intestinal  catarrh.  .  In  prolonged  cases,  there  may  he  developed  polypoid 
cysts  ;  similar  changes  in  the  stomach  may  accompany  intestinal  catarrh. 
Acute  and  chronic  catarrh  of  the  duodenum  are  attended  by  changes  similar 
to  those  which  take  place  in  other  portions  of  the  tract ;  but  in  duodenal 
catarrh,  the  secondary  catarrh  of  the  ductus  communis,  by  obstructing  its 
opening  into  the  duodenum,  leads  to  catarrh  of  the  hepatic  ducts. 

Etiology. — Intestinal  catarrh  is  ordinarily  caused  by  direct  irritation  of 
the  mucous  membrane  by  improper  food,  impure  water,  or  irritating  med- 
icines, or  by  exposure  to  wet  or  cold.  Extensive  burns  will  also  cause  it. 
Certain  atmospheric  conditions  produce  it  in  children  during  dentition, 
or  during  convalescence  from  one  of  the  exanthemata. 

Chronic  intestinal  catarrh  is  often  a  complication  of  chronic  malarial  in- 
fection and  chronic  Bright's  disease.  It  may  also  be  an  accompaniment  of 
hernia.  Obstructed  venous  return,  from  hepatic,  cardiac  or  pulmonary  dis- 
ease, as  cirrhosis  of  the  liver,  chronic  valvular  lesions,  and  pulmonary  em- 
physema, is  a  predisposing  cause.  It  occurs  at  all  ages  ;  one-third  of  the 
diseases  of  children  have  intestinal  catarrh  as  their  primary  or  principal 
lesion.  Its  two  great  predisposing  causes  in  children  are  dentition  and  bad 
hygiene,  especially  during  the  hot  months,  Avhen  there  are  the  greatest  vari- 
ations of  temperature.     It  may  be  epidemic  or  endemic. 

The  membranous  and  phlegmonous  varieties  occur  as  complications  of 
the  exanthemata,  pyaemia,  septicaemia,  puerperal  fever,  and,  in  rare  in- 
stances, acute  tuberculosis,  and  acute  Bright's  disease. 

Symptoms. — As  the  symptoms  of  acute  enteritis  vary  with  the  portion 
of  intestine  involved,  as  well  as  with  its  severity,  the  symptoms  will  be 
considered  without  attempting  a  history  of  its  course. 

Diarrhoea  is  its  earliest  and  most  constant  symptom.  It  is  called  mucous, 
bilious,  or  serous,  according  to  the  varying  character  of  the  discharges.  In 
mucous  diarrhoea  watery  mucus  is  mixed  with  ordinary  faeces.  In  cases 
where  the  stools  consist  almost  exclusively  of  mucus,  rectitis  and  '^colitis" 
may  be  suspected.  In  colitis,  cylindrical  casts  of  varymg  lengths  and  pus 
are  often  present  in  the  discharges.  In  the  so-called  bilious  diarrhoea,  pain 
and  cramps  in  the  calves  of  the  legs  are  not  infrequent.  There  is  vomiting, 
headache,  sallowness  of  the  surface,  furred  tongue,  weight  and  fulness  in 
the  right  hypochondrium,  and  more  or  less  prostration.  The  color  of  the 
stools  is  more  distinctly  green  than  in  any  other  variety.  Serous  diarrhoea 
is  the  most  common,  and  when  the  unqualified  word  diarrhoea  is  employed 
this  form  is  indicated.  At  first  the  dejections  contain  undigested  food  ; 
after  twenty-four  or  forty-eight  hours  the  faecal  odor  of  the  discharges  is 
lost.  At  the  onset  of  duodenitis,  jejunitis,  or  ileitis,  diarrhoea  may  be 
absent  if  the  large  intestine  is  not  simultaneously  involved.  Diarrhoea  may 
occur  independent  of  intestinal  catarrh. 

Pain  is  another  symptom  which,  although  not  always  present,  is  so  con- 
stant that  its  absence  is  the  exception  to  the  rule  ;  sometimes  it  is  colicky 
and  griping  in  character,  at  others  it  is  severe  and  paroxysmal,  or  dull  and 
unremitting.  In  all  cases  it  is  rendered  more  severe  by  the  ingestion  of 
food.     With  the  pain,  there  is  a  sense  of  fulness  and  distention  of  the 


260  DISEASES    or    THE    DIGESTIVE   SYSTEM. 

abdomen,  and  tenderness  on  firm  pressure  ;  yet  moderate  pressure  sometimes 
relieves  the  pain.  In  local  intestinal  catarrh  the  pain  is  confined  to  the 
portion  of  the  intestine  involved. 

Flatulence,  gurgling,  and  tympanitic  distention  of  the  abdomen  are 
usually  present,  and  offensive  borborygmi  occur  with  the  passages  and  with 
eructations  which  may  give  a  sense  of  relief.  When  gurgling  or  borborygmi 
are  prominent  the  small  intestine  alone  is  involved.  When  the  passages 
contain  unchanged  ingesta,  the  large  intestine  is  usually  the  seat  of  the 
catarrh.  Nausea  and  vomiting  indicate  that  gastric  catarrh  is  associated 
with  the  intestinal,  the  combination  being  called  gastro-enteritis .  If 
severe  intestinal  catarrh  has  continued  for  a  long  time,  there  may  be 
nausea,  but  rarely  vomiting. 

The  local  symptoms  of  enteritis  are  usually  preceded  and  accompanied 
by  a  mild  remittent  type  of  fever.  The  skin  is  dry  when  the  temperature 
is  much  elevated,  and  sweating  often  occurs  at  night.  The  change  in  the 
pulse  corresponds  to  the  elevation  of  temperature.  Headache,  thirst  and 
loss  of  appetite  accompany  the  fever,  and  are  more  marked  the  nearer  the 
inflammation  is  to  the  stomach  ;  in  one  case  there  may  be  great  restlessness, 
m  another  extreme  lassitude  and  prostration.  The  tongue  is  usually  dry 
and  heavily  coated;  in  children  it  is  often  glazed  and  ''beefy;"  in 
either  case  the  breath  is  offensive.  The  urine  is  scanty  and  dark,  almost 
black  in  the  bilious  variety. 

When  it  occurs  in  children,  it  has  been  called  gastric  or  ''infantile 
remittent  fever ; "  in  the  evening  the  temperature  may  rise  to  101° 
or  104°  F.,  and  be  normal  the  next  morning.  The  diarrhoea  is  severe 
in  this  class  of  cases,  and  the  abdomen  is  usually  very  much  dis- 
tended. There  is  great  restlessness,  thirst  is  excessive,  and  the  little  pa- 
tients are  constantly  calling  for  cooling  drinks.  The  features  become 
pinched,  the  lips  pale  and  drawn,  and  the  eyes  deeply  sunken.  Yom- 
iting  is  frequent  and  is  "  retching  "  in  character.  The  papillse  of  the  tongue 
are  elevated  and  covered  with  a  yellowish  coating  ;  all  the  other  symp- 
toms of  acute  enteritis  attend  it. 

Duodenitis  rarely  occurs  independently  of  gastric  catarrh,  in  fact  "  gas- 
tro-duodenal  catarrh  "  is  much  more  common  than  simple  duodenitis. 
The  prominent  symptom  of  duodenitis,  independent  of  the  symptoms  of  the 
accompanying  gastric  catarrh,  is  jaundice,  which  results  from  the  secondary 
inflammation  of  the  ductus  communis,  causing  obstruction  to  the  passage 
of  the  bile  into  the  duodenum.  A  very  acute  duodenitis  is  liable  to  com- 
plicate extensive  burns  of  the  surface  ;  in  obscure  cases  the  urine  should 
be  analyzed  for  bile  pigment,  which  may  be  found  before  the  Jaundiced  hue 
of  the  skin  is  apparent.  Some  regard  dyspeptic  symptoms  coming  on  three 
or  four  hours  after  meals  as  indicative  of  duodenal  catarrh,  but  this  symp- 
tom is  only  valuable  in  connection  with  the  others. 

Membranous  enteritis  has  few  distinctive  symptoms,  all  the  symptoms 
of  acute  simple  catarrh  are  much  exaggerated.  The  stools  often  contain 
bloody  mucus  and  pus.  If  shreds  of  false  membrane,  or  cylindrical 
casts  of  segments  of  the  lower  bowel,  are  voided  in  the  diarrhoeal  dis- 


EKTERITIS   OE   INTESTINAL   CATARRH.  261 

charges,  the  diagnosis  is  readily  made,  but  without  these  it  cannot  be 
recognized. 

Phlegmonous  enteritis  is  a  very  grave  disease.  Pain  and  tormina  are  in- 
tense and  come  on  in  paroxysms.  The  abdomen  is  distended,  tympanitic, 
and  extremely  tender,  and  the  position  of  the  patient  is  similar  to  that  as- 
sumed in  peritonitis.  Vomiting  is  frequent,  and  severe;  late  in  the  dis- 
ease it  becomes  fetid  and  even  faecal,  although  in  some  cases  there  is  a  mere 
regurgitation.  The  temperature  rises  to  103°  or  105°  F.,  the  pulse  keeps 
pace  with  the  temperature,  and  is  small  and  compressible.  During  a  par- 
oxysm of  severe  pain,  the  otherwise  dry  skin  becomes  covered  with  a  pro- 
fuse perspiration,  and  the  distended  intestine  may  rupture  and  gas  escape 
into  the  peritoneal  cavity.  Constipation  generally  attends  these  cases,  and 
the  appearance  of  diarrhoea  generally  indicates  the  commencement  of  con- 
valescence, during  which  the  weakness  increases  for  a  time.  With  this 
convalescing  diarrhoea  the  tongue  is  red,  dry  and  glazed.  But  if  a  fatal 
termination  is  to  be  reached,  the  face  becomes  shrivelled,  prostration  be- 
comes extreme,  distressing  hiccough  occurs,  the  extremities  become  cold, 
and  collapse  closes  the  scene,  the  mind  remaining  clear  to  the  last.  The 
urine  is  very  scanty,  and  frequently  suppressed,  a  precursor  of  a  fatal 
termination. 

In  chronic  enteritis  casts  of  mucus,  already  described,  are  passed  with 
the  stools,  and  are  sometimes  thought  by  the  patient  to  be  the  mucous 
membrane  of  the  intestine  or  a  large  intestinal  worm.  If  the  disease  is 
long  continued  there  is  progressive  emaciation,  until  the  wasting  is  greater 
than  in  any  other  disease.  The  skin  has  a  pale  or  dirty  muddy  hue,  and 
the  accompanying  hypochondria  may  lead  to  a  condition  of  melancholia. 
The  tenacious  layer  of  mucus  which  coats  the  intestine  acts  in  the  same 
way  as  in  chronic  gastritis,  the  contents  of  the  intestine  undergo  decompo- 
sition, and  gases  are  set  free  which  distend  the  abdomen,  interfere  with  res- 
piration, and  secondarily  induce  a  passive  hypersemia  in  other  organs.  The 
passage  of  this  flatus,  and  an  occasional  diarrhoeal  attack  afford  great 
relief  to  the  patient.  Chronic  enteritis  in  children  is  marked  by  a  diar- 
rhoea which,  though  at  first  mucous  in  character,  soon  becomes  serous 
and  afterward  dysenteric.  The  mouth  shows  evidences  of  '^thrush," 
and  emaciation  is  steadily  progressive. 

Differential  Diagnosis. — Acute  intestinal  catarrh  may  be  mistaken  for 
dysentery,  hernia,  acute  and  chronic  poisoning,  peritonitis,  or  for  typhoid 
fever.  The  diagnosis  between  intestinal  catarrh  and  dysentery  will  be 
considered  under  the  head  of  dysentery. 

In  hernia,  the  sudden  onset  of  the  symptoms  with  a  history  of  previous 
good  health,  the  localized  pain,  constipation,  vomiting  often  following 
some  sudden  exertion  or  extreme  muscular  effort,  and  the  existence  of  a 
hernial  tumor   establish  the  diagnosis. 

Acute  poisoning  from  certain  articles  of  diet  (as  eating  toadstools  for 
mushrooms)  can  often  only  be  differentiated  in  the  first  twenty-four  hours 
by  the  history  of  the  case.  Poisoning  from  arsenic  or  any  other  chemical 
irritant  causes  severer  gastric  symptoms  than  are  ever  present  in  intestinal 


262  DISEASES    OF   THE   DIGESTIVE   SYSTEM, 

catarrh.  The  vomiting  in  arsenical  poisoning  is  never  stercoraceous,  while 
phlegmonous  enteritis  of  the  same  severity  is  usually  attended  by  stercora- 
ceous vomiting.  A  chemical  analysis  of  the  ejected  matters  will  establish 
the  diagnosis. 

Peritonitis  comes  on  rapidly,  and  at  its  onset  the  abdomen  becomes  ex- 
ceedingly tympanitic  and  tender  to  pressure,  while  the  advent  of  enteritis 
is  comparatively  slow,  and  excessive  tympanitis  is  very  rare.  Vomiting 
rarely  occurs  in  peritonitis  until  the  peritoneum  over  the  stomach  is  in- 
volved, and  then  it  is  *' spinach-green  ;"  in  enteritis  so  severe  as  to  be 
confounded  with  peritonitis,  vomiting  would  be  an  early  symptom  and 
would  not  have  a  spinach-green  character.  There  is  constipation  in  peri- 
tonitis, while  diarrhoea  is  the  rule  in  enteritis.  The  pulse  is  tense  and 
wiry  in  peritonitis,  rapid  and  feeble  in  enteritis.  The  temperature  is 
usually  higher  in  enteritis  than  in  peritonitis.  As  peritonitis  becomes 
general,  there  are  symptoms  of  collapse,  and  the  anxious  face,  thoracic  respi- 
ration, the  immobility  and  the  position  of  the  patient  are  all  characteristic. 

Enteritis,  particularly  gastro-enteritis,  is  sometimes  mistaken  for  typhoid 
fever,  but  in  typhoid  fever  nausea,  vomiting,  and  diarrhoea  follow  the  fe- 
brile movement,  whereas  they  precede  it  in  gastro-enteritis.  The  tempera- 
ture rarely  rises  to  103°  F.  in  gastro-enteritis,  while  it  may  reach  104° 
or  105°  in  typhoid  fever.  The  typical  range  of  temperature  during  the 
first  week  of  typhoid  fever  is  characteristic,  and  is  never  met  with  in 
gastro-enteritis.  In  children  the  diagnosis  is  difficult  without  a  complete 
therm ometrical  record. 

Prognosis. — The  prognosis  in  simple  intestinal  catarrh  is  generally  good, 
particularly  in  children  during  dentition.  The  prognosis  in  membranous 
or  pJilegmonous  enteritis  is  always  bad,  especially  when  it  occurs  with 
pyaemia,  or  Bright's  disease.  The  duration  in  mild  acute  intestinal 
catarrh  is  ordinarily  from  three  to  five  days.  Chronic  intestinal  catarrh 
will  persist  as  long  as  the  cause  which  produces  it  is  in  operation. 
The  signs  which  indicate  recovery  are  subsidence  of  pain,  the  appear- 
ance of  normal  fgecal  discharges,  the  clearing  of  the  tongue,  and  a  hope- 
ful countenance.  But  when  emaciation  is  progressive,  the  pulse  irreg- 
ular, or  continuously  rapid,  constipation  alternating  with  a  serous 
diarrhoea,  and  profuse  sweatings  occurring  at  night  the  prognosis  is 
unfavorable.  Death  may  result  from  exhaustion,  peritonitis,  or  from  some 
of  the  more  serious  complications. 

Treatment. — First,  compel  the  patient  to  remain  in  bed  until  all  active 
symptoms  subside.  If  there  is  reason  to  believe  that  irritating  sub- 
stances in  the  intestine  excite  and  keep  up  the  catarrh,  give  a  dose  of 
castor-oil  or  calomel.  It  is  safe  to  begin  the  treatment  in  every  case  of 
acute  intestinal  catarrh  by  the  administration  of  castor-oil.  The  diet 
should  consist  of  skimmed  milk,  or  milk  with  lime-water,  prepared 
meats,  and  light  broths  containing  but  little  starchy  matter.  The  yolk  of 
eggs  may  be  given  with  the  milk.  No  fats  should  be  allowed,  or  bread  or 
any  form  of  starchy  food.  Young  infants  should  be  immediately  placed 
on   a   healthy  wet-nurse.     When  prostration  is  marked  stimulants  may  be 


DIARKHCEA,  2P)3 

carefully  administered.  The  abdomen  should  he  covered  with  flannel/and 
if  pain  is  excessive  warm  fomentations  of  belladonna  or  opium  may  be 
employed.  Opium  is  the  most  efficient  agent  in  the  treatment  of  all 
varieties.  It  must  be  given  in  sufficient  doses  to  secure  rest  to  the  intes- 
tine, and  to  relieve  the  pain,  half  a  grain  every  two  or  three  hours  is 
usually  sufficient  for  an  adult ;  its  use  must  be  continued  until  the  diar- 
rhoea ceases. 

Reditis  is  the  only  variety  where  astringents  may  be  used.  Here  an 
anodyne  and  astringent  plan  may  be  combined,  the  best  results  having 
been  obtained  by  enemata.  When  the  catarrh  is  of  malarial  origin, 
quinine  must  be  given  in  large  doses.  If  it  has  been  the  result 
of  exposure  to  wet  and  cold  diaphoretics  are  indicated.  In  an  intense 
form  of  enteritis  three  or  four  leeches  may  be  applied  to  the  abdomen, 
around  the  anus,  or  at  the  points  of  tenderness.  Membranous  or  phleg- 
monous enteritis  is  to  be  treated  the  same  as  dysentery. 

Chronic  intestinal  catarrli  may  be  treated  by  astringents  :  the  best  are 
the  nitrate  of  silver,  the  acetate  of  lead,  and  the  sulphate  of  copper.  A 
course  of  mineral  waters  will  in  many  cases  have  a  beneficial  effect,  and 
sea-bathing,  cold  sitz-baths,  or  sponging  the  abdomen  with  cold  salt  water 
may  be  of  service  in  mild  cases.  i 

DIAEEHCEA. 

Diarrhoea  is  the  frequent  discharge  of  fluid  or  semi-fluid  faeces  (without 
tenesmus) ;  it  may  be  acute  or  chronic.  It  is  a  symptom  of  a  variety  of 
morbid  conditions  which  will  be  considered  under  their  appropriate  heads. 

The  following  are  the  principal  varieties  of  acute  diarrhoea  : 

Irritative,  diarrhoea  includes  those  fluxes  attended  by  pain  and  griping  so 
often  met  with  in  children  during  the  summer  months  in  our  large  cities  ; 
those  "brought  up  by  hand"  and  those  who  have  just  been  weaned  are 
most  liable  to  it.  In  adults,  this  form  of  diarrhoea  may  be  caused  by  excess 
of  food,  improper  and  unseasonable  food,  improperly  masticated  food,  foul 
water,  tainted  meats,  etc.  Personal  idiosyncrasies  play  an  important  j^art 
in  its  causation.  The  diarrhoea  produced  by  drugs  causing  hyper-purgation 
is  'irritative."  So  also  the  pseudo-diarrhoea  induced  by  hardened  ffeces, 
the  result  of  long-standing  constipation.  The  presence  of  worms,  excessive 
discharges  from  the  liver  and  intestinal  surface,  especially  if  they  are  in- 
flammatory in  character,  are  causes  of  irritative  diarrhcea. 

Symptor)iatic  diarrhoea  is  part  of  the  natural  history  of  typhoid  fever, 
waxy  intestines,  intestinal  ulcerations,  inflammation  of  the  large  and  some- 
times of  the  small  intestine,  Bright's  disease,  pyaemia,  the  exanthemata, 
Hodgkin's  and  Addison's  diseases,  leukasmia,  and  all  forms  of  cholera. 
The  diarrhoea  of  enteritis  and  proctitis  is  symptomatic. 

Mechanical  diarrhoea  is  that  form  in  which  the  faeces  are  made  fluid  by  a 
large  amount  of  serum  poured  into  the  intestinal  canal,  the  serous  flow  being 
induced  by  the  action  of  salines,  as  Epsom  or  Kochelle  salts.  Hepatic, 
pulmonary,  and  cardiac  diseases  which  retard  the  returning  blood  current 


264  DISEASES  OF  THE   DIGESTIVE   SYSTEM. 

from  the  superior  and  inferior  mesenteric  veins,  will  cause  a  transudation 
of  serum  into  the  intestine,  which  will  dilute  the  fseces  and  wash  out  the 
intestine,  causing  diarrhoeal  discharges. 

Nervous  diarrhoea  may  be  caused  by  fright,  grief,  great  anxiety  and 
severe  pain.  It  is  marked  by  profuse  watery  faecal  discharges,  which,  when 
once  established,  are  apt  to  persist.  It  often  comes  on  so  soon  after  taking 
food  that  the  food  is  passed  undigested,  and  it  is  then  called  Uenteric  diar- 
rhoea.    The  discharges  usually  are  largely  serous. 

Clioleraic  diarrhoea  precedes  an  attack  of  cholera,  and  is  a  prominent 
symptom  in  cholera  morbus. 

Vicarious  diarrhoea  is  usually  compensatory.  When  the  functions  of  the 
skin,  kidneys,  or  lungs  are  suppressed  a  flux  from  the  bowels  affords  relief. 
Some  regard  a  gouty  diarrhoea  as  vicarious.  Chilling  the  body  suddenly 
produces  a  vicarious  diarrhoea,  provided  enteritis  is  not  established.  In  the 
latter  case  the  diarrhoea  would  be  symptomatic.  Intense  heat  brings  on  a 
vicarious  flux.  Many  fevers  and  acute  diseases  attended  by  an  ushering-in 
chill  cause  diarrhoea,  as  much  from  chilling  the  surface  (inducing  a  vicari- 
ous flux)  as  from  the  action  of  their  specific  poison  (in  which  the  flux  would 
be  symptomatic).  Thus  malarial,  puerperal,  and  septic  fevers  are  often 
attended  by  diarrhoea. 

Some  authors  make  different  varieties  of  diarrhoea  according  to  certain 
prominent  symptoms,  and  speak  of  simple,  faecal,  or  stercoraceous  diar- 
rhoea (usually  irritative),  bilious  diarrhoea, — when  the  dejections  con- 
tain a  large  quantity  of  greenish-yellow  fluid, — serous,  mucous,  and 
dysenteric  diarrhoea.  The  discharges  in  the  last  variety  contain  mucus  and 
blood. 

Fatty  diarrhoea  is  the  result  of  faulty  pancreatic  digestion. 

The  term  crapulous  was  formerly  given  to  that  variety  caused  by  over- 
indulgence at  table,  or  the  ingestion  of  unwholesome  food. 

A  diarrhoea  is  critical  when  it  attends  the  crisis  of  a  disease,  not  having 
existed  before  that  time  and  ceasing  directly  after  it. 

A  colliquative  diarrhoea  is  a  copious  watery  flux,  occurring  in  wasting 
diseases  towards  their  close,  e.  g.,  phthisis,  cancer,  Bright's  disease, 
etc. 

The  diarrhoea  accompanying  pyaemia  and  certain  septic  blood-conditions 
is  by  some  called  eliminative.  It  is  a  question  whether  the  flux  carries  away 
the  poison  or  the  poison  induces  the  flux. 

Symptoms. — The  symptoms  of  diarrhoea  are  too  well  known  to  need  repe- 
tition ;  but  cases  vary  greatly,  not  only  in  the  kind  of  fluid  dejections,  but 
in  their  amount  and  frequency.  A  diarrhoea  from  over-eating  may  be 
harmless  or  even  beneficial  in  relieving  an  overtaxed  digestive  system. 
Again,  a  profuse  diarrhoea  may  be  exhausting  enough  to  cause  anaemia,  and 
in  some  chronic  diseases  hastens  the  fatal  issue.  Colicky  pains  and  cramps 
in  the  limbs  almost  always  accompany  diarrhoea  attended  by  profuse  watery 
discharges.  Thirst,  anorexia,  and  febrile  movement  indicate  that  the  diar- 
rhoea has  an  inflammatory  origin.  In  copious  fluxes  (serous  diarrhoeas)  the 
urine  becomes  scanty,  acid  and  albuminous.    Fatty  diarrhoea  may  be  accom- 


DIAREHOEA.  265 

panied  by  the  dejection  of  a  large  quantity  of  fat.'     Jaundice  and  melsena 
accompany  some  cases  of  fatty  diarrhoea. 

Chronic  diarrhoea  is  always  associated  with  some  form  of  chronic  organic 
disease,  e.  g.,  chronic  enteritis,  intestinal  ulcers,  syphilis,  malaria,  scurvy, 
phthisis,  etc.  In  India,  chronic  diarrhoea  is  called  ihe  white  flux.  Anaemia 
and  exhaustion  are  its  most  constant  symptoms.  After  (apparent)  recovery 
there  is  a  strong  tendency  to  its  return. 

Differential  Diagnosis.— Diarrhoea  may  be  mistaken  for  cholera,  dysentery, 
or  a  condition  produced  by  the  prolonged  retention  of  fceces. 

In  cholera,  the  history  of  the  epidemic,  the  watery  stools  resembling  rice- 
water,  the  persistent  vomiting,  the  cramps,  suppression  of  urine,  and  the 
tormina  will  be  sufficient  to  exclude  a  simple  diarrhoea. 

In  dysentery  there  will  be  fever,  rapid  pulse,  early  and  great  exhaustion, 
tormina  and  tenesmus,  scanty  bloody  stools  having  a  dysenteric  odor,  and 
more  or  less  tenderness  along  the  line  of  the  large  intestine. 

A  diarrhoea  dependent  upon  prolonged  retention  of  fceces  is  recognized 
by  the  history  of  previous  constipation  and  the  presence  of  thin  muco- 
feculent  faeces  accompanied  by  straining,  a  sense  of  soreness  in  the  sacral 
region,  and  the  detection  of  a  faecal  mass  by  a  rectal  exploration.  It  is  im- 
portant to  recognize  this  condition  early. 

Prognosis. — The  prognosis  in  symptomatic  and  inflammatory  diarrhoea 
depends  upon  the  primary  causative  disease  with  which  it  occurs.  The 
prognosis  in  simple  diarrhoea  is  good,  yet  the  disease  is  dangerous  in  the 
very  young  and  very  old.  Nervous  diarrhoea  is  apt  to  become  chronic  and 
often  proves  very  obstinate.     In  fatty  diarrhoea  50  per  cent.  die. 

Treatment. — The  treatment  of  diarrhoea  will  be  determined  by  the  causes 
which  produce  it,  and  the  symptoms  which  attend  it ;  if  it  depends  on  un- 
digested food,  the  first  indication  is  to  remove  the  substances  which  are 
causing  the  intestinal  irritation  by  a  full  dose  of  castor-oil,  or  rhubarb  and 
soda.  The  diet  should  be  restricted  to  milk  and  lime-water,  and  rest  in 
bed  should  be  enjoined.  In  the  feeble  a  teaspoouful  of  brandy  may  be 
given  every  two  or  three  hours.  If  the  discharge  continue,  camphor,  kino, 
bismuth  or  dilute  sulphuric  acid  may  be  administered  after  each  passage. 
If  the  discharges  are  accompanied  by  colicky  pains  and  griping,  opium  may 
be  combined  with  bismuth  and  camphor,  or  a  simple  diarrhoea  mixture 
will  be  found  efficacious.'  In  malarial  diarrhoea,  quinine  must  be  given  in 
combination  with  opium  and  capsicum.  In  bilious  diarrhoea  hydrargyrum 
cum  creta  may  be  combined  with  opium.  In  the  summer  diarrhoea  of 
children,  the  treatment  described  under  cholera  infantum  is  indicated.  It 
is  often  rapidly  cured  by  enemata  of  chloral  hydrate  (gr.  ij)  in  two  or 
three  drachms  of  starch  water.     In  nervous  diarrhoea  I  have  found  oxide 

'  Dr.  Bright  stated  that  fatty  diarrhoea  probably  indicated  disorder  of  the  pancreatic  functions  before 
Bernard  discovered  what  these  functions  were. 

2;^    Spt8.lavand.com 5  ij. 

Tr.  opii 3  ij. 

Tr.  rhei 3  ss. 

01.  sassafras  gtt.  x. 

M.— Sig.    Teaspoonful  after  each  movement. 


266  DISEASES    OF   THE    DIGESTIVE   SYSTEM. 

of  zinc  the  most  beneficial.  Scorbutic  diarrhoea  is  not  influenced  by  drugs  ;. 
lemonades,  anti-scorbutics  and  fresh  vegetables  will  usually  check  it  readily. 
A  vicarious  flux  frequently  needs  to  be  encouraged  rather  than  checked  (e.  g. 
in  anaemia).  As  regards  the  treatment  of  fatty  diarrhoea  we  have  but  few 
observations ;  large  quantities  of  olive  oil  in  one  case,  large  quantities  of 
whiskey  in  another,  and  a  change  from  an  indoor  to  an  outdoor  life  in  still 
another  case,  resulted  in  recovery. 

In  lienteric  diarrhoea  arsenic  is  beneficial  ;  it  may  be  combined  with  bis- 
muth or  the  alkalies.  Hydrochloric  acid  is  som^etimes  useful  ;  astringents 
are  not  indicated. 

In  the  treatment  of  chronic  diarrhoea,  bismuth  is  the  most  reliable 
drug.  There  should  be  great  care  in  diet,  and  the  body  should  be  cov- 
ered with  flannel,  even  in  warm  weather.  Sea  voyages  and  change  of 
climate,  are  often  of  service.  Tonics  are  indicated,  and  copper  and  silver 
salts  are  the  best  astringents.  Hope's  mixture — a  well-known  combina- 
tion— will  often  control  it  when  all  other  means  have  failed.  In  chronic 
nervous  diarrhoea,  arsenic  and  the  bromides  are  indicated. 

CHOLERA    MOEBUS. 

Cholera  Morbus,  called  also  cholera  nostras,  English  cholera,  and  sporadic 
cholera,  is  in  reality  idiopathic  entero-catharsis. 

Morbid  Anatomy. — If  any  anatomical  lesion  exists,  it  consists  in  an  acute 
gastro-enteritis  ;  but  the  disease  may  occur  without  any  discoverable  lesions, 
thus  simulating  a  functional  disorder.  It  is  so  rarely  fatal,  that  there 
has  been  little  opportunity  to  study  its  morbid  changes.  In  the  few  cases 
where  post-mortems  have  been  made,  no  adequate  lesions  have  been  dis- 
covered. Death  may  occur,  and  the  intestinal  tract  may  exhibit  no  mor- 
bid changes.  Sometimes  there  is  cerebral  anaemia  with  serous  effusion  into 
the  sub-arachnoid  spaces. 

Etiology.— Cholera  morbus  almost  always  occurs  during  the  summer 
months.  In  this  country  it  is  most  prevalent  in  July  and  August.  Sud- 
den checking  of  the  perspiration,  or  suddenly  chilling  the  surface  of  the 
body  by  external  cold,  or  iced  drinks,  and  sudden  changes  in  the  tempera- 
ture after  a  heated  term  will  produce  it.  Its  most  frequent  cause  is  undi- 
gested food,  as  shell-fish,  unripe  fruit,  cucumbers,  etc.  Sudden  arrest  of 
the  digestive  process  from  mental  emotion  is  said  to  induce  it.  .  Some  claim 
that  malaria  will  cause  it,  especially  in  those  greatly  exhausted.  Overdoses 
of  tartar  emetic  and  elaterium  bring  on  attacks  of  vomiting  and  purging 
very  similar  to  cholera  morbus.  Its  prevalence  during  certain  seasons  seems 
to  indicate  a  specific  cause,  perhaps  some  peculiar  atmospheric  condition. 
It  is  infrequent  in  old  age.  It  attacks  males  oftener  than  females.  In  many 
cases  its  only  discoverable  cause  is  intense  nervous  disturbance,  on  account 
of  which  the  peristaltic  action  of  the  intestines  is  greatly  exaggerated. 

Symptoms. — The  symptoms  of  cholera  morbus  are  familiar.  An  attack 
usually  begins  at  night  by  vomiting  and  purging.  The  matters  vomited 
are  first,  undigested  food,  gastric  mucus  and  bile ;  afterward  large  quan- 


CHOLERA   MOEBUS.  267 

titles  of  acid  or  bilious  fluid.  The  vomiting  is  projectile  in  character,  and 
there  is  temporary  relief  after  each  attack.  The  bitter  fluid  ejected 
leaves  a  burning  sensation  in  the  mouth  and  throat.  Although  the  thirst 
is  intense,  fluids  as  well  as  solids  are  immediately  rejected.  In  some  in- 
stances, instead  of  an  abrupt  onset,  the  attack  is  preceded  for  several  hours 
or  a  day  by  nausea,  general  malaise,  or  sense  of  weight  and  uneasiness  in 
the  epigastrium  and  lower  part  of  the  abdomen,  occasionally  accompanied 
by  colicky  pains.  Evacuations  from  the  bowels -follow  each  other  in 
quick  succession,  the  dejections  becoming  watery  and  profuse,  and  having 
a  mouse-like  odor.  In  some  cases  purging  alone  is  present.  After  an  at- 
tack has  continued  for  some  hours  the  discharges  become  watery  and  odor- 
less, but  they  always  contain  bile.  Pain  generally  accompanies  or  precedes 
every  act  of  vomiting  or  purging,  which  either  occur  together  or  rapidly 
succeed  each  other.  The  larger  the  evacuations  the  lighter  their  color,  and 
greater  the  thirst. 

In  all  severe  cases  there  are  cramps  in  the  lower  extremities,  es- 
pecially in  the  calves  of  the  legs  and  feet.  Both  vomiting  and  purging 
occur  suddenly  and  without  premonition.  The  skin  is  cool  and  covered 
with  a  profuse  perspiration.  The  pulse  grows  weak  and  rapid  as  the 
vomiting  and  purging  become  more  severe.  The  abdomen,  at  first  dis- 
tended, becomes  retracted  ;•  sometimes  the  abdominal  muscles  are  knotted 
by  cramps.  The  urinary  secretion,  after  the  excessive  watery  discharges 
from  the  alimentary  track,  is  greatly  diminished,  and  traces  of  albumen 
and  desquamated  epithelium  may  be  found  in  it.  These  severe  symptoms, 
although  seeming  to  threaten  the  life  of  the  patient,  usually  continue  only 
for  a  few  hours,  and  the  patient  rapidly  convalesces.  If  the  attack  is 
protracted,  the  pulse  becomes  flickering  and  imperceptible  at  the  wrist,  the 
countenance  pale  and  shrunken,  the  voice  feeble  and  the  surface  icy  cold. 
This  condition  is  called  the  algid  stage  of  cholera  morbus,  and  the  patient 
may  pass  into  a  state  of  collapse,  which  may  be  followed  by  death.  In  all 
cases  the  mind  is  perfectly  clear,  and  recovery  or  death  occurs  within  twenty- 
four  or  forty-eight  hours  from  the  beginning  of  the  attack.  A  fatal  issue 
in  adults  is  exceedingly  rare.  Sometimes  a  fever,  attended  by  typhoid 
symptoms,  follows  the  stage  of  collapse,  called  "the  reaction  fever."  Gen- 
erally, the  stools  become  normal  in  character  the  day  after  the  commence- 
ment of  the  attack,  and  the  patient  is  simply  weak.  There  are  rarely  any 
febrile  symptoms  during  its  active  period. 

Differential  Diagnosis. — During  a  cholera  epidemic,  it  is  difficult  to  differ- 
entiate cholera  morbus  from  either  cholerine  or  true  Asiatic  cJiolera.  When 
not  prevailing  as  an  epidemic,  Asiatic  cholera  is  differentiated  by  the  ab- 
sence of  fsecal  odor,  by  the  color  of  the  stools  and  by  the  duration  of  the 
attack.  Cholera  morbus  rarely  continues  longer  than  twelve  or  eighteen 
hours.  In  cholera,  collapse  comes  on  early  and  the  discharges  have  the  dis- 
tinctive rice-water  appearance  from  its  commencement. 

Cholera  morbus  may  be  mistaken  for  the  effects  of  irritant  poisons.  In 
cases  of  poisoning,  the  mouth  and  pharynx  are  usually  intensely  hj- 
peraemic,  and  the  pain  is  more  intense  and  constant  than  in  cholera  morbus. 


268  DISEASES    OF   THE    DIGESTIVE    SYSTEM, 

If  there  is  diarrhoea,  the  discharges  are  blood-stained,  and  this  never  occurs 
in  cholera  morbus.  In  poisoning,  the  pain  over  the  stomach  is  more  severe, 
and  an  analysis  of  the  vomited  matters  quickly  decides  the  question. 

Cholera  morbus  is  differentiated  from  typhlitis  and  perityplilitis,  by  the 
absence  of  a  tumor,  the  short  duration  of  the  attack,  and  by  the  intens- 
ity and  character  of  the  gastric  symptoms.  Typhlitis  is,  in  the  majority 
of  cases,  accompanied  by  constipation  ;  cholera  morbus  by  diarrhoea. 

Prognosis. — Cholera  morbus  is  rarely  a  fatal  disease.  Its  duration  va- 
ries from  two  hours  to  two  days.  In  the  aged,  and  in  the  feeble,  the  prog- 
nosis is  more  unfavorable  than  in  healthy  adults.  It  is  also  more  unfa- 
vorable when  cholera  and  dysentery  prevail  epidemically,  or  when  there  is 
co-existing  renal  disease.  When  a  patient  passes  into  the  algid  stage  or 
stage  of  collapse  there  is  always  danger. 

Treatment. — In  mild  cases  of  cholera  morbus,  ice  may  be  given  to  check 
the  vomiting,  and  sinapisms  applied  to  the  eiDigastrium.  In  the  severer 
cases,  a  quarter  of  a  grain  of  morphine  hypodermically  will  generally  re- 
lieve the  distressing  symptoms.  In  all  cases  sinapisms  should  be  applied 
over  the  abdomen,  and  if  there  is  great  coldness  of  the  surface,  dry  Tieat 
should  be  applied  to  the  extremities.  If  there  is  great  prostration,  with 
coldness  of  the  extremities,  alcoholic  stimulants  must  be  given  with  mor- 
phine, and  if  there  is  hepatic  tenderness,  one-half  grain  of  calomel  every 
hour  for  six  hours  will  be  of  service.  Small  doses  of  the  mineral  acids  are 
often  beneficial  after  the  vomiting  is  relieved. 

If  the  diarrhoea  is  protracted,  vegetable  astringents  may  be  given.  All 
remedies  should  be  given  in  small  doses.  After  the  subsidence  of  the 
attack,  care  should  be  exercised  in  the  diet  for  several  days,  and  the  patient 
should  be  kept  in  bed. 

CHOLERA    INFANTUM. 

Cholera  infantum,  or  summer  complaint  in  children,  is  a  very  common 
disease  in  cities  and  large  towns  during  the  heat  of  summer. 

Morbid  Anatomy. — Its  principal  lesions  are  found  in  the  colon  next  to 
the  ileum,  but  sometimes  the  whole  intestinal  tract  is  involved.  Patches 
of  arborescent  injection  are  scattered  over  the  intestinal  mucous  surface, 
which  sometimes  assumes  a  bright  red  color  and  becomes  more  or  less  tume- 
fied. The  most  constant  change  is  enlargement  and  softening  of  the  fol- 
licles. Peyer's  patches  present  the  shaven-beard  appearance,  and  in  pro- 
tracted cases  the  mucous  membrane  is  studded  with  follicular  ulcers.  Over 
the  inflamed  patches  the  peritoneum  may  be  reddened  and  covered  with 
lym]3h.  The  intestines  usually  contain  a  thin  rice-water  fluid,  more  rarely 
fluid  fffices.  The  mesenteric  glands  are  sometimes  enlarged  and  the  liver 
congested.  Death  may  occur  and  the  intestinal  tract  exhibit  no  morbid 
change. 

Etiology. — The  prevalence  of  cholera  infantum  in  summer  is  in  direct 
proportion  to  the  height  of  the  temperature.  Teething  children  are  es- 
pecially liable  to  it.     Those  over  three  years  are  less  liable  to   it.     Over- 


CHOLERA    IXFANTUM.  269 

crowded  and  anti-hygienic  surroundings  predispose  to  it.  It  prevails 
extensively  among  the  children  of  tenement-house  districts  and  in  asylums. 
The  greatest  mortality  occurs  during  hot,  still,  sultry  days.  Gases  from 
cesspools  and  malarial  influences  are  powerful  predisposing  causes. 
The  improper  feeding  of  children  which  prevails  in  the  densely  packed 
tenement-house  districts  of  New  York  City,  where  the  death-rate  from 
this  disease  is  twice  that  of  any  other  city  in  the  world,  has  as  much  to 
do  with  its  prevalence  as  the  high  temperature.  Artificially  fed  children 
are  more  subject  to  it  than  those  who  nurse. 

Symptoms. — It  begins  either  with  vomiting  or  diarrhoea,  or  both.  There 
may  be  prodromata,  but  they  are  vague  and  inconstant.  The  child  rejects 
all  food,  and  becomes  peevish  or  languid  and  aj^athetic.  Purging  is  always 
present,  and  the  passages  are  watery  and  greenish  in  color,  rarely  colorless, 
and  contain  curdy  masses  mixed  with  mucus.  There  is  a  peculiar  odor  to 
the  discharges  which  is  characteristic  of  the  affection.  Sometimes  the  stools 
contain  particles  of  undigested  food  that  have  passed  through  the  intestinal 
tract  unchanged.  The  discharges  are  more  or  less  slimy,  sometimes  frothy, 
and  at  first  have  a  distinctly  sourish  odor.  The  child  is  constantly  thirsty, 
although  all  liquids,  even  its  mother's  milk,  are  instantly  rejected.  Prostra- 
tion and  emaciation  begin  almost  with  the  first  discharges,  and  two  or  three 
days  suffice  to  bring  the  healthiest  child  into  an  extremely  exhausted  con- 
dition. The  reaction  of  the  vomited  matter  varies  ;  it  maybe  acid  or  alka- 
line. 

The  patient  becomes  stupid,  with  a  marked  tendency  to  coma.  Con- 
vulsions are  not  infrequent.  The  temperature  is  rarely  above  the  normal,  ex- 
cept during  the  first  few  hours,  and  then  it  is  remittent  in  character.  The 
urinary  secretion  is  diminished,  and  ursemic  symptoms  often  precede  a  fa- 
tal termination.  The  number  of  passages  varies  from  six  to  seventy-five  in 
the  twenty-four  hours  ;  the  abdomen  at  first  may  be  distended  and  tympa- 
nitic ;  later,  it  is  retracted,  and  always  tender.  The  pulse  varies  from  1 20  to 
160,  and  there  is  often  marked  dyspnoea.  These  little  patients  die  from 
inanition,  or  rapidly  recover  after  having  seemingly  been  on  the  verge  of 
death.  Not  infrequently  they  gradually  pass  into  a  condition  where  months 
will  elapse  before  normal  intestinal  digestion  is  re-established.  The  disease 
usually  lasts  a  week,  at  the  end  of  which  death  or  recovery  takes  place. 
Deceptive  remissions  may  occur,  only  to  be  followed  by  graver  and  often 
fatal  symptoms.  Tenderness  on  pressure  is  generally  marked  along  the 
whole  line  of  the  colon,  and  the  diffuse  erythema  about  the  anus  causes  in- 
tense pain  whenever  a  passage  occurs. 

Diiferential  Diagnosis. — Cholera  infantum  may  be  mistaken  for  Asiatic 
cholera.  The  points  already  given  for  the  differential  diagnosis  of  cholera 
and  cholera  morbus  will  suffice  to  establish  the  diagnosis. 

A  spurious  liydroceplialus  sometimes  follows  cholera  infantum,  the  symp- 
toms of  which,  and  the  termination  in  coma,  resemble  very  closely  those  of 
acute  hyilroce2}Tialus.  In  spurious  hydrocephalus  there  is  diarrhoea  and  a 
history  of  previous  vomiting  and  purging.  In  acute  hydrocephalus,  there 
is  constipation.     In  spurious  hydrocephalus,  the  pupils  are  dilated  buo  reg- 


270  DISEASES    OF   THE    DIGESTIVE    SYSTEM. 

ular,  while  in  tubercular  meningitis  they  are  contracted  and  irregular.  In 
sj)urious  hydrocephalus  the  pulse  is  accelerated  but  regular,  while  in  acute 
hydrocephalus  it  is  slower  than  normal,  irregular  and  intermittent.  In 
acute  hydrocephalus  the  abdomen  is  retracted  ;  in  spurious  hydrocephalus 
it  is  distended  and  tympanitic.  The  hydrocephalic  cry  and  convulsions, 
on  the  one  hand,  and  the  age  of  the  patient  and  the  mode  of  the  attack  on 
the  other,  will  further  aid  in  the  diagnosis. 

Prognosis. — The  prognosis  in  a  severe  attack  of  cholera  infantum  is  always 
unfavorable.  Its  duration  depends  upon  the  vigor  of  the  child  and  the  se- 
verity of  the  attack.  It  may  continue  a.  week,  or  death  may  occur  in  twenty- 
four  hours.  Children  who  are  artificially  fed  are  less  likely  to  recover  than 
those  who  receive  the  breast.  The  rate  of  mortality  is  greater  in  those  liv- 
ing in  badly  ventilated  tenements  than  in  those  with  better  hygienic  sur- 
roundings. Continued  vomiting,  excessive  purging,  stupor,  or  great  rest- 
lessness and  convulsions,  are  unfavorable  symptoms.  The  prognosis  is 
favorable  when  the  vomiting  and  purging  are  not  excessive.  Death  may 
occur  from  exhaustion,  or  cerebral  effusion  causing  convulsions  and  coma. 
Oedema  of  the  lungs  may  result  from  heart- failure,  and  this,  with  hypo- 
static congestion,  may  cause  death.  In  all  cases  the  prognosis  must  be 
guarded. 

Treatment. — The  treatment  of  cholera  infantum  is  mainly  prophylactic ; 
the  diet  and  hygienic  surroundings  are  the  most  important.  Occurring  as  it 
does  in  large  cities  in  the  summer  it  is  best  treated  by  removing  the  children 
of  the  poor  to  the  sea-shore.  When  this  is  impossible,  the  child  must  spend 
the  morning  and  evening  in  the  fresh  air.  The  first  indication,  then, 
is  change  of  air  and  location.  The  establishment  of  various  seaside  sani- 
tariums for  children  during  the  summer  months  in  the  neighborhood  of 
large  cities  is  the  most  important  advance  that  has  been  made  in  the 
management  of  this  disease.  At  the  same  time  great  care  must  be  exer- 
cised in  the  diet ;  fresh  cow's  milk  with  barley  and  lime-water  added,  is 
the  best  artificial  diet ;  a  good  wet-nurse  is  always  to  be  preferred.  The 
amount  of  food  taken  should  be  regulated  by  the  capacity  of  each  case  to 
retain  it.  At  the  onset  of  the  attack  a  few  drops  of  brandy  in  a  teaspoon- 
ful  of  barley-water  is  all  that  should  be  allowed,  and  absolute  rest  in  the 
horizontal  position  should  be  maintained  as  long  as  the  vomiting  con- 
tinues. To  relieve  the  intense  thirst  the  child  may  suck  pounded  ice  in  a 
linen  bag.  The  only  drug  that  I  have  found  efficacious  in  controlling  the 
vomiting  is  calomel,  which  should  be  given  dry  on  the  tongue  in  minute 
doses,  1-12  of  a  grain  every  half-hour.  Some  claim  excellent  results  from 
the  administration  of  bismuth  and  carbolic  acid.  Both  bismuth  and  calo- 
mel are  efficacious  when  the  stools  contain  large  quantities  of  mucus.  If 
the  intestinal  symptoms  persist  after  the  vomiting  is  relieved,  camphor 
and  opium  may  be  given — five  or  ten  drops  of  the  tr.  opii  camph.  every  two 
hours. 

In  malarial  districts,  quinine  should  be  given  as  soon  as  the  stomach  will 
retain  it.  When  vomiting  is  slight  and  purging  is  excessive  with  great 
prostration,  benefit  will  be  obtained  from  camphor  and  brandy.     The  vege- 


IJSrTESTIKAL   DYSPEPSIA.  271 

table  astringents,  siicli  as  liaematoxylon,  kino,  and  catechu,  are  of  service 
incontrolling  the  diarrhoea  which  so  often  follows  a  severe  attack  of  cholera 
infantum.  During  convalescence,  wine-whey  may  be  given  in  connection 
with  cod-liver  oil,  and  the  phosphates  and  oils  may  be  applied  to  the  sur- 
face as  a  means  of  sustaining  the  strength  of  the  child.  Seaside  resorts 
and  salt  water  baths  are  especially  beneficial  to  this  class  of  patients  after 
the  severity  of  the  attack  has  passed.  Spiced  poultices  wet  with  brandy 
and  worn  over  the  epigastrium  are  of  service. 

Flannel  should  be  worn  next  the  surface  during  convalescence,  and  great 
care  should  be  exercised  to  avoid  exposing  the  surface  to  changes  of  tem- 
perature, for  capillary  bronchitis  carries  off  a  large  number  of  convales- 
cents. 

IT^TESTINAL    DYSPEPSIA. 

Closely  connected  with  diarrhoea  is  a  functional  disturbance  of  the  intes- 
tines which  may  be  designated  intestinal  dyspepsia.  It  depends  upon  a 
derangement  of  the  functions  of  the  small  intestine  independent  of  any 
organic  lesion. 

Etiology.— Intestinal  dyspepsia  may  be  a  primary  disease,  or  it  may  be 
secondary  to  gastric  dyspepsia,  diseases  of  the  liver  and  large  intestine. 
Its  causes  are  similar  to  those  of  gastric  dyspepsia,  such  as  structural 
changes  in  the  mucous  membrane,  altered  conditions  of  the  secretions  of 
the  small  intestine,  the  presence  of  undigested  food,  or  the  ingestion  of 
improper  food  ;  an  altered  condition  of  the  muscular  coat  of  the  intestine 
often  accompanies  general  malnutrition. 

Symptoms. — Pain,  which  is  generally  a  constant  symptom,  is  of  a  dull, 
aching  character  and  not  circumscribed,  but  radiates  over  the  upper  por- 
tion of  the  abdomen.  It  is  rarely  acute  like  that  of  peritonitis,  nor  as  sud- 
den in  its  advent  as  the  pain  of  colic,  nor  does  it  bear  any  relation  to  the 
ingestion  of  food.  Nausea  and  vomiting,  when  present,  depend  more 
upon  the  accompanying  stomach  derangement  than  upon  any  intestinal 
disturbance.  Constipation  and  gaseous  distention  of  the  large  intestine 
are  prominent  symptoms.  It  is  only  after  repeated  attacks  that  the 
patient's  health  becomes  impaired,  so  that  he  loses  flesh  and  strength  and 
begins  to  worry  about  himself,  fearing  some  serious  organic  lesion.  It  is  a 
peculiar  fact  that  the  appetite  is  seldom  if  ever  impaired. 

Treatment. — Hygienic  measures  are  the  most  important  and  should  first 
be  tried.  If  possible  the  patient  should  travel ;  if  this  cannot  be  done, 
out-of-door  exercise,  such  as  horseback  riding  and  walking,  will  be  most 
beneficial.  This  class  of  patients  should  abstain  from  all  fats  and  starches, 
eat  principally  meat,  and  vegetables  containing  but  little  starch  ;  of  the 
drugs  which  yield  the  best  results,  ipecacuanha  and  cubebs  in  the  form 
of  a  powder  stand  first,  although  some  prefer  bismuth  combined  with  iron 
and  quinine. 


272 


DISEASES    OF   THE    DIGESTIVE    SYSTEM. 


DTSENTEET. 


Dysentery  is  a  specific  febrile  disease,  with  a  characteristic  local  lesion. 
Its  local  lesion  is  an  inflammation  of  the  mucous  membrane,  and  of  the 
solitary  and  tubular  glands  of  the  large  intestine,  which  may  be  catarrhal 
or  croupous  in  character.  It  has  points  of  resemblance  to  acute  infectious 
diseases,  being  attended  by  fever,  and  having  a  characteristic  local  lesion. 
It  may  be  acute  or  chronic,  epidemic,  endemic,  or  sporadic. 

Morbid  Anatomy. — The  difference  between  sporadic  or  simple  dysentery 
and  epidemic,  often  malignant,  dysentery,  is  that  in  the  former  tlie  ana- 
tomical changes  do  not  pass  to  extensive  ulceration,  and  it  attacks  com- 
paratively few  individuals  in  the  same  locality.  In  mild  cases,  the  lesions 
are  confined  to  the  lower  portion  of  the  large  intestine,  while  in  severe 
cases  the  whole  length  of  the  large  intestine  is  involved. 

The  first  change  which  takes  place  in  the  pathological  process,  in  the 
mild  as  well  as  in  the  severe  types,  is  a  more  or  less  intense  hypergemia  of 
the  intestinal  mucous  membrane.  Its  color  varies  from  a  slight  inflamma- 
tory blush  to  a  purplish  red  ;  this  change  in  color  is  never  uniform  through- 
out the  affected  portion.  With  the  change  in  color,  the  mucous  mem- 
brane becomes  swollen  and  softened,  from  oedema  of  the  mucous  and  sub- 
mucous tissue ;  the  latter  being  infiltrated  with  inflammatory  products 
which  give  it  a  "cloudy"  appearance.  The  thickening  and  softening 
are  more  marked  at  some  points  than  at  others.  They  are  usually  most 
distinct  at  the  summit  of  the  folds  of  the  mucous  membrane.  In  mild 
cases,  only  a  small  number  of  prominences  indicate  the  localities  which 

are  involved,  whereas  in  severe  cases  these 
prominences  are  so  numerous  that  they 
give  the  membrane  a  lobulated  appear- 
ance. In  the  first  stage,  the  solitary  fol- 
licles become  distinct,  enlarged,  promi- 
nent, and  vary  in  size  from  a  millet-seed 
to  a  small  pea.  Each  is  surrounded  by  a 
zone  of  turgid  and  enlarged  vessels.  These 
glands  enlarge,  become  distended  with  a 
whitish,  albuminous  exudation,  having  a 
dark  central  spot  surrounded  by  a  vascular 
ring.  The  next  change^in  most  instances, 
is  rupture  of  some  of  the  distended  capil- 
laries in  the  wall,  thereby  filling  the  fol- 
licular cavity  with  blood.  Molecular  dis- 
integration of  the  gelatinoid  contents  now 
Mucous  Surface  of  lower  portion  of  Large  occurs,  and  ulccrs  are  formed   after  the 

Intestine  in  the  First  Stage  of  Acute  Dysen-    contents  of  the  follicleS  are  discharged. 

A,  A.  Enlarged  follicles.  Thcsc  ulccrs  are  at  first  round  ;  later 

B.  Small  ulcers.  ,  i  in  i  i    ± 

they  gradually  enlarge,  and  two  or  more 
may  coalesce,  their  edges  becoming  everted  and  flattened,  and  assume  au 


DYSENTERY. 


273 


irregular,  serpentine,  or  rodent  shape.  The  long  axis  of  the  ulcer  usually 
corresponds  to  the  told  of  mucous  membrane  circumscribing  the  intestinal 
canal.  The  condition  of  the  different  ulcers  in  the  same  case  yaries  ;  one 
is  pale  and  superficial,  another  deep,  angry,  and  irritable  ;  again  they  may 
be  covered  by  a  more  or  less  dense  layer  of  lymph,  or  a  thin  film  of 
serous  fluid.  The  adjoining  tubular  glands  are  involved.  Sometimes 
ulceration  destroys  everi/  solitary  follicle  of  the  involved  part.  The  floor 
of  the  ulcer  may  be  on  the  muscular  or  on  the  peritoneal  layer  of  the  intes- 
tine. Between  the  ulcers  is  often  found  a  polypoid  growth,  which  is  simply 
h  flaccid,  vascular  tuft  of  mucous  membrane. 

As  the  mucous  membrane  of  the  large 
intestine  has  the  poorest  blood  supply  of 
any  mucous  membrane,  a  very  acute  dys- 
enteric process  may  cause  the  Avhole  length  of 
the  intestine  to  become  a  black,  shaggy,  gan- 
grenous, pus-infiltrated  slough.  In  high 
grades  of  dysentery,  large  tracts  of  the  mu- 
cous membrane  are  converted  into  dark  brown 
or  black,  ecchymotic,  and  nodular  carbonified 
masses  (sphacelus)  more  or  less  friable,  and 
underneath  them  the  submucous  tissue  is 
sometimes  infiltrated  with  pus.  When  this 
occurs  around  the  ileo-caecal  valve,  invagina- 
tion and  obstruction  may  result.  This  puru- 
lent infiltration  must  be  regarded  as  part  of  a 
*' reactive  inflammation,"  following  the  re- 
moval of  the  charred-looking  mass.  Some 
observers,,  however,  are  of  the  opinion  that  in 
rapidly  sloughing  dysentery  the  process  begins 
by  a  submucous  purulent  cellulitis,  which  detaches  the  mucous  mem- 
brane, this  membrane  then  becoming  gangrenous.  Many  pathologists 
regard  coagulation-necrosis  as  the  basis  of  all  dysenteric  processes  in  the  fol- 
licles and  tubular  glands. 

In  some  of  the  severe  forms,  the  submucous  cellular  tissue  becomes  infil- 
trated with  a  sero-sanguinolent  fluid,  and  its  vessels  become  filled  with  black 
masses  of  altered  blood.  The  muscular  coat  of  the  intestine  is  sometimes 
condensed,  friable,  and  of  a  pale  ashy-gray  color.  In  severe  epidemics,  a 
thin  dark-colored  exudation  covers  the  peritoneal  investment  of  the  affected 
portion  of  the  intestine.  In  many  cases  the  intestine  becomes  dilated,  and 
is  filled  with  dark  blood  and  disintegrating  inflammatory  products.  When 
the  intestine  contains  a  putrid,  coffee-ground  fluid,  the  case  must  be  re- 
garded as  malignant.  I  have  sometimes  found  the  intestine  collapsed  and 
empty  at  the  post-mortem  of  one  who  had  suffered  from  severe  dysenteric 
symptoms.  In  the  mildest  form  of  dysentery,  cicatrization  is  accompanied 
by  an  exudation  of  lymph,  which  rapidly  organizes.  This  lymph  exuda- 
tion first  appears  upon  the  floor  of  the  ulcer  ;  the  edges  become  rounded,, 
and  are  then  drawn  down  towards  the  base,  and  so  cicatrization  is  com- 
18 


ortion    of 
Stage  of 


Fig.  60. 
Mucous  Surface  of    lower   p 

Large  Intestine  in   Second 

Acute  Dysentery. 
Ulcers  are  seen  of  varying  size,  fron 

that  of  the  single  follicle  to  larger  onei 

formed  by  their  coalescence. 


274  DISEASES    OF   THE    DIGESTIVE    SYSTEM. 

pleted.  When  a  large  extent  of  the  mucous  membrane  is  removed,  the 
edges  of  the  ulcer  are  not  approximated.  The  cicatrices  which  remain 
after  the  deep  structures  have  been  destroyed  often  cause  *' valve-like"  or 
"annular"  folds,  which  constrict  the  colon. 

Perforation  and  peritonitis  may  result  from  an  ulcer  perforating  the  in- 
testinal walls.  If  the  cascum  is  perforated,  faecal  abscesses  may  form  in  the 
right  iliac  fossa.  The  liver  is  frequently  congested,  and  it  may  be  the  seat 
of  multiple  abscesses.  The  mesenteric  glands  are  enlarged,  softened,  and  of 
a  dark  blue  color.  The  lower  part  of  the  small  intestine,  in  rare  instances, 
may  be  involved  .in  the  dysenteric  process.  In  the  croupous  variety,  the 
mucous  membrane  of  the  large  intestine  undergoes  changes  similar  to  those 
which  occur  in  croupous  inflammation  of  other  mucous  membranes.  It 
usually  occurs  in  patches  ;  the  size  of  the  patches  will  correspond  to  the 
severity  of  the  inflammation.  If  the  inflammation  is  mild  in  character, 
the  membranous  exudation  will  disappear  after  a  few  days,  and  the  mucous 
membrane  return  to  its  normal  condition.  If  it  is  severe,  and  the  sub- 
mucous tissues  become  infiltrated,  there  will  be  destruction  of  the  mucous 
membrane  and  the  formation  of  ulcers.  These  ulcers  may  involve  the 
muscular  and  peritoneal  coats  of  the  intestine.  They  behave  the  same  as 
those  already  described. 

In  chronic  dysentery,  the  mucous  membrane  of  the  large  intestine  is 
studded  either  with  ^laty-blue  cicatrices  or  pigmented  ulcers.  In  the  ma  • 
jority  of  cases,  complete  cicatrization  of  the  ulcers  does  not  occur.  The 
edges  of  these  ulcers  are  always  made  up  of  unhealthy  tissue.  Multiple 
abscesses  in  the  liver  are  often  met  with  in  chronic  dysentery.  These  ulcera- 
tions are  especially  marked  at  the  sigmoid  flexure  and  in  the  rectum,  while 
the  mucous  membrane  in  the  remainder  of  the  large  intestine  is  thickened, 
tough  and  pigmented.  In  some  cases  the  intestinal  walls  atrophy  and  are 
thinner  than  normaly  but  generally,  on  account  of  the  changes  in  the  sub- 
mucous connective-tissue,  they  are  thickened  and  indurated  ;  consequently, 
there  is  more  or  less  rigidity  of'  the  whole  intestine,  with  narrowing  of  its 
calibre.  Sometimes  sinuses  exist  between  the  layers  of  the  intestine  ;  these 
are  most  often  found  about  the  rectum.  In  chronic  dysentery,  more  fre- 
quently than  in  acute,  are  annular  and  valve-like  constrictions  formed, 
which  cause  subsequent  constipation.  Small  polypoid  tumors  sometimes 
form  and  project  into  the  intestine. 

Etiology. — Dysentery  is  especially  liable  to  prevail  in  malarial  districts. 
There  are  localities  in  which  it  is  endemic,  and  others  in  which  it  is  epi- 
demic. It  seems  possible  that  there  is  a  specific  dysenteric  miasm,  and  that 
the  discharges  from  a  dysenteric  patient,  when  they  have  undergone  certain 
changes,  are  capable  of  causing  the  disease.  This  may  account  for  the  oc- 
currence of  the  disease  in  hot  climates  and  in  early  fall  in  our  own  climate, 
under  conditions  similar  to  those  which  favor  the  development  of  typhoid 
fever.  Impure  air  and  water  are  recognized  causes  of  its  development ; 
thus,  seamen  and  those  who  live  in  crowded  barracks  are  especially  liable 
to  it.  In  districts  where  it  prevail  ^,  exposure  to  cold  or  chilling  the  sur- 
face is  often  an  exciting  cause.     Bad  or  insufficient  food,  or  a  diet  wanting 


DYSEHTEBT. 


275 


in  vegetables,  alcoholismus,  mental  anxiety,  and  excessive  fatigue  are  among 
its  predisposing  causes. 

Symptoms. — Dysentery  is  preceded  by  loss  of  appetite,  a  furred  tongue, 
constipation,  or  constipation  alternating  with  diarrhoea,  a  dry  skin,  and  a 
feeling  of  general  malaise.  Tlie  severer  forms  of  acute  dysentery  commence 
with  a  chill  or  distinct  rigor,  followed  by  a  slight  rise  in  temperature,  ac- 
companied by  anorexia  and  nausea.  The  temperature  usually  ranges  from 
101°  to  103°  ;  it  may  reach  105°  F.  The  pulse  is  increased  in  fre- 
quency, small  and  compressible. 
Wibh,  or  following  these  constitu- 
tional symptoms,  there  is  a  constant 
desire  to  go  to  stool,  with  tormina, 
both  during  and  after  a  passage 
from  the  bowels.  The  evacuations 
are  at  first  semifeculent  mucus, 
watery  looking,  and  contain  lumps 
of  hard  faeces,  ''scybalse."  After 
and  during  stool,  there  occurs  that 
painful  straining  with  bearing  down, 
called  "tenesmus."  The  tenesmus 
is  due  to  the  abnormal  sensibility 
of  the  lower  bowel,  and  the  invol- 
untary action  of  the  muscular  fibres 
of  the  rectum.  At  the  very  onset 
of  the  attack,  the  nervous  depres- 
sion is  very  marked,  the  strength  is 
diminished,  and  the  face  assumes  a 

pale,  anxious  expression.  The  discharges  soon  become  scanty  and  more  fre- 
quent, containing  blood  and  mucus  (the  "  bloody  flux  "),  and  have  the  pecu- 
liar dysenteric  odor.  Twenty  or  thirty  discharges  from  the  bowels  may  occur 
in  twenty-four  hours,  although  they  usually  do  not  exceed  eight  or  twelve. 

If  the  disease  has  its  seat  at  the  upper  part  of  the  large  intestine,  altered 
biliary  secretions  will  be  intimately  mingled  with  the  blood  and  mucus.  If 
the  dysenteric  process  is  confined  to  the  lower  portion  of  the  intestine,  the 
blood  will  be  separated  from  the  mass  and  occur  in  streaks.  As  the  disease 
progresses,  the  patient  becomes  more  nervous  and  anxious,  irritable  and 
restless,  and  his  countenance  will  be  expressive  of  intense  suffering.  There 
is  seldom  much  abdominal  pain  or  tenderness  on  pressure  during  the  first 
few  days,  but  the  slightest  amount  of  solid  food  taken  into  the  stomach 
causes  tormina.     The  tongue  is  moist  and  covered  with  a  thick  whitish  fur. 

As  the  disease  advances,  in  the  severe  type,  the  stools  change  in  character ; 
they  contain  sloughy  shreds  of  exudative  matter,  looking  like  "  washed  raw 
meat,"  mixed  with  blood  and  purulent  matter,  or  they  are  of  a  greenish 
color  resembling  spinach.  The  thickened  intestine  may  now  be  felt  through 
the  abdominal  parietes.  The  abdomen  becomes  tympanitic  and  tender ; 
the  tenderness  is  usually  most  marked  at  some  point  along  the  line  of  the 


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Temperature  Record  in  a  case  of  Acute 
Dj'sentery. 


276  DISEASES   OF   THE   DIGESTIVE    SYSTEM. 

large  intestine.  In  some  cases  the  stools  become  brownish,  serous  in  char- 
acter, and  are  often  so  copious  as  to  cause  extreme  exhaustion.  The  pulse 
increases  in  frequency,  and  is  extremely  small  and  feeble  ;  the  tympanitis 
increases,  the  tongue  becomes  dry,  its  centre  brown  or  black,  and  its  edges 
red.  The  restlessness  increases,  with  a  mild  delirium  at  night,  which  some- 
times becomes  violent.  The  urine  is  dark  and  scanty.  There  may  be  great 
difficulty  in  passing  it,  only  a  few  drops  at  a  time  being  voided, — stran- 
gury. If  the  case  tends  to  a  fatal  termination,  irregular  febrile  exacerba- 
tions and  remissions  occur,  the  stools  have  a  cadaverous  or  gangrenous  odor  ; 
hiccough,  subsultus  tendinum,  cold  perspiration,  a  flickering  pulse,  deeply 
sunken  eyes,  and  cyanosis  of  the  extremities  usher  in  the  fatal  termination. 
If  recovery  is  to  take  place,  the  discharges  during  the  second  week  become 
less  frequent  and  acquire  a  faecal  odor.  The  temperature  falls,  the  pulse 
diminishes  in  frequency  and  gains  in  force.  The  tympanitis  subsides  and 
gases  are  discharged  from  the  bowels  with  the  faecal  discharges.  As  recov- 
ery is  reached,  the  face  loses  the  anxious,  despondent  expression  which  it 
had  during  the  active  period  of  the  disease.     Convalescence  is  slow. 

Microscopically  examined,  the  stools  voided  at  the  height  of  dysentery 
are  found  to  contain  fat  spherules,  blood  globules,  pus  corpuscles,  vibri- 
ones,  triple  phosphates,  and  traces  of  ingesta,  all  crowded  into  a  molecular 
mass  ;  while,  if  examined  in  a  test  tube,  the  amount  of  albumen  present 
causes  the  entire  contents  of  the  tube  to  coagulate  on  the  application  of 
heat. 

Acute  dysentery  in  children  is  often  accompanied  by  vomiting  and  convul- 
sions.    In  some  cases  tenesmus  is  so  great  that  prolapsus  ani  occurs. 

A  malarial  dysentery  is  recognized  by  the  periodicity  of  its  febrile 
symptoms.  The  temperature  is  higher  than  in  non-malarial  dysentery,  and 
exacerbations  and  remissions  of  all  its  symptoms  occur  at  regular  inter- 
vals ;  the  hepatic,  renal  and  splenic  changes  are  the  same  as  in  malarial 
fevers.  The  stomach  is  very  irritable,  and  the  stools  are  likely  to  be 
serous  from  the  onset,  showing  but  slight  traces  of  blood. 

In  malignant  dysentery  the  typhoid  state  is  present  with  the  first  dysenteric 
stool  ;  the  passages  soon  assume  a  gangrenous  odor  and  contain  gan- 
grenous shreds  of  membrane,  with  abundant  serum  and  blood.  The  coun- 
tenance is  not  anxious,  but  listless  and  apathetic,  the  pulse  is  rapid  and 
weak,  the  voice  feeble,  the  stomach  irritable,  the  skin  cold  and  covered 
with  a  cold  perspiration — indeed,  a  state  of  collapse  is  very  quickly  reached. 
The  urine  may  be  entirely  suppressed,  but,  if  passed,  scalds,  and  has  a 
fetid  odor.  Not  infrequently,  just  before  death,  large  amounts  of  blood 
are  discharged  from  the  bowels  and  also  from  the  mouth  and  nose. 

When  all  the  causes  of  '*  scurvy  "  are  added  to  those  of  dysentery,  the 
symptoms  of  scurvy,  namely,  great  prostration,  emaciation,  a  pale  muddy 
skin,  darting  pains  in  the  limbs,  the  scurvy  sore  mouth,  and  the  petechial 
spots,  will  be  added  to  the  dysenteric  symptoms,  and  the  stools  will  contain 
blood  from  the  very  onset,  and  are  as  fetid  as  in  the  malignant  variety.  In 
scorhutic  dysentery,  profuse  and  fatal  hemorrhages  are  liable  to  occur  after 
the  first  few  days. 


DYSENTEEY.  377 

Chronic  dysentery  is,  in  most  instances,  the  direct  sequela  of  the 
acute  form.  In  a  few  cases  dysentery  is  chronic  from  the  beginning,  and 
its  cause  then  lies  in  fatty  or  waxy  degeneration  of  the  liver  or  spleen,  or 
both,  or  in  a  strumous  or  scorbutic  taint.  The  temperature  usually  ranges 
above  the  normal.  In  some  instances  hectic  fever  may  attend  it.  The 
evacuations  are  scanty  and  frequent,  tormina  and  tenesmus  are  present  in 
most  cases,  and  the  stools  contain  mucus.  At  times  they  are  serous,  pale, 
slimy,  or  frothy,  but  always  fluid  ;  occasionally  they  contain  faecal  matter 
and  are  brown  and  watery.  The  patient  progressively  loses  flesh  and 
strength,  although  the  appetite  may  remain  good.  Defective  nutrition  is 
shown  by  furuncles,  a  dry,  scaly  skin,  a  red,  glazed,  and  often  deeply  fis- 
sured tongue,  falling  of  the  hair,  and  a  worn  and  feeble  expression  of 
countenance. 

Differential  Diagnosis. — Dysentery  may  be  mistaken  for  acute  rectitis  or 
intestinal  catarrh,  iov  diarrhoea  complicated  with  hemorrlioids,  and  for  ca7i- 
cer  ov polypus  of  the  rectum.  Acute  i-ectitis  begins  with  colicky  pains  and 
constipation ;  while  dysentery  commences  with  a  distinct  chill  or  rigor, 
diarrhoea,  and  a  permanent  elevation  of  temperature.  Dysenteric  dis- 
charges contain  mucus,  pus,  blood,  and  scybalae. 

In  acute  intestinal  catarrh  there  is  no  blood  mingled  with  mucus  in  the 
discharges,  and  the  latter  do  not  have  the  dysenteric  odor  which  is  so 
characteristic  of  dysentery.  Tenesmus  is  always  present  in  dysentery, 
and  never  in  intestinal  catarrh.  The  discharges  are  j)rofuse  in  intestinal 
catarrh,  scanty  in  dysentery.  The  pain  in  acute  enteritis  is  more  intense 
and  paroxysmal  than  in  dysentery.  The  constitutional  symptoms  are  much 
more  severe  in  dysentery  than  in  enteritis. 

A  simple  diarrhoea  in  one  suffering  from  hemorrhoids  may  be  accom- 
panied by  bloody  discharges  and  tenesmus,  but  the  absence  of  constitutional 
symptoms  and  an  examination  of  the  rectum  will  readily  establish  the  diag- 
nosis. 

In  the  same  way  cancerous  or  polypoid  growths  in  the  rectum,  from 
which  pus  or  blood  is  frequently  discharged,  can  readily  be  differentiated 
from  dysentery. 

Prognosis. — The  prognosis  in  simple,  acute,  and  malarial  dysentery  is 
good.  In  the  malignant,  or  asthenic  and  scorbutic  varieties,  it  is  exceed- 
ingly bad.  The  ordinary  duration  of  acute  dysentery  is  from  eight  to  ten 
days ;  malignant  dysentery  may  terminate  fatally  in  two  or  three  days. 
Sporadic  dysentery  in  children  usually  lasts  about  a  week.  Chronic  dys- 
entery may  continue  for  years.  The  favorable  symptoms  in  any  case  are 
absence  of  a  gangrenous  odor  to  the  stools,  absence  of  great  nervous 
depression  and  of  an  anxious,  sodden  expression  of  countenance,  the  gradual 
subsidence  of  the  tenesmus  and  of  the  peculiar  dysenteric  stools.  The  unfa- 
vorable indications  are  a  large  quantity  of  blood  in  the  discharges,  a  sunken 
aspect  of  the  countenance,  hiccough,  vomiting,  a  distended,  tympanitic 
abdomen,  great  nervous  depression,  a  typhoid  condition,  great  restlessness, 
suppression  of  urine,  and  marked  cerebral  disturbances.  Dysentery  may 
be  complicated  by  extreme  anaemia,    by  prolapsus    ani,    by  hepatic    ab- 


278  DISEASES   OF  THE   DIGESTIVE   SYSTEM, 

scess,  by  bronchitis  and  lobular  pneumonia,  by  malaria,  typhoid  fever,  pur- 
pura, scurvy,  the  hemorrhagic  diathesis,  enlargement  of  the  spleen  and 
liver,  any  one  of  which  renders  the  prognosis  unfavorable.  Death  may  occur 
from  exhaustion,  from  hemorrhage,  from  perforation  and  peritonitis,  or 
from  secondary  pysemic  abscess.  In  all  cases,  however,  the  immediate 
cause  of  death  is  asthenia. 

Treatment. — The  preventive  treatment  of  dysentery  consists  in  disinfect- 
ing  the  evacuations  as  soon  as  they  are  discharged,  in  the  same  way  as  in 
typhoid  fever,  and  the  avoidance  of  all  those  conditions,  such  as  bad 
hygienic  surroundings,  insufficient  clothing,  and  improper  food,  which  act 
as  predisposing  causes.  A  patient  with  dysentery  miust  be  kept  in  bed, 
and  all  irritating  matter  removed  from  the  intestinal  tract  by  a  full 
dose  of  castor-oil ;  to  accomplish  this  an  enema  of  one  to  two  quarts  of  warm 
water  is  recommended  by  East  Indian  physicians.  The  diet  should  be 
chiefly  of  milk  with  light  meat  broths  ;  no  solids  should  be  allowed. 
If  at  the  very  onset  there  is  great  tenesmus,  two  or  three  leeches  about 
the  anus  will  often  give  great  relief.  Medicinally,  opium  is  the  drug 
almost  universally  employed,  and  should  be  given  to  semi-narcot- 
ism.' 

Its  direct  action  is  three-fold — narcotic,  sedative  and  astringent ;  secondly, 
it  controls  the  inflammatory  process  by  its  action  on  the  sympathetic  nerv- 
ous system.  When  the  rectum  is  chiefly  involved,  it  is  best  administered 
per  rectum,  but  when  the  temperature  is  high  and  the  tenesmus  is  intense, 
the  rectal  use  of  opium  is  contra-indicated.  In  such  cases  ipecacuanha  in 
large  or  small  doses  has  been  found  most  efficacious.  Some  recommend 
that  it  should  be  given  in  thirty-grain  doses,^  but  ib  seems  to  me  just 
as  efficacious  when  given  in  |-grain  doses  every  half-hour.  When  larger 
doses  are  given,  it  must  be  administered  when  the  stomach  has  been 
empty  for  some  hours,  and  no  fluid  should  be  taken  for  some  time  after 
its  administration ;  my  own  experience  has  led  me  to  rely  upon  the 
J-grain  doses  of  ipecacuanha  with  sufficient  morphine  hypodermically  to 
relieve  the  pain  and  restlessness.  Ipecacuanha  is  markedly  beneficial  in 
children,  combined  with  bismuth,  chalk,  or  bicarbonate  of  soda. 

Hot  fomentations  or  poultices  over  the  abdomen  are  always  grateful  to 
the  patient  and  are  not  contra-indicated.  Finely  pounded  ice  introduced 
into  the  rectum  and  ice-bags  externally  are  recommended,  but  they  have 
seemed  to  me  to  increase,  rather  than  arrest  the  inflammatory  process.  In 
malarial  dysentery,  quinine  must  be  given  in  full  doses  with  the  ipe- 
cacuanha, and  when  there  is  evidence  of  hepatic  congestion  one  or  two 
grain  doses  of  calomel  act  beneficially.  All  treatment  of  malignant 
dysentery  is  unsatisfactory ;  it  is  summed  up  in  the  treatment  of  symp- 
toms, and  in  supporting  the  patient  with  concentrated  nutrition  and 
stimulants.     In    the    scorbutic    variety,    in    addition  to   the   opium    and 

'  Opium  may,  by  semi-narcotism,  maslc  tlie  true  picture  of  the  disease,  and  sudden  death  may  unexpect- 
edly occur  when  the  friends  regard  the  case  as  doing  well. 

"^  Ewart  states  that  we  possess  in  ipecacuanha  "a  non-spoliative  antiphlogistic,  a  certain  cholagogue 
and  unirritating  purgative,  a  powerful  sudorific,  and  a  harmless  sedative  to  the  heart  and  muscular  fibres 
of  the  intestines."    Quain's  Dictionary,  pp.  414-415. 


TYPHLITIS.  279 

ipecacuanha,  lemon  and  lime-juice,  fresh  vegetables  and  milk,  and  ripe 
fruit  should  be  freely  given.  The  "grape  cure"  has  received  a  deserved 
reputation  in  the  treatment  of  this  variety.  During  convalescence  iron, 
bark,  and  the  mineral  acids  are  indicated. 

Patients  with  chronic  dysentery  should  reside  in  a  mild,  dry,  equable 
climate,  and  wear  flannel  next  the  surface,  especially  over  the  abdo- 
men. With  some  a  sea-voyage  will  effect  a  cure.  The  diet  should  be 
most  carefully  regulated ;  each  case  is  a  law  unto  itself ;  and  the 
articles  of  diet  can  only  be  determined  by  trial.  Astringents,  as 
the  acetate  of  lead,  sulphate  of  copper  and  nitrate  of  silver,  combined 
with  small  doses  of  opium,  are  recommended,  but  I  have  found  the 
greatest  benefit  from  the  prolonged  use  of  cod-liver  oil  and  the  pernitrate 
of  iron.     Quinine  is  recommended  by  East  Indian  physicians. 

TYPHLITIS. 

Typhlitis,  sometimes  called  "caecitis,"  although  a  catarrhal  inflamma- 
tion of  the  caecum  and  vermiform  appendix,  might  properly  be  classed 
under  the  head  of  intestinal  ulcerations,  since  the  inflammation  of  the 
mucosa  is  commonly  accompanied  by  ulceration. 

Morbid  Anatomy. — Typhlitis  begins  as  an  acute  local  catarrh  of  the 
mucous  membrane  of  the  cfficum,  which  soon  involves  the  submucous  tis- 
sue ;  the  muscular  coat  loses  its  contractile  power,  so  that  the  intestine 
becomes  dilated  and  allows  of  large  -faecal  accumulations,  which  are 
usually  attended  by  ulceration  of  the  mucous  and  submucous  tissue.  The 
faecal  accumulation  constitutes  a  typhlitic  tumor.  The  catarrh  may  extend 
to  the  vermiform  appendix,  or  an  independent  inflammation  of  the  appen- 
dix may  occur  ;  in  either  case  it  becomes  dilated  and  forms  a  sac  with 
thin  walls,  which  is  filled  with  a  semi-transparent  fluid.  The  termina- 
tions of  the  ulcerations  which  occur  in  the  caecum  are,  1st,  rupture  and 
general  peritonitis  ;  2d,  an  extension  of  inflammation  through  the  intes- 
tinal walls  to  its  peritoneal  covering,  and  a  local  peritonitis  ;  3d,  exten- 
sion of  the  inflammation  to  the  connective- tissue  at  the  posterior  wall  of 
the  caecum,  where  the  peritoneum  is  wanting,  and  a  consequent  suppura- 
tion or  adhesive  cellulitis,  which  may  bind  the  colon  to  the  iliac  fascia, 
and  develop  a  suppurative  "  perityphlitis  ; "  or,  4th,  adhesions  may  form  be- 
tween the  caecum  and  small  intestine,  matting  them  together,  and  binding 
them  to  neighboring  organs. 

Etiology. — More  than  two-thirds  of  the  cases  of  typhlitis  are  excited  by 
the  presence  of  foreign  bodies,  or  by  impaction  of  faecal  matter,  from  mus- 
cular atony  of  the  intestine,  the  result  of  the  habitual  distention  accom- 
panying constipation  ;  bilious  and  intestinal  concretions  and  masses  of  lum- 
brici  sometimes  cause  it.  It  may  also  result  from  acute  or  chronic  intestinal 
catarrh.  It  is  most  frequently  met  with  in  males  from  twelve  to  thirty 
years  of  age. 

Symptoms. ^The  premonitory  signs  of  typhlitis  are  vague  :  sometimes 
there  may  be  dull,  uneasy  pains  in  the  right  iliac  fossa,  usually  of  a  distinct 


280  DISEASES    OF   THE    DIGESTIVE    SYSTEM. 

colicky  character,  or  a  dull,  heavy,  d.raggmg  sensation  ;  diarrhoea  often  al- 
ternates with  constipation  ;  the  abdomen  is  more  or  less  distended  and  tym- 
panitic. The  faeces,  for  some  time  before  the  attack,  will  be  described  by 
the  patient  as  hard  round  balls  ;  if  it  end  in  resolution,  these  symptoms 
gradually  subside,  and  after  a  week  or  two  the  patient  regains  his  former 
health.  In  some  cases,  these  premonitory  signs  are  absent.  In  either  case, 
the  actual  symptoms  begin  with  a  severe  pain  in  the  csecal  region  and  right 
hip,  increased  by  pressure  and  by  motion  of  the  parts.  On  account  of  a 
loss  in  the  contractile  power  of  the  muscular  coat  of  the  intestine,  there  is 
nausea  and  vomiting.  At  first,  the  contents  of  the  stomach  are  ejected, 
then  bilious  matters,  and  finally  (in  some  instances)  the  ejected  matter  is 
stercoraceous  in  character.  The  pain  is  often  remitting ;  the  patient  is 
most  comfortable  on  the  right  side.  With  these  symptoms  there  may  be 
a  slight  rise  in  temperature,  but  this  is  not  constant,  nor  does  it  follow  any 
rule  ;  the  temperature  may  rise  to  103°  or  104"  F.,  accompanied  by  a  pulse 
of  130  per  minute  ;  with  these  symptoms  the  patient  often  suddenly  passes 
into  a  condition  of  collapse. 

If  recovery  now  occurs,  the  bowels  will  move  spontaneously,  and  large 
quantities  of  faeces  are  discharged,  accompanied  by  severe  griping  pains,  and 
the  typhlitic  tumor  may  entirely  disappear ;  sometimes  it  remains,  after 
copious  discharges  from  the  bowels,  on  account  of  the  infiltrated  state  of 
the  intestinal  walls.  This  is  called  "  chronic  typhlitis."  A  local  perito- 
nitis may  remain  after  the  typhlitis  has  disappeared,  but  if  peritonitis  has 
occurred,  it  usually  subsides  with  the  typhlitis.  When  peritonitis  occurs 
it  will  mask  the  ordinary  symptoms  of  typhlitis. 

Physical  Signs. — Inspection  may  show  a  swelling  in  the  right  iliac  fossa. 

Palpation  discovers  a  superficial,  sausage-shaped  tumor  just  above  Pou- 
part's  ligament,  its  long  axis  pointing  inwards  and  downwards,  and  some- 
times reaching  laterally  to  the  median  line,  and  vertically  to  the  free  border 
of  the  ribs.  It  is  tender,  slightly  movable,  .and  may  give  a  ''gurgling  "  on 
pressure.  It  is  not  to  be  forgotten  that  in  chronic  typhlitis  with  peritonitis, 
the  tumor  loses  its  characteristic  sausage-shape  and  grows  broader. 

Percussion. — There  is  dulness  on  slight  percussion  over  the  tumor,  and 
the  limits  of  the  tumor  can  be  well  defined. 

Diiferential  Diagnosis. — If  a  typhlitic  tumor  develops  slowly,  it  may  be  con- 
founded with  other  abdominal  tumors,  as  ovarian,  renal,  cancerous  and  an- 
eurismal.  But  in  all  cases  the  latter  are  covered  by  the  intestine,  whereas 
typhlitic  tumors  are  superficial.  The  perforating  peritonitis  of  typhlitis  may 
be  mistaken  for  peritonitis  from  other  causes,  when  it  comes  on  suddenly, 
and  a  diagnosis  is  only  reached  by  careful  study  of  the  previous  history, 
which  in  typhlitis  is  characteristic. 

Prognosis. — The  prognosis  is  always  doubtful,  but  in  the  majority  of  cases 
favorable,  statistics  showing  75  per  cent,  of  recoveries.  The  duration  in 
severe  cases  may  be  only  three  days,  and  again  it  may  continue  for  three  or 
four  weeks  ;  the  average  duration  is  from  eighteen  to  twenty  days.  The 
peritoneal  changes  may  be  permanent.  Typhlitis  may  be  complicated  by 
perityphlitis,  peritonitis,  periproctitis,  perinephritis,  fsecal  fistula,  pylephle* 


PERITYPHLITIS.  281 

bitis  and  thrombosis  of  the  femoral  vein.     Death  always  occurs  from  some 
of  the  complicating  conditions. 

Treatment. — Typhlitis  dema-nds  prompt  treatment.  Leeches  should  be 
applied  over  the  caecum,  and  followed  by  hot  fomentations  over  the  tumor. 
If  there  are  no  evidences  of  peritonitis,  large  enemata  of  tepid  water  may 
be  administered,  preceded  by  a  full  dose  of  castor  oil  ;  drastic  purges  should 
never  be  employed.  If  free  evacuations  from  the  bowels  are  obtained,  the 
case  soon  terminates  in  recovery,  for  the  swelling  which  often  goes  on  in- 
creasing afterward,  is  not  due  to  f?ecal  accumulation,  but  to  a  local  inflam- 
mation. If  there  are  evidences  of  local  or  general  peritonitis,  opium  must 
be  administered  in  sufficiently  large  doses  to  give  complete  relief  from  jDain, 
and  it  should  be  continued  until  all  signs  of  peritonitis  have  disaj)peared. 
If  the  bowels  do  not  then  move  spontaneously,  a  full  dose  of  castor  oil  may 
be  given,  followed  by  an  enema  of  warm  water. 

PEEITYPHLITIS. 

Perityphlitis  is  an  inflammation  of  the  connective-tissue  which  attaches 
the  ascending  colon  to  the  iliac  fascia,  rarely  extending  beyond  the  region  of 
the  caecum.  By  some  it  is  regarded  as  a  form  of  peritonitis,  and  it  has  also 
received  the  name  of  periccecal  abscess.  In  nearly  all  cases  the  inflamma- 
tion is  propagated  from  the  caecum,  the  vermiform  appendix,  or  the  as- 
cending colon.  It  may  occur  as  a  primary  inflammation  from  traumatic 
causes. 

Morbid  Anatomy. — The  ulcerative  processes  within  the  caecum  are  usu- 
ally accompanied  by  localized  congestion  of  the  peritoneum  over  it.  Fre- 
quently the  congested  peritoneum  is  covered  with  a  thin  layer  of  partially 
organized  lymph.  The  new  connective-tissue  formation  binds  together 
the  appendix  vermiformis  and  the  caecum,  and  attaches  either  or  both  of 
them  to  the  adjacent  parts.  When  typhlitic  ulceration  extends  into  this 
new  tissue  a  perityphlitic  abscess  is  formed.  In  rare  instances  recovery 
takes  place  without  an  abscess.  If  an  abscess  formg,  its  seat  is  in  the  cel- 
lular tissue,  between  the  colon  and  quadratus  lumborum,  or  in  the  cellular 
tissue  between  the  iliac  fascia  and  the  caecum.  Many  perityphlitic  ab- 
scesses are  undoubtedly  peritoneal  abscesses.  These  abscesses  are  deep  and 
irregular  in  shape,  owing  to  the  great  resistance  of  the  fascia  in  this  neigh- 
borhood. 

The  pus  may  infiltrate  the  connective-tissue  as  far  up  as  the  level  of 
the  eleventh  rib  and  reach  the  under  surface  of  the  liver,  or  may  extend 
as  far  down  as  the  rectum.  It  may  burrow  and  point  near  the  anus, 
or  it  may  make  a  direct  external  opening  in  the  groin  or  loin,  or,  as  most 
frequently  happens,  it  may  perforate  the  adjoining  wall  of  the  caecum  and 
be  voided  through  the  bowel  and  anus.  After  the  pus  has  burrowed  it 
may  form  a  sinus  or  a  series  of  sinuses  which  never  become  obliterated, 
although  they  grow  smaller  and  smaller  as  time  advances  ;  faecal  matter 
may  at  times  escape  from  such  sinuses.  In  many  instances  a  perityphlitic 
abscess  opens  into  the  bladder.     The  pus  may  escape  through  the  skin  of 


282  DISEASES   OP  THE   DIGESTIVE   SYSTEM. 

the  thigh,  or  it  may  perforate  the  peritoneal  sac  and  induce  general  and 
quickly  fatal  peritonitis.  In  most  cases  peritoneal  adhesions  prevent  the 
opening  of  the  abscess  into  the  peritoneal  cavity.  When  the  veins  are 
pressed  upon  by  the  abscess  there  will  be  more  or  less  oedema  of  the  ex- 
tremity. In  some  cases  the  inflammation  does  not  assume  an  intense  or 
acute  form,  but  is  rather  sub-acute  in  character,  and  then  its  area  is  lim- 
ited, and  the  accompanying  adhesions  are  firmer  and  more  extensive. 

Etiology. — Perityphlitis  is  usually  the  result  of  extension  of  inflamma- 
tion from  the  vermiform  appendix  or  its  rupture  from  ulceration.  It  may  be 
due  to  the  extension  of  tubercular,  typhoid,  or  dysenteric  ulcers  in  the  cae- 
cum, and  to  the  lodgment  of  foreign  bodies  in  the  vermiform  appendix. 
Caries  of  the  spine  or  of  the  pelvis  has  induced  it.  Traumatism  is  an  oc- 
casional cause  ;  it  is  rarely  of  spontaneous  origin. 

Symptoms. — In  a  few  instances  of  perityphlitis,  especially  those  super- 
vening on  typhlitis,  there  will  be  a  history  of  colicky  pains  which  radiate- 
outward  from  the  ceecal  region,  with  more  or  less  irregularity  in  the  ac- 
tion of  the  bowels.  There  is  pain  in  the  thigh,  accompanied  by  numb- 
ness and  a  sense  of  formication  in  the  right  lower  extremity,  due  tO' 
pressure  of  the  tumor  upon  the  nerves.  This  pain  is  deep-seated  and 
much  increased  by  flexing  the  thigh  upon  the  abdomen.  Eigors  and  fe- 
brile movement  are  usually  slight.  In  extensive  perityphlitis  the  patient 
cannot  raise  the  right  thigh,  either  on  account  of  the  pain,  or  from  inter- 
ference with  functions  of  the  nerves  from  the  pressure^  When  the  abscess 
is  of  large  size  there  may  be  oedema  of  the  limb.  The  parts  in  the  vicin- 
ity of  the  caecum  are  very  tender  to  pressure,  and  the  patient  usually  lies 
on  the  right  side,  with  his  thigh  semi-flexed  so  as  to  relax  the  psoas  and 
iliac  muscles.  As  the  abscess  increases  in  size,  there  is  in  adults  consti- 
pation, and  a  tendency  to  vomit.  In  children  the  bowels  are  commonly 
loose,  and  pain  in  the  stomach  will  have  been  an  early  and  prominent 
symptom.  When  a  perityphlitis  arises  as  a  typhlitis  is  disappearing,  a. 
painful  tumor,  more  deeply  seated  than  in  typhlitis,  will  make  its  appear- 
ance. 

Physical  Signs. — Inspection  reveals  a  tumor  in  the  right  iliac  region, 
which  may  extend  upward  and  to  the  left,  as  far  as  the  umbilicus.  In  chil- 
dren the  tumor  is  often  elongated,  reaching  from  the  ramus  of  the  pubis  to 
the  free  border  of  the  ribs. 

Palpation. — If  suppuration  has  occurred,  palpation  may  show  the  exist- 
ence of  fluctuation  over,  and  to  the  right  of  the  tumor.  In  children 
these  tumors  sometimes  have  a  brawny  hardness.  Careful  manipulation 
shows  the  tumor  to  be  deeply  seated. 

Percussion  may  give  a  tympanitic  resonance  on  account  of  the  gaseous 
distention  of  the  caecum,  the  tumor  being  behind  this  portion  of  the  intes- 
tine. More  often  the  percussion  note  has  an  obscure  tympanitic  resonance, 
for  the  caecum  is  either  tumefied,  or  contains  faecal  matter. 

Differential  Diagnosis. — Perityphlitis  may  be  mistaken  for  typhlitis.  In 
typhlitis  there  will  be  a  history  of  colicky  pains,  dyspepsia,  irregular  action 
of  the  bowels,  and  tympanitis,  all  of  which  are  present  before  a  tumor  is 


PEKITYPHLITIS.  283 

developed  ;  in  perityphlitis  a  tumor  is  present  before  any  other  symptoms 
are  developed.  In  typhlitis  the  pain  is  superficial  and  unaffected  by  the 
motion  of  the  thigh,  in  perityphlitis  it  is  deep-seated  and  increased  by 
motion  of  the  right  thigh.  There  is  no  sense  of  numbness  or  formication 
in  the  right  lower  extremity  in  typhlitis,  but  this  is  more  or  less  marked 
in  perityphlitis.  There  is  no  evidence  of  suppuration  (fluctuation),  etc., 
in  typhlitis,  while  evidence  of  fluctuation  is  present  in  ^perityphlitis  as 
soon  as  suppuration  occurs.  The  tumor  of  typhlitis  is  superficial  and 
sausage-diaped,  that  of  perityphlitis  deep  and  irregular.  A  typhlitic 
tumor  gives  a  flat  percussion  sound,  a  perityphlitic  tumor  an  obscure  tym- 
panitic resonance. 

A.  psoas  abscess  has  no  intestinal  symptoms,  and  the  purulent  discharge 
is  of  a  very  different  character,  lacking  the  fascal  odor.  Renal  and  ova- 
rian tumors  will  not  be  mistaken  for  perityphlitis  if  the  early  history  of 
the  case  is  carefully  analyzed. 

Prognosis. — In  the  majority  of  cases  in  which  the  peritonitis  is  localized, 
and  intestinal  perforation  does  not  occur,  recovery  takes  place.  If  a  peri- 
typhlitic abscess  opens  externally,  or  into  the  ascending  colon,  or  if  the 
pus  burrows  and  points  in  the  region  of  the  thigh,  buttock,  or  scrotum, 
the  prognosis  is  more  favorable  than  when  it  opens  into  the  peritoneal 
cavity,  or  into  the  bladder.  If  chills,  hectic,  emaciation,  and  extreme  ex- 
haustion are  present  the  prognosis  is  unfavorable.  The  average  rate  of 
mortality  is  about  25  per  cent.  If  recovery  from  the  primary  attack 
occurs,  there  still  may  be  narrowing  of  the  intestine,  or  such  alteration  in 
the  relative  position  of  the  parts  that  there  will  be  more  or  less  intestinal 
obstruction  for  the  remainder  of  the  individual's  life.  One  of  the  most 
unfortunate  sequela?  of  perityphlitis  is  the  formation  of  a  faecal  sinus. 

Treatment. — The  first  and  most  important  thing,  after  aspiration  has 
determined  the  character  of  the  tumor  and  shown  the  presence  of  pus,  is 
to  make  an  incision  into  the  abscess,  cutting  cautiously  through  the 
abdominal  wall  at  the  seat  of  the  swelling.  Free  drainage  must  be  kept 
up  by  means  of  a  drainage  tube.  Previous  to  the  evidences  of  suppu- 
ration, leeches  may  be  applied  over  the  tumor,  followed  by  warm  poul- 
tices. Absolute  rest  is  all  important  to  the  successful  management  of 
these  cases.  Some  prefer  to  open  at  once,  i.  e.,  before  fluctuation 
occurs.  After  an  artificial  or  spontaneous  opening,  or  after  the  occur- 
rence of  absorption,  care  must  be  taken  to  avoid  any  pressure  upon  that 
part  of  the  intestine  for  some  time.  The  exhaustion  from  the  suppura- 
tion must  be  combatted  by  iron  and  the  vegetable  tonics.  The  diet 
throughout  should  be  highly  nutritious  and  easy  of  digestion.  Opium 
should  be  employed  when  the  least  indication  of  peritonitis,  local  ©r  gen- 
eral, appears,  and  laxatives  and  purgatives  must  not  be  administered  un- 
til the  reparative  processes  are  well  established. 


384  DISEASES   OF  THE   DIGESTIVE   SYSTEM. 


ESTTESTIN'AL    ULCEES. 

The  Duodenal  Ulcer. — The  round  or  perforating  duodenal  nicer  may  be 
regarded  as  the  analogue  of  the  peptic  gastric  ulcer. 

Morbid  Anatomy. — This  ulcer  in  its  nature  and  appearance  closely  resem- 
bles the  gastric  nicer,  and  its  subsequent  changes  are  the  same,  its  most 
frequent  seat  is  the  ascending  portion  of  the  duodenum,  it  is  rarely  found 
in  its  descending  or  transverse  portions.  Not  infrequently  duodenal  and 
gastric  ulcers  coexist.  The  cicatrix  which  results  from  the  healing  of  a 
duodenal  ulcer  may  cause  dilatation  of  the  stomach,  and  of  that  portion 
of  the  duodenum  between  the  cicatrix  and  the  pylorus.  This  constric- 
tion and  subsequent  dilatation  will  induce  chronic  gastric  and  duodenal 
catarrh,  and  in  rare  cases  the  vena  portse  is  completely  obliterated  by  the 
constriction  of  a  duodenal  cicatrix,  or  the  ductus  communis  may  be  oc- 
cluded, thus  giving  rise  to  obstructive  jaundice.  Atrophy  of  the  pancreas 
has  resulted  from  occlusion  of  the  pancreatic  duct,  and  in  this  connection 
it  may  be  mentioned  that  duodenal  ulcers  near  the  head  of  the  pancreas 
rarely,  if  ever,  perforate.  Another  result  is  the  formation  of  a  fistula 
communicating  with  the  gall-bladder.  A  duodenal  ulcer  may  perforate 
the  duodenal  walls  into  the  peritoneal  cavity  and  cause  peritonitis,  or  hav- 
ing perforated  the  walls  of  the  duodenum  it  may  involve  the  liver,  pan- 
creas or  gall-bladder,  which  becomes  adherent  to  it  at  the  seat  of  the 
ulcer.  It  may  perforate  directly  outward  at  the  seventh  intercostal  space, 
or  indirectly  outward  after  having  first  opened  into  the  loose  cellular  tis- 
sue behind  the  bowel.  Abscesses  resulting  from  such  perforation  have  bur- 
rowed through  the  mediastinum  into  the  tissues  of  the  neck  and  opened 
posteriorly  near  the  shoulder-blade. 

Etiology. — Compared  with  gastric  ulcers,  duodenal  ulcers  stand  in  the 
proportion  of  one  to  thirty.  The  cause  of  the  round  duodenal  ulcer  is  the 
same  as  that  of  round  ulcer  of  the  stomach.  An  emiolus  obstructs  a  ves- 
sel, or  blood  is  extravasated,  necrosis  results,  and  the  action  of  the" intestinal 
juices  rapidly  establishes  the  ulcerative  process,  just  as  the  gastric  juice 
causes  a  gastric  ulcer  ;  an  ulceration  resulting  from  turns  is  much  more  lia- 
ble to  be  duodenal  than  gastric.  Duodenal  ulcers  occur  more  frequently 
in  males  than  in  females  ;  occasionally  they  are  met  with  in  children. 

Symptoms.— The  symptoms  of  duodenal  ulcers  are  obscure,  the  first  and 
only  symptom  being,  in  many  cases,  a  sudden  and  fatal  peritonitis.  When 
perforation  occurs,  it  ordinarily  takes  place  after  a  hearty  meal,  or  from  ef- 
forts made  in  vomiting  or  defecation.  The  patient  rapidly  passes  into  a 
condition  of  collapse,  the  face  becoming  "  Hippocratic,"  the  pulse  small  or 
imperceptible,  the  extremities  cold,  and  suppression  of  urine  often  precedes 
the  fatal  issue.  A  fatal  gastric  hemorrhage  has  been  the  only  sign  of  duo- 
denal ulcer.  Pain  is  less  pronounced  than  in  gastric  ulcer.  The  pain  may 
be  limited  to  the  right  hypochondrium,  or  it  may  be  localized  over  the  du- 
odenum. It  commences  from  two  to  four  hours  after  eating.  The  loca- 
tion of  the  pain  and  the  time  of  its  occurrence,  are  the  diagnostic  signs  of  a 


INTESTINAL   ULCERS.  285 

duodenal  ulcer.  It  giyes  rise  to  intestinal  hemorrhages  more  frequently 
than  to  peritonitis.  If  Jaundice  occur  with  these  symptoms,  it  aids  in  its 
diagnosis.  If  the  pancreas  is  secondarily  enlarged  and  indurated,  there 
will  be  a  tumor  in  the  right  hypochondrium. 

Prognosis. — The  prognosis  is  not  as  good  as  in  gastric  ulcers,  for  cicatriza- 
tion is  not  so  likely  to  occur.  Duodenal  ulcers  are  to  be  treated  in  the  same 
manner  as  gastric  ulcers. 

Follicular  Ulcers. — Though  the  morbid  anatomy  of  this  variety  of  in- 
testinal ulcers  is  almost  inseparable  from  that  of  enteritis  (q.  v.),  its  symp- 
toms are  distinct,  and  are  better  considered  under  a  separate  head. 

Symptoms. — Following  a  long-continued  intestinal  catarrh,  especially  in 
cachectic  subjects, where  the  diarrhoeal  discharges  have  been  distinctly  mu- 
co-purulent,  and  have  alternated  with  natural  faecal  discharges  coated  with 
blood  and  mucus,  there  will  ajjpear  in  the  dejections  transparent  masses  of 
mucus,  looking  like  "boiled  sago,"  and  having  the  form  of  the  conical- 
shaped  ulceration  of  the  follicles  of  Lieberkiihn.  AVith  follicular  ulceration 
there  is  great  emaciation  and  marasmus.  In  children,  where  this  form  of 
ulceration  is  often  extensive,  death  often  results  from  inanition.  If  long 
continued,  there  may  be  tormina  and  tenesmus,  while  the  stools  become 
uniformly  opaque,  puriform  and  yellowish  white.  If  recovery  takes  place, 
the  resulting  cicatrices  give  rise  to  obstinate  constipation.  Death  may 
occur  from  ^perforation,  peritonitis,  or  from  marasmus. 

Diffused  Catarrhal  Ulcers  are  never  met  with  apart  from  acute  enteritis. 

Morbid  Anatomy. — Acute  intestinal  catarrh  may  be  accompanied  by  a  sup- 
purative process,  which  will  cause  the  destruction  of  an  irregularly  circular 
portion  of  the  intestinal  wall,  including  the  mucous,  submucous,  and  often 
the  muscular  coats,  and  lead  to  perforating  peritonitis.  The  margin  of 
these  ulcers  is  usually  well  defined.  Their  centres,  which  are  irregularly 
depressed,  contain  a  grayish  shreddy  mass  ;  between  the  ulcerated  patches 
the  mucous  membrane  is  congested.  If  cicatrization  takes  place  rapidly, 
stricture  of  the  intestine  at  the  corresponding  point  may  result.  If  cicatri- 
zation takes  place  slowly,  portions  of  the  intestine  will  be  matted  together 
in  coils,  and  will  become  more  or  less  adherent  to  the  adjacent  organs. 

Etiology. — The  etiology  of  catarrhal  ulcers  is  the  same  as  that  of  catarrhal 
enteritis.  They  are  especially  liable  to  be  induced  by  foreign  bodies  and 
fgecal  impaction.  The  condition  occurs  most  frequently  when  an  acute  be- 
comes ingrafted  on  a  chronic  intestinal  catarrh.  The  symptoms,  prognosis 
and  treatment  are  identical  with  those  of  chronic  enteritis. 

Tuberculous  Ulcers. — Under  this  head  I  shall  consider  the  so-called  ''fol- 
licular "  or  strumous  enteritis. 

Morbid  Anatomy. — The  csecum  is  the  region  which  is  most  frequently 
the  seat  of  these  ulcers  ;  next  the  lower  portion  of  the  ileum.  The  large 
and  small  intestines  are  often  equally  affected.  Peyer's  patches  and  the 
solitary  follicles  are  the  primary  points  of  invasion.  At  first  they  become 
swollen  and  congested,  hyperplasia  of  their  lymphatic  elements  causing  nu- 
merous projections  on  the  mucous  surface.  These  projections  are  small, 
gray,  translucent,  elastic  nodules,  "  the  gray  miliary  tubercle."     They  usu- 


286 


DISEASES    OF   THE    DIGESTIVE    SYSTEM. 


ally  occur  in  isolated  patches,  but  may  become  confluent  over  a  consider- 
able portion  of  the  intestine.  After  a  time  these  gray  nodules  become  yel- 
low, dry,  and  cheesy,  increase  in  size  and  constitute  the  "yellow  tubercle," 
and  afterward  soften  and  form  ulcers. 

The  primary  tubercular  ulcer  is  a 
small,  round,  crater-like  mass  with  indu- 
rated base  and  walls.  Several  primary 
ulcers  in  one  Peyerian  patch  may  be  sep- 
arated from  each  other  only  by  thin  septa, 
and  then  the  patch  presents  a  honeycomb- 
like appearance  ;  or  several  follicles  form 
an  elevated  patch,  which  ulcerates  in 
points.  Diffuse  inflammation  of  the  sub- 
mucous tissue  occurs  in  the  vicinity  of 
these  patches.  The  villi  are  matted  to- 
gether at  their  base,  and  free  at  their 
apex.  Tuberculous  ulcers  spread  by  the 
development  of  small  fresh  nodules  in  the 
walls  of  the  blood-vessels  so  that  they 
extend  transversely,  sometimes  forming 
girdles  half  an  inch  wide  around  the 
whole  internal  surface  of  the  intestine. 
In  this  way  the  oval  tuberculous  ulcers 
outside  of  Peyer's  patches  have  their  long 
axis  transversely.  As  these  ulcers  in- 
crease in  size,  they  cause  contraction  and 
narrowing  of  the  calibre  of  the  intestine. 
These  ulcers  rarely  cicatrize  and  rarely 
cause  hemorrhage  or  perforation  of  the 
intestine.  If  a  tuberculous  ulcer  extends 
to  the  serous  coat  of  the  intestine,  the  latter  becomes  thickened,  reddened, 
and  somewhat  clouded,  and  is  covered  with  a  fibrinous  exudation  which 
mats  the  intestines  together.  It  is  at  these  points  that  the  peritoneum  is 
covered  with  minute  tubercle-granules.  A  more  or  less  severe  intestinal 
catarrh  accompanies  tubercular  ulceration.  The  process  may  extend  to  the 
mesenteric  glands,  or  these  may  be  primarily  involved,  constituting  what  is 
called  "tabes  mesenterica." 

Etiology. — The  strumous  or  tuberculous  diathesis  is  the  essential  cause 
of  tubercular  intestinal  ulcers.  As  the  primary  manifestation  of  scrofula, 
it  appears  almost  exclusively  in  children  under  five  years  of  age,  while  tu- 
bercular inflammation  of  the  intestines  and  mesenteric  glands  of  adults  is 
always  secondary  to  tubercle  elsewhere,  especially  pulmonary  tuberculosis. 
The  causes  which  in  non -tubercular  subjects  would  excite  simple  enteritis 
will  in  this  class  excite  a  tubercular  inflammation. 

Symptoms. — The  symptoms  of  tubercular  intestinal  ulceration  are  never 
diagnostic.  Diarrhoea  is  its  most  constant  symptom.  Pain  in  many  cases 
precedes  the  diarrhoea,  which  consists  of  thin  green  mucus,  or  more  rarely 


B. 

Fig.  62. 
Tubercular  Ulcers  of  the  Ileum. 

A.  Mucous  coat. 

B.  Peritoneal  coat. 


INTESTINAL   HEMORRHAGE.  287 

is  yeasty  in  character.  Blood  is  not  often  present  in  the  discharges.  An 
inordinate  desire  for  food  is  often  a  prominent  symptom.  There  is  early 
tympanitic  distention  of  the  abdomen,  which  causes  it  to  become  round 
and  protuberant,  and  this  pot-belly  presents  a  marked  contrast  to  the 
wasted  chest  and  limbs.  Ascites  is  sometimes  present,  and  enlargement  of 
the  abdominal  veins  is  quite  common.  The  general  health  is  much  im- 
paired and  there  is  progressive  emaciation,  although  there  are  intervals  of 
apparent  improvement.  The  sleep  is  disturbed  and  muscular  twitchings 
and  convulsions  occasionally  occur  in  children.  During  the  whole  course 
of  this  disease  there  is  a  continuous  rise  of  a  degree  or  two  in  temperature. 
When  the  end  is  near,  the  diarrhoea  which  has  continued  thi'ough  the  dis- 
ease in  many  cases  gives  place  to  obstinate  constipation. 

Physical  Signs. — Palpation  may  reveal  localized  tenderness,  especially 
about  the  csecal  region.  The  enlarged  mesenteric  glands  may  sometimes 
be  felt  through  the  abdominal  walls,  although  tympanitic  distention  often 
so  interferes  with  the  examination  that  they  cannot  be  detected. 

DijSerential  Diagnosis. — Tubercular  disease  of  the  intestine  may  be  mis- 
taken for  tubercular  meningitis  and  tubercular  peritonitis.  The  abdomen 
is  distended  in  tubercular  intestinal  ulceration  and  retracted  in  meningitis 
There  is  constipation  in  tubercular  meningitis,  and  diarrhoea  in  intestinal 
ulceration.  Vomiting,  projectile  in  character,  is  a  marked  and  constant 
sign  of  tubercular  meningitis,  while  vomiting  is  rare  in  intestinal  ulcers, 
and  when  present  is  retching  in  character.  The  pulse  is  slower  than  nor- 
mal early  in  meningitis,  while  it  is  accelerated  in  tuberculous  ulcer  of  the 
intestine.  The  pupils  are  normal  in  size  in  intestinal  disease,  and  con- 
tracted or  dilated  in  meningitis. 

Tubercular  joeriYo^ztVis  is  often  associated  with  intestinal  ulceration.  If 
peritonitis  exists,  the  abdomen  is  more  rigid  than  in  intestinal  ulceration, 
the  tenderness  and  paroxysmal  pain  are  much  more  severe,  and  emaciation 
is  not  so  prominent  a  sign  or  so  progressive.  Enlarged  cervical  glands  are 
more  frequent  with  ulceration  than  with  peritonitis. 

Prognosis. — This  is  always  unfavorable.  It  is  essentially  a  chronic  disease. 
Death  may  occur  from  exhaustion  incident  to  the  diarrhoea  and  maras- 
mus, or  from  intercurrent  tubercular  complications. 

Treatment. — The  prophylactic  treatment  is  similar  to  that  of  general  tuber- 
culosis. If  the  diarrhoea  is  copious  and  exhaustive,  astringents  with  opium 
may  be  employed.  Inunctions  of  cod-liver  oil  and  iodine  may  be  made 
over  the  abdomen,  which  should  be  covered  with  a  flannel  bandage.  When 
pain  is  severe  anodyne  poultices  may  be  applied  locally  to  relieve  it. 

INTESTINAL    HEMORRHAGE. 

Intestinal  hemorrhage  may  be  a  symptom  of  local  or  of  general  disease. 
The  bleedings  may  be  slight  when  they  are  capillary,  profuse  when  they 
come  from  vessels  of  considerable  size.  Blood  from  the  stomach  which  is 
passed  with  the  dejections  cannot  strictly  be  regarded  as  intestinal  hemor- 
rhage. 


288  DISEASES  OF  THE   DIGESTIVE   SYSTEM. 

Morbid  Anatomy. — At  the  post-mortem  of  one  who  has  died  during  or 
soon  after  an  intestinal  hemorrhage  the  intestinal  mucous  membrane  may 
be  found  either  hyperaemic  or  anaBmic,  according  as  the  hemorrhage  has 
been  slight  or  profuse.  The  intestinal  canal  will  contain  dark  grumous 
blood  or  small  clots.  If  the  hemorrhage  is  caused  by  ulcers  in  the  intes- 
tine, coagula  generally  adhere  to  the  ulcers,  and  the  edges  and  base  of  the 
latter  are  suffused  with  blood.  In  a  few  instances  the  mucous  membrane 
appears  normal,  especially  when  the  hemorrhage  is  due  to  obstruction  of 
the  portal  circulation. 

Etiology.— Any  disease  in  which  there  is  extensive  obstruction  to  the 
portal  circulation  may  be  a  cause  of  intestinal  hemorrhage  ;  with  the  ex- 
ception of  intestinal  ulcers,  cirrhosis  or  atrophy  of  the  liver  is  its  most  fre- 
quent cause.  It  is  a  very  frequent  attendant  upon  typhoid  and  dysenteric 
ulcerations.  Foreign  bodies  and  traumatism  act  mechanically  in  producing 
it,  and  it  may  be  induced  by  powerful  chemical  and  mechanical  irritants 
acting  directly  on  the  intestinal  mucous  membrane.  It  occurs  in  waxy  de- 
generation of  the  intestine,  and  may  be  causied  by  the  rupture  of  an  aneu- 
rism into  the  intestinal  canal. '  It  frequently  attends  the  development  of 
intestinal  cancer,  and  is  a  common  symptom  of  internal  hemorrhoids.  It 
occurs  in  yellow  fever  and  in  the  pernicious  malarial  fevers,  and  a  vicari- 
ous hemorrhage  may  take  the  place  of  the  menstrual  discharge.  Subsidence 
of  the  fiery-red  tint  of  the  face  in  erysipelas  has  been  followed  by  remit- 
tent intestinal  hemorrhage.  Chronic  constipation  and  the  pressure  of  large 
tumors  may  cause  it  by  impeding  the  venous  return.  It  has  occurred  in  a 
few  cases  of  intestinal  invagination  and  with  embolism  of  the  mesenteric 
artery.  It  is  a  common  symptom  in  purpura  hemorrhagica,  and  in  that 
condition  known  as  haemophilia.  Acute  yellow  atrophy  and  splenic  leuco- 
cythaemia  may  be  attended  by  intestinal  hemorrhage.  Those  affected  with 
a  scorbutic  or  syphilitic  taint  are  always  predisposed  to  it.  It  occurs  oft- 
ener  in  men  than  in  women.  The  aged  are  subject  to  a  passive  intestinal 
hemorrhage,  without  apparent  cause. 

Symptoms.— If  the  hemorrhage  is  slight  it  frequently  passes  unnoticed, 
for  it  gives  rise  to  no  symptoms.  When  it  occurs  in  dysentery,  typhoid  and 
yellow  fevers,  the  symptoms  which  attend  it  will  vary  with  the  amount,  num- 
ber and  persistence  of  the  bleedings  as  well  as  with  the  stage  of  the  disease  in 
which  it  occurs.  Its  color  will  be  determined  by  its  seat  and  the  length  of 
time  it  remains  in  the  intestinal  canal.  When  it  comes  from  the  upper 
portion  of  the  intestinal  tract,  it  is  of  a  dark  red  color,  grumous  and  tarry, 
when  its  seat  is  near  the  rectum  it  is  of  a  IrigJit  red  color  and  fluid.  The 
tarry  color  and  consistence  given  to  the  faeces  by  the  presence  of  blood  is 
called  ''  melasna." 

The  symptoms  which  attend  a  large  intestinal  hemorrhage  are  a  feel- 
ing of  faintness,  a  feeble  pulse,  a  deadly  pallor,  ringing  in  the  ears,  bright 
flashes  before  the  eyes  and  coldness  of  the  surface,  followed  bv  syncope 
which   may   end   in   death.      Immediately  following  or   preceding   these 

1  Bambei-g  places  diphtheritic  inflammation  of  the  intestines  as  its  second  most  frequent  cause,  dysen* 
terj'  being  the  first. 


INTESTIITAL  OBSTRUCTIOK.  289 

symptoms  there  may  be  a  large  discharge  of  blood  from  the  bowels.  In 
most  instances,  after  a  few  hours  the  patient  recovers  from  the  shock 
of  the  hemorrhage.  There  may  be  abdominal  pain  at  the  time  of  the 
hemorrhage  accompanied  by  a  sensation  as  if  warm  water  was  being 
poured  into  the  abdominal  cavity.  A  continuation  or  succession  of  large 
hemorrhages  will  rapidly  give  rise  to  the  characteristic  signs  of  ansemia. 
If  the  normal  dejections  are  coated  with  blood,  the  origin  of  the  hemor- 
rhage is  within  the  large  intestine.  When  the  hemorrhage  is  from  intes- 
tinal ulcers,  pus  will  be  mingled  with  the  blood.  Intestinal  hemorrhages 
may  cause  death  when  there  has  been  no  discharge  of  blood  from  the 
anus. 

Differential  Diagnosis.— The  diagnosis  of  intestinal  hemorrhage  is  not  dif- 
ficult, it  is  usually  made  by  the  patient.  Its  source  can  only  be  determined 
by  a  careful  history  of  the  case.  In  acute  infectious  diseases  its  seat  is  in 
the  small  intestine  ;  in  chronic  disease  it  usually  has  its  seat  in  the  large 
intestine.  When  diseases  of  the  liver  can  be  excluded,  local  causes  in  the 
rectum  should  be  sought  for. 

Prognosis. — The  prognosis  will  depend  upon  the  seat  and  cause  of  the 
bleeding.  In  yellow,  typhoid  and  malarial  fevers,  in  dysentery  and  cirrho- 
sis, it  is  always,  unfavorable.  Arterial  hemorrhages  are  far  graver  than 
capillary.  The  condition  of  the  patient  at  the  time  of  the  hemorrhage 
influences  the  prognosis.  It  is  less  dangerous  in  vigorous  than  in  feeble 
and  ansemic  subjects.  Death  may  occur  from  a  single  large  hemorrhage, 
or  from  the  asthenia  produced  by  repeated  smaller  bleedings. 

Treatment. — The  first,  and  perhaps  the  most  important,  indication  is  ab- 
solute rest.  The  patient  should  be  kept  in  bed  in  a  cool,  quiet  room,  and 
should  not  be  allowed  to  change  the  position  of  the  body.  Peristalsis  must 
be  arrested  by  opium  ;  fluid  nourishment  should  be  given  at  short  intervals 
and  in  small  quantities.  Cold  compresses  or  ice-bags  should  be  placed  over 
the  abdomen,  and  styptics  should  be  administered  by  the  mouth  or  by  the 
rectum,  according  to  the  supposed  seat  of  the  hemorrhage.  Alum-whey, 
perchloride  of  iron,  acetate  of  lead,  tannin,  or  any  of  the  haemostatics  may  be 
given  by  the  mouth  or  rectum.  Ergot  internally  or  ergotine  hypodermatic- 
ally  should  be  administered  in  sufficient  quantities  to  produce  the  physio- 
logical effect  of  the  drug.  When  the  bleeding  has  been  excessive,  stimu- 
lants—alcohol, ether  or  musk— should  be  administered,  and  it  may  be 
necessary  to  practice  transfusion.  Everything  taken  by  the  patient  by 
the  mouth  or  rectum  must  be  ice-cold.  The  use  of  the  mineral  acids  as 
beverages  has  been  advocated.  ISTo  irritating  food  or  drinks  should  be 
allowed  for  many  days  after  all  signs  of  hemorrhage  have  ceased.  If 
intestinal  hemorrhage  occurs  in  one  who  gives  the  evidence  of  purpura  or 
hgemophilia,  .the  salts  of  iron  or  potassa,  combined  with  vegetable  acids, 
are  serviceable. 

IITTESTINAL    OBSTRUCTION'. 

By  the  term  intestinal  obstruction  is  meant  a  narrowing,  closure,  invagi- 
nation, or  twisting  of  some  portion  of  the  intestine,  so  that  its  calibre  is 
19 


290  DISEASES  OF  THE   DIGESTIVE   SYSTEM. 

diminished  and  the  passage  of  its  contents  retarded  or  prevented.  In  all 
cases  there  is  a  mechanical  impediment  situated  either  within  or  without, 
or  in  the  wall  of  the  intestine.  When  a  foreign  body  prevents  the  onward 
progress  of  the  contents  of  the  intestines,  by  becoming  an  actual  plug,  the 
obstruction  is  said  to  be  within  the  intestine  ;  when  some  abdominal  tumor 
presses  on,  and  n-arrows  almost  to  closure,  some  portions  of  the  bowel,  it  is 
said  to  be  toitliout  the  intestine  ;  and  when  a  deep  ulcer,  involving  the  whole 
wall  of  the  intestine,  contracts  and  forms  a  stricture,  or  other  changes  take 
place  in  its  walls  which  diminish  or  obliterate  its  calibre,  it  is  said  to  be  in 
the  intestinal  walls.  It  is  impossible  to  sejDarate  the  etiology  of  intestinal 
obstruction  from  its  morbid  anatomy,  and  they  can  best  be  considered  to- 
gether. 

Morbid  Anatomy. — I  shall  first  consider  intestinal  obstruction  from  causes 
which  have  their  seat  in  tlie  ivall  of  the  intestine.  In  this  group  stricture 
and  intussusception  are  the  chief  lesions.  Intussusception,  or  invagination, 
consists  in  the  descent  or  prolapse  of  a  portion  of  the  intestine  into  that 
which  immediately  succeeds  it,  like  a  glove-finger  drawn  j)artially  within 
itself.  It  always  occurs  from  above  downward.  In  this  condition  the  two 
mucous  and  the  two  serous  surfaces  are  opposed  to  each  other,  so  that  a 
section  exhibits  three  cylinders,  one  within  the  other,  called  respectively — 
the  receiving  layer,  the  entering  layer,  and  the  returning  layer.  Sometimes 
the  intussusception  is  lateral  and  partial.  The  me- 
sentery belonging  to  the  invaginated  portion  lies 
between  the  middle  and  internal  layers.  By  the 
traction  of  the  mesentery,  the  central  part  of  the  in- 
testine is  curved  laterally.  Invagination  which  occurs 
during  the  last  moments  of  life  is  unimportant ;  it  is 
chiefly  found  in  children  who  die  of  brain  disease. 
The  occurrence  of  intussusception  is  regarded  by  most 
as  the  result  of  the  sudden  passage  of  a  spasmodically 
contracted  portion  of  the  intestine  into  a  flaccid 
Diagram  iiiustraling  intus-  °^  paralyzcd  portiou.  An  exaggeration  of  the 
susceptioE.  normal  peristaltic  wave   can   produce   it,   especially 

a' SrilTSer"'^'''^^^^'''^'  ^^^®"  *^^®^®  ^^  ^^^^^   gascous   distention  of  the  in- 

B.  Returning  layer.  tcstinc.      Some   obscrvcrs   state   that  it  is  the  par- 

C.  Receiving  layer.  ... 

alyzed  portion  which  is  thrust  forward  by  a  sudden 
increase  in  peristaltic  action  of  the  intestine. 

Its  most  frequent  seat  is  in  the  neighborhood  of  the  ileo-csecal  valve.  It 
may  occur  in  any  portion  of  the  intestine.  The  whole  colon  may  be  filled 
by  the  ileum,  and  the  latter  may  even  project  outside  of  the  anus.  It  is 
more  common  in  the  young ;  50  per  cent,  of  all  the  cases  occur  in  child- 
hood. Males  are  more  subject  to  it  than  females.'  The  mucous  membrane 
of  the  invaginated  portion  is  intensely  congested,  its  villi  are  swollen,  soft- 
ened, friable,  and  sometimes  united  by  a  pseudo-membrane.  The  single  and 
the  agminated  glands  are  hypertrophied,  infiltrated  with  fluid,  and  ulcerated 

'  In  the  Croonian  Lectures,  1657,  intussusception  appears  to  be  ileo-csecal  in  50  per  cent.,  iliac  in  28  pei 
cent.,  jejunal  in  4  per  cent.,  and  colonic  in  12  per  cent. 


Fig.  63. 


TNTESTTN'AL  OBSTRUCTION".  291 

at  the  centre.  The  snb-serous  cellular  tissue  is  infiltrated  with  blood,  and 
is  ecchymotic.  The  intestine  above  the  obstruction,  when  the  latter  has 
existed  for  some  time,  is  dilated.  In  many  cases  there  is  more  or  less  twist- 
ing besides  the  invagination.  Sometimes  blood  extravasates  into  the  mu- 
cous tissue  and  into  the  mesentery.  The  invaginated  portion  may  become 
gangrenous,  slough,  and  be  discharged  per  rectum.  During  the  sloughing 
the  peritoneal  cavity  may  be  opened. '  In  the  neighborhood  of  the  obstruc- 
tion the  mucous  membrane  may  be  the  seat  of  intense  catarrh.  Sometimes 
the  intussusception  is  restored.  Polypoid  growths  in  the  rectum  or  sig- 
moid flexure,  besides  inducing  intussusception,  may  themselves  cause  in- 
testinal obstruction. 

The  other  causes  within  the  intestine  which  induce  obstruction  are  can- 
cerous and  non-cancerous  stricture.  These  diminutions  in  the  calibre  of 
the  intestine  may  be  due  either  to  contraction  of  cicatrices,  or  to  infiltra- 
tion of  the  intestinal  walls.  Such  obstructions  are  developed  gradually, 
and  are  rarely  complete.  Intestinal  stricture  may  be  merely  a  thin  fold  of 
mucous  membrane,  or  four  or  five  inches  of  intestine  may  be  included. 
Above  the  stricture  there  is  well-marked  dilatation  and  hypertrophy  ;  below, 
atrophy  of  the  intestine.  The  accumulation  of  matter  above  a  stricture 
often  leads  to  ulceration  and  perforation.  About  seventy-five  per  cent,  of 
all  strictures  are  in  the  large  intestine,  and  most  of  these  are  m  the  rectum. 
About  half  of  all  intestinal  strictures  are  of  cancerous  origin.  Congenital 
stricture  is  a  surgical  disease. 

Intestinal  obstruction  may,  secondly,  have  its  cause  outside  the  wall  of  the 
intestine.  Folds  of  the  intestine  may  be  caught  in  bands  of  adhesion  formed 
by  an  old  peritonitis,  or  may  be  forced  through  openings  in  the  abdom- 
inal walls  and  become  strangulated,  causing  internal  or  external  hernia. 
The  small  intestine  is  strangulated  by  hernia,  diverticula,  and  bands  of 
new  formation,  more  frequently  than  the  large  intestine.  Internal 
strangulation  occurs  oftener  in  men  than  in  women.  It  may  occur  at 
any  age,  although  it  is  met  with  most  frequently  in  those  about  thirty. 
Volvulus  or  twisting  of  the  intestine  may  occur,  so  as  to  produce  in- 
testinal obstruction  ;  the  mesentery  or  a  coil  of  intestine  may  be  the 
axis  about  which  certain  parts  revolve.  Again,  a  coil  of  intestine  may, 
with  another,  form  a  knot.  Both  of  these  occurrences  are  most  frequent 
about  the  sigmoid  flexure.  An  abnormally  relaxed  mesentery  predisposes 
to  it.  Half  a  turn  is  sufficient  to  cause  obstruction.  In  the  old  the  sig- 
moid flexure  may  become  twisted,  by  shrinking  of  the  mesentery.  Any 
abdominal  tumor  may  induce  by  pressure  more  or  less  diminution  in  the 
calibre  of  the  intestine  and  intestinal  obstruction. 

The  third  class  of  causes  which  give  rise  to  intestinal  obstruction 
are  situated  wWiin  the  intestinal  canal.  Under  this  head  are  included 
obstruction  from  gall-stones,  impacted  faeces  and  foreign  bodies  of  various 
kinds.  Gall-stones  are  most  frequently  impacted  in  the  ileum  near  the 
ileo-csecal  valve  and  in  the  duodeno- jejunal  region.     The  larger  and  thin- 

1  In  one  instance  the  whole  of  the  caecum  and  ascending  colon  uloughed  away,  and  recovery  took  place. 
— 6uy''8  Ilogj).  Rfpo-'^i". 


292  DISEASES    OE   THE   DIGESTIVE   SYSTEM. 

ner  the  calculus,  the  more  liable  is  obstruction  to  occur.  In  some  cases 
gall-stones  cause  a  fatal  obstruction,  but  usually  the  obstructions  continue 
only  for  two  or  three  days.  Gall-stones  of  immense  size  have  been  found 
completely  plugging  an  intestine.  These  obstructions  rarely  have  their  seat 
in  the  large  intestine  and  are  met  with  more  frequently  after  fifty  years  of 
age,  and  in  females  oftener  than  in  males. 

Hardened  fffical  masses  mixed  with  the  phosphate  of  magnesia  and  lime, 
concretions  of  chalk  and  magnesia,  ammonio-magnesian  phosphate,  inspis- 
sated mucus,  and  large  oval  masses  consisting  chiefly  of  cholesterin,  are 
among  the  commoner  forms  of  the  so-called  "enteroliths."  Concretions 
of  hardened  fgeces  rarely  cause  fatal  obstruction.  The  list  of  foreign  bodies 
which  have  caused  intestinal  obstruction  is  very  large,  but  they  all  act  in 
the  same  way. 

The  changes  which  follow  all  forms  of  intestinal  obstruction,  are  dila- 
tation of  the  intestine  above,  and  atrophy  below,  the  seat  of  the  obstruc- 
tion. The  peritoneum  over  the  site  of  the  obstruction  is  the  seat  of  acute 
or  chronic  peritonitis.  G-angrene  may  occur  at  the  point  of  greatest  press- 
ure. There  is  always  more  or  less  extensive  intestinal  catarrh  in  every 
case  of  intestinal  obstruction. 

Symptoms. — The  symptoms  of  intestinal  obstruction  vary  with  its  seat, 
extent,  and  cause.  The  symptoms  which  are  common  to  all  varieties 
are  obstinate  constipation,  and  vomiting.  The  matters  vomited  consist 
first  of  the  contents  of  the  stomach,  then  mucus,  and  after  a  time  bile 
and  stercoraceous  matter.  The  accompanying  pain  varies  in  character 
and  intensity  :  sometimes  it  resembles  that  of  a  colic,  sometimes  that  of 
peritonitis.  When  the  obstruction  is  low  down  there  is  tympanitis.  When 
the  upper  part  of  the  small  intestine  is  obstructed  there  is  hiccough.  Ac- 
companying these  symptoms  there  is  prostration  and  often  collapse.  The 
skin  is  cold  and  the  countenance  assumes  an  Hippocratic  expression.  In 
a  few  cases,  portions  of  the  intestine  that  have  become  invaginated  can 
be  seen  projecting  from  the  anus.  A  careful  analysis  of  these  prominent 
symptoms  will  often  enable  one  to  determine  the  seat  and  character  of  the 
obstruction.  When  gall-stones  and  other  foreign  bodies  or  intestinal 
worms  obstruct  the  intestme,  constipation  will  come  on  suddenly. 

In  intussusception,  constipation  does  not  occur  suddenly,  for  thin  liquid 
faeces  are  able  to  pass  the  narrowed  orifice.  When  invagination  occurs  in 
the  small  intestine,  the  discharges  are  accompanied  by  a  copious  flow  of  blood. 
But  when  the  lower  bowel  is  invaginated  the  blood  is  mingled  with  the  dis- 
charges, and  they  are  dysenteric  in  character.  When  intussusception  be- 
comes chronic,  diarrhoea  may  develop  and  become  exhausting,  especially 
in  children.  When  sloughing  occurs  gangrenous  masses  mingled  with 
mucus  and  blood  will  be  discharged. 

If  thin  bands  of  fgeces  are  passed,  it  indicates  the  existence  of  an  in- 
complete stricture  of  the  large  intestine.  Slow  but  steadily  increasing 
constipation,  the  bands  of  the  fseces  becoming  gradually  smaller,  indicates 
the  growth  of  a  stricture  or  the  enlargement  of  a  tumor  compressing  the 
intestine.     If  obstruction  occurs  suddenly,  the  rectum  retains  its  contrac* 


INTESTINAL   OBSTRUCTION.  293 

tile  power  and  is  empty,  while  if  the  obstruction  comes  on  gradually  it  is 
patulous.  Vomiting  is  present  in  most  cases ;  when  the  obstruction  is  • 
high  up  the  vomiting  is  bilious,  and  occurs  within  an  hour  or  two  after  its 
occurrence  ;  when  near  the  cascum,  the  obstruction  is  accomj)anied  by 
faecal  or  stercoraceous  vomiting  ;  when  low  down,  two  or  three  da3's  may 
elapse  before  the  vomiting  occurs.  In  the  so-called  chronic  forms  of 
obstruction,  vomiting  occurs  at  intervals,  and  is  more  persistent  the  higher 
the  obstruction.  Copious  stercoraceous  vomiting  is  evidence  that  the 
obstruction  is  at  the  ileo-csecal  valve.  ^  In  children  vomiting  occurs  very 
readily,  and,  with  the  pain,  is  the  first  well-marked  sign  of  the  obstruc- 
tion. When  gall-stones  are  lodged  high  up,  vomiting  comes  on  early  and 
continues  until  death  occurs,  or  the  stone  is  dislodged. 

Enteroliths  usually  give  rise  to  typhlitic  symptoms.  The  pain  which 
accompanies  or  precedes  the  vomiting  is  colicky  or  paroxysmal  at  first,  after- 
ward it  becomes  constant  and  severe.  Sometimes  patients  can  locate  the  spot 
where  the  pain  originates,  at  other  times  it  resembles  a  stitch  in  the  side. 
When  the  constriction  has  come  on  slowly  the  j)ain  resembles  that  of  ordi- 
nary colic.  If  the  small  intestine  near  the  csecum  or  jejunum  is  strangulated, 
there  is  pain  in  the  region  of  the  umbilicus.  When  the  colon  is  obstructed 
the  pain  is  located  at  the  seat  of  the  obstruction.  Pain  in  the  groin  or  in 
the  left  iliac  fossa  indicates  obstruction  at  the  sigmoid  flexure.  There  is 
usually  no  tenderness  at  the  onset.  When  tenderness,  local  or  diffuse,  is 
extreme,  peritonitis  is  indicated. 

In  all  cases  except  those,  where  the  obstruction  is  near  the  duodenum,  the 
abdomen  gradually  becomes  distended  from  gaseous  accumulation  in  the 
intestine  above  the  seat  of  the  obstruction, — tympanitis.  It  occurs  first  near 
the  obstruction.  When  twisting  of  the  intestine  occurs  the  portion  consti- 
tuting the  loop  often  forms  a  tympanitic  tuhaor.  The  tympanitic  note  is 
readily  elicited  as  the  abdominal  muscles  become  rigid.  Vomiting  relieves 
the  tympanitis  to  a  greater  or  less  degree.  The  higher  the  obstruction 
the  greater  the  relief  from  the  vomiting. 

Intestinal  cancer,  large  gall-stones,  faecal  masses,  and  other  abdominal 
tumors  which  gradually  compress  the  intestine  may  usually  be  accurately 
located  and  definitely  mapped  out.  invagination  sometimes  gives  rise  to  a 
soft,  sausage-shaped  tumor,  which  can  be  distinctly  felt,  especially  when  it 
occurs  at  the  csecum.  In  intussusception  of  the  small  intestine  a  central 
tumor  may  often  be  felt  near  the  umbilicus.  If  invagination  occurs  low 
down,  the  slit-like  opening  in  the  invaginated  portion  may  be  felt  per  rec- 
tum. Faecal  tumors  along  the  line  of  the  colon  are  quite  distinct  on  pal- 
pation, and,  while  firm,  continued  pressure  gives  no  pain,  their  situation 
and  form  may  gradually  be  altered ;  attention  to  these  points  will  prevent 
mistaking  faecal  for  malignant  tumors. 

Percussion  over  these  tumors  elicits  dulness  corresponding  to  their  extent. 
If  the  obstruction  is  in  the  duodenum,  there  is  an  almost  total  suppression 

'  Brinton  Bug<,'ests  that  a  double  current  is  produced;  the  intestinal  contents  are  propelled  along  the 
wall  of  the  intestine  until  they  meet  the  obstruction,  and  then  a  return  current  passes  up  in  the  centre  of 
the  intestine.  This  retrofrrade  movement  continues  until  the  vomited  matters  are  the  same  as  those  at  the 
Beat  of  the  stricture. 


394  DISEASES   OF   THE    DIGESTIVE   SYSTEM. 

of  urine ;  when  in  the  jejunum  or  ileum,  there  is  marked  diminution  ; 
but  when  the  lower  bowel  is  occluded  the  flow  is  abundant  and  limpid.  In 
many  cases  of  intestinal  obstruction  there  is  a  sudden  shock  at  the  time  of 
its  occurrence,  similar  to  the  shock  in  peritonitis  ;  this  is  often  followed  bj 
symptoms  of  collapse.  During  the  whole  course  of  intestinal  obstruction, 
the  temperature  is  rarely  elevated.  If  the  obstruction  is  complete,  the  face 
becomes  ''drawn,"  the  extremities  and  the  surface  cool,  the  pulse  rapid 
and  small,  the  patient  lies  on  his  back  witli  the  knees  flexed,  and  carefully 
avoids  movements  which  induce  pain  and  vomiting.  Later  on  symptoms  of 
collapse  are  developed,  the  breathing  becomes  rapid  and  superficial,  thirst 
is  intense,  the  voice  is  husky,  the  pulse  becomes  imperceptible,  and  the 
patient  dies  as  in  collapse,  from  peritonitis  which  will  be  found  in  most 
cases  after  death.  If  the  obstruction  is  in  the  small  intestine  hiccough  is 
a  constant  and  annoying  symptom.  The  mind  is  undisturbed  to  the 
last.  In  slowly  developed  intestinal  obstruction,  as  in  cancer-strictures 
and  compression  from  tumors,  the  patient  loses  flesh  and  strength,  becomes 
anaemic  and  melancholic,  and  the  countenance  bears  the  aspect  of  one 
suffering  from  malignant  disease.  Torsion  or  twisting  of  the  intestine 
is  attended  by  acute  and  rapidly  fatal  enteritis. '  In  these  cases  all  the 
symptoms  of  severe  enteritis  are  present. 

Differential  Diagnosis.  — It  is  important  in  every  case  to  determine  the  seat 
and  cause  of  the  intestinal  obstruction.  Intussusception  occurs  most  fre- 
quently in  children,  it  begins  suddenly  with  intense  colicky  pains,  and  there 
is  blood  mingled  with  the  scanty  mucous  discharges.  Faecal  vomiting  occurs 
early,  and  there  is  commonly  a  distinct  tumor,  firm  pressure  on  which  some- 
times relieves  the  pain  ;  in  a  few  cases  the  invagination  may  be  determined 
by  a  rectal  examination.  The  patient  rapidly  passes  into  collapse.  When 
this  train  of  symptoms  occurs  suddenly  in  a  child,  previously  healthy,  and 
without  appreciable  cause,  intussusception  may  be  suspected. 

Internal  hernia  occurs  suddenly.  The  pain  is  fixed  at  one  point  and 
paroxysmal  in  character,  faecal  vomiting  comes  on  after  a  few  hours,  accom- 
panied by  obstinate  constipation  and  rapidly  developing  tympanitis  ;  in  a 
day  or  two  the  patient  may  pass  into  a  state  of  collapse.  The  large  in- 
testine is  usually  empty.  In  a  few  cases  the  patient  will  have  "felt  some- 
thing give  way  in  the  abdominal  cavity."  Its  symptoms  resemble  those  of 
an  external  strangulated  hernia  and  intussusception  combined. 

Twisting,  volvulus,  and  the  sudden  incarceration  of  loops  of  the  intestine 
under  bands  of  adhesion  or  diverticula  are  attended  by  similar  symptoms. 

Foreign  bodies  usually  have  their  seat  in  the  caecal  region  and  give  rise 
to  typhlitic  tumors.  When  gall-stones  are  the  cause  of  the  obstruction 
there  is  usually  a  history  of  hepatic  colic,  and  the  seat  of  the  obstruction  is 
high  up  ;  this  will  be  indicated  by  the  vomiting  and  urinary  suppression. 

Obstruction  from  cicatrices,  and  from  the  pressure  of  tumors  is  of  slow 
growth,  there  will  be  the  history  of  frequent  attacks  of  constipation,  gradu- 
ally increasing  in  duration  and  severity,  coils  of  distended  and  displaced 

'  Bristowe  supposes  the  enteritis  may  occur  first,  may  weaken  the  parts,  and  that  the  volvulus  is  a 
eecondary  phenomenon. 


INTESTINAL   OBSTRUCTION.  295 

intestine  are  easily  detected,  the  centre  of  the  abdomen  has  a  dough}'  feel, 
and  a  tumor  can  often  be  made  out. 

Intestinal  obstruction  may  be  mistaken  for  colic  (or  enteralgia)  peri- 
tonitis, exterfial  hernia,  acute  poisoning  (as  from  arsenic,  antimony,  etc.), 
hepatic  or  renal  colic,  and  enteritis.  In  colic  the  discharges  from  the 
bowels  will  be  normal,  or  there  may  be  diarrhoea.  In  intestinal  obstruction 
there  is  obstinate  constipation.  The  pain  of  colic  is  of  short  duration  and 
is  usually  relieved  by  pressure,  while  in  intestinal  obstruction  the  pain  is 
persistent  and  not  relieved  by  pressure.  Fsecal  vomiting,  tympanitis,  and 
symptoms  of  collapse  are  present  in  obstruction  and  absent  in  colic. 

Peritonitis  is  attended  by  a  rise  in  temperature,  by  great  tenderness  on 
pressure,  by  a  tense,  hard,  wiry  pulse,  and  by  rigidity  of  the  abdominal 
walls  ;  while  obstruction,  if  it  begins  with  colicky  pains,  is  soon  attended 
by  fsecal  vomiting,  the  pain  is  localized,  there  is  a  sub-normal  temperature 
and  more  distention  of  the  abdomen. 

Internal  hernia  may  be  confounded  with  femoral  or  inguinal  hernia  ;  a 
careful  examination  of  the  inguinal  regions  and  the  history  of  the  case  are 
usually  sufficient  to  establish  a  diagnosis. 

In  cases  of  acute  poisoning  there  will  be  evidences  in  the  mouth  and  phar- 
ynx of  the  action  of  an  irritant  poison  ;  the  gastric  symptoms,  especially  the 
sense  of  heat  in  the  epigastrium,  will  be  marked  ;  there  will  be  diarrhoea,  no 
faecal  vomiting,  no  tympanitis,  and  the  vomited  matters  will  contain  traces  of 
the  poison. 

.  In  hepatic  colic  the  pain  is  persistent  and  radiates  from  the  region  of  the 
gall-bladder  to  the  back.  There  is  no  fsecal  vomiting  and  no  tympanitis, 
but  the  stools  are  clay-colored,  and  the  calculus  may  be  detected  in  the 
fseces  after  the  attack  ceases.  The  urine  contains  bile,  and  if  the  attack  is 
prolonged  jaundice  occurs. 

In  renal  colic  the  bowels  are  normal,  the  pain  shoots  from  the  back  down 
the  ureter  to  the  end  of  the  penis,  and  the  testicle  on  the  affected  side  is  re- 
tracted. Relief  immediately  follows  the  passage  of  the  calculus  into  the 
bladder,  which  is  followed  by  a  copious  flow  of  bloody  urine  ;  in  intestinal 
obstruction  there  is  no  hsematuria,  no  symptoms  referable  to  the  urinary  or- 
gans, the  bowels  are  constipated,  and  there  is  tympanitis  and  fsecal  vomit- 
ing. 

Enteritis  is  distinguished  from  intestinal  obstruction  by  copious  mucous 
discharges  from  the  bowels,  by  the  rise  in  temperature,  and  the  absence  of 
fsecal  vomiting,  excessive  tympanitis,  and  the  symptoms  of  collapse. 

Prognosis. — The  length  of  time  for  which  an  intestinal  obstruction  may 
exist  before  causing  death  varies  with  its  seat  and  its  character  ;  a  weak  child 
may  die  in  eight  or  ten  hours  from  the  shock  of  intussusception,  and  an 
adult  whose  intestine  is  gradually  being  occluded  by  the  presence  of  some 
slow-growing  tumor,  may  live  for  months.  As  a  rule,  the  nearer  the  stom- 
ach the  obstruction,  the  more  rapidly  death  ensues.  Volvulus,  strangula- 
tion, internal  hernia  of  the  small  intestine,  and  obstruction  by  large  gall- 
stones and  enteroliths  induce  death  more  rapidly  than  stricture,  compres- 
sion, and  intussusception,  especially  of  the  large  bowel.     Intussusception 


296  DISEASES   OF   THE    DIGESTIVE    SYSTEM. 

may  be  recovered  from  when  a  gangrenous  process  throws  off  the  invagina* 
ted  portion,  and  it  is  possible  for  it  to  slip  back  into  its  normal  relations. 
The  prognosis  is  favorable  in  intussusception  when  a  portion  of  the  invagi- 
nated  bowel  is  discharged,  It  is  better,  the  lower  the  seat  of  the  obstruc- 
tion. Of  all  forms  of  obstruction,  ftecal  tumors  are  the  least  grave.  The 
complications  of  intestinal  obstruction  are  enteritis,  with  or  without  per- 
foration, septicaemia,  phlebitis,  ulceration  and  gangrene  within  the  canal, 
and  perforation  of  the  intestine  above  the  stricture.  After  recovery  from 
the  primary  obstruction,  the  attending  peritonitis  may  cause  permanent 
constriction  of  the  intestine.  Another  sequela  is  the  formation  of  internal 
fistulae. 

Treatment. — Whenever  there  is  reason  to  suspect  intestinal  obstruction 
of  a  non-faecal  origin,  free  catharsis  should  be  avoided.  It  is  better  not  to 
relieve  a  simple  constipation,  than  to  attempt  to  force  fseces  through  an 
internal  hernia.  AVhatever  may  be  the  seat  or  character  of  the  obstruction, 
the  therapeutical  indications  are  the  same,  whereas  a  knowledge  of  the  site 
and  variety  of  the  obstruction  is  demanded  before  surgical  interferemce 
should  be  resorted  to.  E.est  is  demanded  in  every  case  ;  hence  opium  is  to 
be  given  in  sufficient  quantities  to  relieve  pain.  The  more  sudden  and 
severe  the  onset,  and  the  more  urgent  the  symptoms,  the  more  serviceable 
is  opium.  The  condition  of  the  patient  alone  regulates  the  quantity  to  be 
administered. 

Nourishment  should  be  given  per  rectum  in  the  form  of  defibrinized 
"blood,  and  peptoni_ed  fluids.  Each  injection  should  contain  from  three  to 
five  grains  of  chloral,  to  retard  decomposition.  Ice  may  be  given  to  relieve 
the  thirst.  If  the  tympanitis  is  excessive,  it  may  be  relieved  by  aspiration, 
or  by  the  introduction  of  a  tube  into  the  colon.  Instead  of  ice,  warm  com- 
presses seem  to  relieve  the  pain  and  soreness,  but  they  have  no  other  value. 
There  is  no  objection  to  saline  laxatives  in  stricture  or  in  compression, 
where,  though  not  wholly  occluded,  the  intestine  is  gradually  narrow- 
ing, and  only  a  small  opening  remains  through  which  liquid  fasces  can 
pass. 

When  the  obstruction  is  faecal,  opium  should  not  be  given ;  the  bow- 
els should  be  acted  on  by  those  drugs  which  produce  copious  watery 
evacuations  without  drastic  action ;  at  the  ^ame  time  the  rectum  must  be 
emptied  by  mechanical  means,  or  by  enemata  of  warm  water  and  glycerine. 
Much  patience  is  often  required  to  remove  these  faecal  obstructions.  The 
most  efficient  method  of  mechanically  overcoming  obstruction  is  to  make 
large  injections  of  warm  water  through  long  rubber  tubes,  which  must  be 
inserted  as  far  as  possible.  In  order,  however,  to  overcome  by  enemata  an 
obstruction  situated  high  up,  the  patient  must  be  brought  under  the  influ- 
ence of  ether  or  chloroform,  and  during  the  administration  of  the  enema 
careful  manipulation  of  the  bowels  must  be  practised.  Taxis  is  to  be  prac- 
tised according  to  the  rules  which  surgery  lays  down  for  the  reduction  of 
hernia.  Instead  of  warm  water,  air  and  gas  have  been  injected  in  order  to 
distend  the  intestines.  Whatever  injection  is  employed,  it  should  be  thrown 
in  very  slowly,  and  in  very  large  quantities.     It  has  been  suggested  to  de« 


WAXY    DEGBNEUATION    OP   THE   INTESTINES.  297 

velop  gas  inside  the  patient  by  successively  injecting  solutions  of  soda 
bicarbonate  and  of  tartaric  acid  ;  rupture  of  the  intestine  may  result  from 
such  a  procedure.  Before  injections  are  given  or  taxis  practised,  it  is  well 
for  the  patient  to  take  a  prolonged  and  moderately  hot  bath.  As  an  aid  to 
the  reduction  of  an  intestinal  obstruction,  the  hips  may  be  elevated  or  the 
patient  may  assume  the  knee-elbow  position.  The  use  of  the  constant  cur- 
rent is  advocated  by  some,  to  produce  active  peristalsis ;  this  must  not  be 
resorted  to  unless  there  is  no  danger  of  exciting  peritonitis  by  the  active 
peristalsis.  If  the  long  tube  is  used  for  the  purpose  of  giving  injections,  it 
must  be  introduced  with  the  utmost  care,  for  perforation  has  been  caused 
by  its  careless  introduction. 

If  at  any  time  symptoms  of  collapse  come  on,  alcoholic  stimulants,  musk, 
ammonia,  etc.,  should  be  freely  administered.  As  regards  surgical  meas- 
ures, colotomy  and  laparotomy  are  the  proceedings  which  have  been  pro- 
posed. The  mortality  after  laparotomy  is  not  exactly  known,  some  statistics 
showing  68  |)er  cent.,  others  73  per  cent.,  and  still  others  75  per  cent,  of 
deaths.  Laparotomy  is  applicable  especially  in  acute  intussusception,  and 
should  be  performed  with  as  little  delay  as  possible.  The  dangers  from  co- 
lotomy seem  to  be  less  than  those  of  any  other  operation.  The  statistics  of 
lumbar  colotomy  exhibit  the  low  rate  of  33  per  cent,  of  deaths.  Laparo- 
enterotomy  has  a  mortality-rate  below  sixty,  but  concerning  laparo-colot- 
omy,  laparo-typhlotomy,  etc.,  the  number  of  operations  is  too  small  to  give 
reliable  statistics. 

WAXY    DEGENEEATIOX    OF    THE    USTTESTHSTES. 

Statistics  show  that  after  the  kidney,  spleen,  and  liver,  the  intestines  are 
most  frequently  the  seat  of  waxy  degeneration. 

Morbid  Anatomy. — The  primary  seat  of  amyloid  change  in  the  intestines 
is  in  the  arterioles.  The  small  intestine  is  more  often  involved  than  the  large. 
The  mucous  membrane  is  pale,  shining,  and  slightly  cedematous  ;  on  the 
application  of  the  iodine  test  small  maroon  colored  spots  appear  in  the  villi, 
where  the  earliest  changes  occur  ;  later  the  muscular  coat  is  involved,  and 
finally  the  entire  wall  of  the  intestine  is  fused  into  a  homogeneous  mass. 
Peyer's  patches  are  less  affected  than  the  surrounding  tissues,  but  there  is 
annular  infiltration  about  the  solitary  glands. 

Etiology. — Its  causes  are  all  those  conditions  which  predispose  to  waxy 
changes  in  other  organs.  It  is  usually  a  late  complication  of  waxy  kidney 
and  liver. 

Symptoms. — Its  symptoms  are  masked  by  those  of  waxy  liver  and  kidney, 
with  which  it  is  always  associated.  When  general  amyloid  degeneration  of 
the  entire  intestinal  canal  exists,  the  nutritive  disturbances  are  great ;  ex- 
haustion, emaciation,  and  ansemia  are  more  marked  than  in  any  other  con- 
dition. The  countenance,  the  appearance  of  the  skin,  and  the  other  consti- 
tutional symptoms  are  identical  with  those  of  waxy  liver  and  kidney,  hut 
in  addition  to  these  there  is  a  serous  diarrhoea  which  is  persistent  an^ 
exhausting. 


298  DISEASES   OF   THE    DIGESTIVE   SYSTEM. 

Differential  Diagnosis. — The  diagnosis  is  made  by  the  presence  of  diar 
rhoea  associated  with  the  evidences  of  waxy  changes  in  other  organs. 

Prognosis. — This  is  very  unfavorable  ;  more  so  than  when  the  amyloid 
change  is  confined  to  other  organs,  for  it  indicates  that  the  changes  which 
usually  precede  a  fatal  termination  have  already  occurred  in  those  organs. 

Treatment. — The  treatment  is  altogether  palliative ;  the  diet  should  be  re- 
stricted to  meat  and  milk  taken  in  small  quantities  and  at  short  intervals. 
In  addition  to  the  general  constitutional  treatment  of  waxy  degeneration, 
the  diarrhoea  may  be  checked  by  the  vegetable  astringents — hgemafcoxylon, 
tannin,  and  catechu,  or  when  these  fail,  the  mineral  astringents  can  be 
given.  Iodide  of  potassium  and  iron  will  be  found  especially  beneficial  in 
these  cases. 

CAlSrCEE    OF    THE    INTESTINE. 

Carcinoma  is  the  most  common  variety  of  intestinal  neoplasm.  It  is  less 
frequent  than  carcinoma  of  the  stomach,  and  is  almost  always  primary.  In 
rare  instances,  it  may  be  secondary  to  cancer  of  the  peritoneum,  uterus,  or 
bladder.  It  almost  exclusively  affects  the  large  intestine  ;  the  rectum  is 
its  most  frequent  seat,  then  the  anus,  the  csecum,  the  sigmoid  flexure  of 
the  colon,  and  lastly  the  duodenum  and  jejunum. 

Morbid  Anatomy. — The  primary  development  of  intestinal  cancer  is  com- 
monly in  the  mucosa  and  extends  into  the  submucous  connective-tissue  ; 
the  infiltration  extends  in  a  ring  around  the  intestine.  Sometimes  its 
primary  development  is  in  the  epithelium  of  the  follicles.  It  may  involve 
an  inch  or  three  or  four  inches  of  the  intestine.  In  any  case  it  causes 
more  or  less  diminution  in  the  calibre  of  the  intestine  ;  the  intestinal  wall 
becomes  infiltrated  and  ulceration  may  be  established,  which  will  destroy 
the  mucous  membrane  covering  the  cancerous  mass,  and  temporarily  re- 
move the  intestinal  obstruction.  Frequently  cancerous  masses  project  from 
the  anus  looking  like  cutaneous  growths  about  its  margin,  or  they  may 
project  from  the  anus  in  the  form  of  fungous  masses. 

Before  ulceration  occurs  scirrhus  cancer  presents  a  smooth,  nodulated 
surface  ;  encephaloid  is  soft,  vascular,  and  often  forms  a  tumor,  or  series  of 
tumors  projecting  into  the  intestine  ;  these  tumors  are  round,  lobulated  or 
villous.  Often  where  the  upper  part  of  the  rectum  seems  to  be  the  seat  of 
cancer,  the  disease  will  be  found  to  have  its  seat  at  the  sigmoid  flexure, 
which  has  been  pushed  down  into  the  pelvis,  as  the  result  either  of  the 
obstruction  which  it  has  caused,  or  of  its  own  weight. 

When  ulceration  occurs,  fungoid  masses  may  spring  up  upon  the  elevated 
surface  and  lobulated  tumors  may  rapidly  develop,  or  a  smooth  excavation 
may  be  fojmed,  with  hard,  well-defined  edges.  Cancerous  ulcerations  may 
extend  through  the  intestinal  walls,  and  cause  peritonitis  or  fgecal  abscess, 
or  establish  communication  with  the  bladder,  urethra,  uterus,  vagina,  or 
with  other  portions  of  the  intestine.  Scirrhus,  more  often  than  either  of 
the  other  varieties,  produces  stricture  of  the  intestine.  In  a  few  cases  both 
large  and  small  intestines  are  studded  with  small  cancer-nodules,  whose  fa- 
vorite locality  seems  to  be  the  Peyerian  patches.     In  any  form  of  cancer. 


CANCER   OF   THE   INTESTINE.  299 

esj'iecially  scirrhus,  there  may  be  great  distention  of  the  intestine  above  the 
seat  of  the  cancer.  There  may  be  catarrh  of  the  intestinal  mucous  mem- 
brane above  and  below  the  seat  of  the  cancer.  In  cancer  of  the  rectum  the 
disorganization  may  be  so  rapid  and  extensive  that  dilatation  occurs  at  the 
site  of  the  cancer.  Stricture,  hemorrhage,  perforation,  fistulae,  and  matting 
together  and  deformity  of  the  organs  in  the  neighborhood,  are  common 
pathological  sequelae  of  intestinal  cancer.  The  neighboring  lymph  glands 
are  always  more  or  less  involved.  If  cancer  commences  outside  of  the  in- 
testine and  extends  inward,  it  will  be  most  extensive  along  the  line  of  the 
attachment  of  the  peritoneum.  The  loose  tissue  around  the  rectum,  cae- 
cum, or  duodenum  may  be  so  extensively  infiltrated  that  the  intestine 
within  is  merely  a  narrow  rigid  channel. 

Etiology. — Intestinal  cancer  is  rare  before  thirty,  and  more  frequent  be- 
tween forty  and  sixty.  Sex  has  no  marked  influence  over  its  development ; 
statistics  give  cancer  of  the  rectum  as  occurring  three  and  one-half  times 
as  often  in  males  as  in  females.  Its  etiology  is  obscure  ;  cancer  of  the 
colon  seems  to  develop  most  frequencly  in  the  cicatrix  of  an  ulcer  or  after 
traumatism. 

Symptoms. — The  symptoms  of  intestinal  cancer  vary  with  its  seat.  It 
comes  on  insidiously,  with  vague  abdominal  pains,  a  sense  of  unrest,  and  a 
marked  decline  in  health  and  strength. 

Duodenal  cancer  simulates  hepatic  and  gastric  cancer ;  it  is  often 
attended  by  coffee-ground  vomiting  coming  on  several  hours  after  taking 
food.  Sometimes  there  will  be  jaundice  from  pressure  of  the  tumor  on 
the  common  bile  ducts.  The  tumor  may  be  felt  near  the  cartilage  of  the 
right  tenth  rib. 

Cancer  of  the  ccecum  is  attended  by  pain  in  the  right  iliac  fossa  and  a. 
tumor  will  be  felt  in  the  region  of  the  CEecam,  usually  much  larger  than  the 
cancerous  mass  and  formed  by  the  accumulation  of  faeces  above  the  stenosed 
portion.  Manipulation  in  these  subjects  causes  movement,  and  diminution 
in  size  of  the  fsecal  tumor,  leaving  distinct  the  cancer  nodule,  which  is  ten- 
der. In  colloid  cancer  of  the  caecum,  the  tumor  is  large,  hard,  and  smooth. 
In  most  instances  there  is  "  tympanitic  dulness  "  on  percussion,  over  th& 
tumor. 

Cancer  of  the  rectum  first  causes  the  symptoms  due  to  a  stricture,  the  bow- 
els are  constipated  and  the  stools  are  not  cylinders,  but  narrow  bands.  "  Sa- 
cral" pains  darting  down  the  limbs,  of  a  stabbing,  lancinating  character, 
giving  rise  to  most  intense  suffering,  are  often  present.  When  the  bowels 
move,  there  is  a  sensation  as  if  the  parts  were  being  burned,  accompanied  by 
more  or  less  tenesmus.  The  bowels  usually  are  at  first  constipated,  but  some- 
times an  irregular  diarrhoea  is  present  from  its  commencement ;  later  in  all 
cases,  there  is  diarrhoea,  the  thin  stools  containing  blood,  pus,  m^^cus,  and 
shreds  of  sloughing  and  gangrenous  matter.  The  invasion  of  the  sphincter 
is  followed  by  loss  of  power  to  retain  the  faeces,  and  then  a  brownish,  watery, 
offensive  fluid  continually  oozes  from  the  anus.  Communications  with  the 
vagina  or  urethra  are  followed  by  the  escape  of  liquid  faeces  through  these - 
channels.     A  physical  examination  of  the  rectum  (the  patient  being  ether- 


300  DISEASES    OP   THE    DIGESTIVE    SYSTEM. 

ized)  reveals  numerous  hard  nodular  masses,  with  a  cartilaginous  feel,  or  a 
soft,  fungoid,  friable  mass  having  a  hard  base.  A  portion  of  the  mass 
removed  and  examined  microscopically,  will  usually  decide  its  character. 
At  times,  an  irregular,  angry  red,  fungoid  mass  protrudes  from  the  anus, 
and  on  inspection  it  is  readily  recognized  as  cancer.  The  finger  may 
detect  a  septum  thrown  across  the  gut,  or,  in  colloid  disease,  a  large, 
round,  smooth  tumor  projects  forward,  to  occlude  the  rectum.  The 
symptoms  of  epithelial  cancer  of  the  rectum  are  the  least  urgent  and 
serious  in  appearance  of  all  forms  of  rectal  cancer.  It  may  exist  for  a 
long  time  without  producing  either  constipation,  pain,  or  cachexia. 

The  prominent  symptoms,  which  are  common  to  all  varieties  of  intes- 
tinal cancer,  are  pain,  cachexia,  constipation,  and  the  presence  of  a  tumor. 
As  soon  as  the  cancerous  development  has  reached  sufficient  size  to  cause 
pressure,  there  is  constant  pain,  which  may  be  dull,  vague,  and  dragging 
in  character,  or  sharp  and  lancinating.  In  upper  rectal  and  sigmoid  can- 
cer, the  seat  of  pain  is  in  the  left  iliac  fossa  and  loins  ;  in  lower  rectal  can- 
cer, it  is  in  the  loins,  upper  part  of  the  thigh,  and  sometimes  in  the  testes. 
In  other  situations  the  pain  is  at  the  site  of  the  cancer.  A  cachexia 
usually  develops  with  the  commencement  of  the  cancerous  development, 
accompanied  by  emaciation,  loss  of  strength  and  flesh  ;  the  skin  is  dry, 
'^ scaly,"  and  assumes  the  dirty  greenish  ''cancer  color,"  the  hair  and 
nails  become  harsh  and  dry,  and  easily  split.  With  the  growth  of  the 
cancerous  mass,  exhaustion  and  cachexia  gradually  and  steadily  increase, 
and  in  some  cases  are  the  direct  cause  of  death.  As  Avith  cancer  elsewhere, 
the  disease  may  run  its  entire  course  without  pain,  anaemia,  or  marasmus. 
Constipation  is  the  rule  :  at  first  there  is  fiatulence,  nausea,  and  vomiting  ; 
later  these  symptoms  vary  according  to  the  locality  of  the  obstructions,  as, 
for  example,  if  the  cancerous  growth  is  high  up  in  the  rectum,  or  at  the 
sigmoid  flexure  there  is  marked  distention  of  the  colon.  A  free  evacu- 
ation of  the  bowels  temporarily  relieves  the  distress ;  diarrhoea  may  alter- 
nate with  the  constipation,  attended  by  rapidly  increasing  exhaustion.  In 
some  instances  intestinal  cancer  is  attended  only  by  the  symptoms  of  intes- 
tinal obstruction.  Cancer  high  up  in  the  colon  is  more  often  attended  by 
diarrhoea  than  in  the  other  localities.  In  long-standing  cases  of  intes- 
tinal cancer,  the  lymphatic  glands  in  the  neighborhood  of  the  cancer 
will  be  found  enlarged,  and  there  will  be  occasional  intestinal  hemor- 
rhages, dropsy,  and  thrombosis  of  the  neighboring  veins.  The  discovery 
of  a  tumor  along  the  line  of  the  intestine  is  essential  to  the  diagnosis  of 
intestinal  cancer.  When  it  is  developed  in  the  ascending  and  descending 
colon  and  caecum,  the  tumor  is  always  felt  in  the  normal  position  of  the 
intestines,  but  when  it  is  developed  in  the  small  intestine  and  transverse 
colon,  the  mobility  of  the  parts  and  the  weight  of  the  tumor  may  cause  it 
to  occupy  an  abnormal  position. 

Differential  Diagnosis. — Cancer  of  the  duodenum  cannot  at  first  be  dis- 
tinguished from  hepatic  or  gastric  cancer  ;  later  on,  however,  the  situation 
of  the  tumor,  the  character  of  the  vomiting,  and  the  time  of  its  occurrence 
after  meals  will   often   enable  one  to   recognize  its  seat  and  character. 


KECTITIS  :    PROCTITIS.  301 

Cancer  of  the  pancreas  cannot  be  distinguished  from  that  of  the  duo- 
denum. Abdominal  a7ieurism  may  be  distinguished  from  a  pulsating 
duodenal  cancer  by  the  alteration  which  it  causes  in  the  pulsation  of  the 
femoral  artery. 

Cancer  of  the  intestine  is  to  be  distinguished  from  floating  kidney  by  the 
absence  of  the  cancerous  cachexia  in  the  latter,  and  fi-om  the  fact  that  the 
kidney  tumor  is  heliind  and  the  cancer  tumor  m.  front  of  the  intestine.  Can- 
cer maybe  distinguished  from  enteritis,  colic  or  intestinal  ulceration  by  the 
cachexia,  tumor,  and  constipation.  The  age  of  the  patient  and  a  history  of 
gradual  development  will  aid  in  the  diagnosis.  The  diagnosis  of  cancer  of 
the  rectum  from  other  growths  in  it,  or  from  proctitis  or  hemorrhoids,  is 
made  by  a  digital  and  ocular  examination  of  the  rectum  and  by  a  microscop- 
ical examination  of  a  portion  of  the  mass. 

Prognosis. — The  prognosis  is  always  unfavorable.  When  the  disease  is 
situated  in  the  rectum  or  at  the  anus,  surgical  interference  may  prolong 
life.  After  it  is  possible  to  recognize  the  existence  of  cancer  of  the  intestine 
a  fatal  termination  will  generally  be  reached  within  a  year. 

Duodenal  cancer  gives  rise  to  more  distressing  symptoms,  and  is  more 
rapidly  fatal  on  account  of  its  situation,  than  any  other  variety.  Death 
may  result  from  exhaustion  and  anaemia  (''cancer  marasmus")  from  small 
hemorrhages,  or  from  a  single  large  hemorrhage,  from  rupture  of  the 
intestine  and  peritonitis,  and  from  secondary  complications.  Death  some- 
times occurs  with  all  the  symptoms  of  sudden  intestinal  obstruction,  at- 
tended by  large  accumulations  of  faeces  above  the  site  of  the  cancer. 
Pyaemia,  thrombosis,  and  embolism  are  sometimes  the  immediate  causes  of 
death. 

Treatment. — The  treatment  of  intestinal  cancer  is  only  palliative.  The 
diet  should  be  restricted  to  such  articles  as  will  produce  the  least  faecal 
matter,  such  as  milk,  nutritive  broths,  and  eggs  ;  saline  waters  should  always 
be  taken  freely  to  keep  the  faeces  semi-fluid,  without  at  any  time  causing 
diarrhoea.  Pain  must  be  relieved  by  the  hypodermatic  use  of  morphine  ; 
hemorrhages  may  be  checked  by  balsams  and  astringents.  If  at  any  time 
hardened  faeces  collect  at  the  sigmoid  flexure,  warm  water  injections  are  to 
be  given  through  a  long  tube.  The  formation  of  an  artificial  anus,  the 
operations  of  colotomy,  typhlotomy,  etc.,  are  surgical  means  for  prolonging 
life.  Extirpation  of  the  rectum  for  cancer  has  been  performed  with  suc- 
cess. 

BECTITIS:    PEOCTITIS. 

Eectitis,  or  proctitis,  is  a  localized  catarrh  of  the  rectum  ;  it  rarely  occurs 
except  as  the  result  of  traumatism,  or  from  the  pressure  of  foreign  bodies. 
It  may  be  acute  or  chronic. 

Morbid  Anatomy. — The  morbid  changes  in  rectal  catarrh  are  similar  to 
those  which  occur  in  catarrh  of  other  portions  of  the  intestinal  canal.  The 
colon  is  distended,  and  there  may  be  faecal  impaction  above  the  sigmoid 
flexure.  The  results  of  chronic  rectal  catarrh  are  periproctitis,  peritonitis, 
abscess,  fistulas  into  the  adjacent  tissues  and  organs,  cicatricial  contrac- 


302  DISEASES   OF  THE   DIGESTIVE   SYSTEM. 

tions,  and  thrombosis  of  the  hemorrhoidal  veins,  with  subsequent  emholit 
hepatic  abscess. 

Etiology. — Acute  catarrh  of  the  rectum  may  result  from  blows,  the  pres. 
ence  of  foreign  bodies,  irritation  produced  by  hardened  faeces,  and  the  long 
continued  use  of  purgatives  which  act  on  the  lower  bowel.  It  may  arise 
from  an  extension  of  inflammation,  as  in  enteritis  or  dysentery ;  in  the 
latter  case  it  will  be  accompanied  by  ulceration  ;  some  regard  rectitis  as  a 
mild  form  of  dysentery,  but  it  has  none  of  the  constitutional  symptoms  of 
dysentery,  although  it  is  attended  by  tenesmus,  and  blood  may  appear  in 
the  stools.  Hemorrhoids,  may  excite  it,  and  then  it  is  often  called  "the 
hemorrhoidal  catarrhal  flux.''' 

Syphilitic  disease  of  the  anus  or  rectum,  fistula  in  ano,  mucous  patches, 
ulcerations  of  tertiary  syphilis,  and  exposure  to  cold,  as  sitting  on  the  damp 
earth  or  on  wet  sand-bags,  may  cause  it. 

Symptoms. — The  first  symptom  of  proctitis  is  tenesmus, — a  feeling  of  ful- 
ness and  heat  in  the  rectum  with  straining  at  stool,  which  gives  rise  to 
burning,  scalding  pains  that  shoot  from  the  anal  region  into  the  loins  and 
back.  The  stools  contain  gelatinous  mucus,  and  frequently  there  are  quite 
profuse  hemorrhages.  There  is  spasm  and  excessive  tenderness  of  the 
sphincter  ani,  and,  after  violent  efforts  to  expel  supposed  contents,  rectal 
prolapse  occurs,  and  causes  the  most  intense  suffering.  At  no  time  does 
the  patient  feel  that  the  rectum  has  been  completely  emptied.  There  is 
frequent  urination  without  relief.  After  these  symptoms  have  existed  for 
some  time,  scybalous  masses  are  mingled  with  the  muco-purulent  dis- 
charges, and  strangury,  hemorrhoids,  headache,  nausea  and  restlessness 
may  be  present.  Hard  f?ecal  masses  can  often  be  felt  along  the  line  of  the 
colon.  It  may  terminate  in  recovery  in  from  four  to  eight  days,  or  it  may 
become  chronic. 

Chronic  proctitis  is  attended  by  purulent  or  sero-purulent  discharges,  in 
which  are  scybalous  masses  and  shreds  of  sloughing  mucous  tissue.  The 
discharges  are  foul  smelling.  It  is  usually  accompanied  by  constipation. 
A  digital  examination  of  the  rectum  gives  the  sensation  of  a  rigid  cicatrical 
tube. 

Diiferential  Diagnosis.— Proctitis  may  be  mistaken  for  dysentery,  liemor- 
rhoids,  or  cancer  of  the  rectum,  and,  in  women,  for  displacement  of  the 
uterus.  Dysentery  is  an  acute  febrile  disease,  attended  by  severe  pain  in 
the  abdomen  and  great  exhanstion,  and  the  discharges  have  a  characteristic 
dysenteric  color  and  odor.  On  the  other  hand,  the  symptoms  of  proctitis 
are  local,  and  a  digital  examination  of  the  rectum  readily  establishes  the 
diagnosis.  The  presence  or  absence  of  hemorrhoids  is  also  determined  by  a 
digital  examination  ;  the  two  conditions,  however,  may  frequently  be  asso- 
ciated. 

Cancer  is  accompanied  by  the  characteristic  cachexia  ;  it  develops  slowly, 
and  the  form  of  the  stools  is  for  a  long  time  modified  by  the  constriction. 
A  small  portion  of  the  cancerous  mass  may  sometimes  be  removed,  and 
when  examined  microscopically  will  exhibit  the  characteristics  of  the  can- 
cer-tissue.    In  mal-positions  of  the  uterus,  symptoms  analogous  to  those 


PERIPROCTITIS.  303 

of  rectitis  are  often  present,  but  the  introduction  of  a  uterine  sound  at  once 
determines  the  condition. 

Prognosis. — The  prognosis  in  acute  proctitis  is  good  ;  its  average  duration 
is  about  a  week,  and  its  only  dangers  are  chronic  proctitis,  peritonitis,  fis- 
tulas, and  abscess.  When  proctitis  is  the  result  of  cancer,  or  of  tumors 
pressing  on  the  rectum,  the  prognosis  is  unfavorable.  Chronic  rectal  ca- 
tarrh is  difficult  to  cure,  and  cicatrices  following  attendant  ulceration  may 
lead  to  intestinal  obstruction.  When  any  disease  of  the  liver,  lungs,  or 
heart  is  present  which  interferes  with  the  venous  return,  recovery  is  rarely 
reached. 

Treatment.— A  patient  with  acute  rectitis  should  be  kept  in  bed  ;  a  mild 
laxative,  castor-oil,  should  bo  given,  and  the  intestine  thoroughly  evacua- 
ted ;  a  milk  and  farinaceous  diet  only  should  be  allowed.  Sedative  ene- 
mata,  opium  and  belladonna,  or  morphine,  alternating  with  copious  warm 
water  enemata,  are  the  most  successful  methods  of  treatment.  If  there  is 
intense  pain,  with  tenesmus  and  local  engorgement,  a  hypodermatic  of  mor- 
phine may  be  given,  and  leeches  applied  about  the  anus.  Hot  hip  baths 
often  give  marked  relief.  Chronic  rectal  catarrh,  if  mild,  is  to  be  treated 
by  the  local  application  of  any  of  the  vegetable  astringents ;  and  when 
severe,  the  tough  and  ulcerating  membrane  should  be  brushed  over  every 
few  days  with  a  forty-grain  solution  of  nitrate  of  silver.  Constijoation 
should  be  avoided,  and  aperient  enemata  should  be  employed  rather  than 
cathartics.  Local  treatment  is  always  more  successful  than  internal  med- 
ication. 

PERIPEOCTITIS. 

Periproctitis  is  an  inflammation  of  the  connective-tissue  surrounding  the 
rectum,  and  is  usually  suppurative  in  character  ;  the  resulting  abscess  may 
open  either  into  the  lower  bowel  or  internally. 

Morbid  Anatomy. — The  manner  of  the  extension  of  the  inflammation 
through  the  coats  of  the  intestine  to  the  adjacent  connective-tissue,  and  the 
course  of  the  morbid  processes  excited,  are  identical  with  those  of  perityph- 
litis following  typhlitis.  The  infiltrated  tissue  forms  a  tumor  which  can 
readily  be  detected  through  the  rectum.  After  fluctuation  occurs  in  the 
tumor,  its  subsequent  course  varies.  A  spontaneous  cure  by  absorption  and 
induration  may  take  place,  or  the  abscess  may  open  and  a  complete  fis- 
tula be  established,  having  an  internal  opening  communicating  with  the  rec- 
tum. These  fistulous  tracts  are  very  tortuous,  and  are  always  accompanied 
by  a  suppurative  cellulitis  in  the  adjacent  cellular  tissue.  These  fistulous 
openings  in  the  rectum  are  high  up,  and  the  tracts  are  separated  from  the  rec- 
tum by  indurated  connective-tissue.  Fistulse  may  also  be  established  with 
the  bladder  or  vagina.  Suppurating  granulations  surround  the  irregular 
sinuses,  and  in  cases  of  long  standing  they  may  have  an  epithelial  lining 
similar  to  that  of  the  anal  mucous  membrane.  Chronic  periproctitis  may 
lead  to  stricture  and  intestinal  obstruction. 

Etiology. — Periproctitis  is  very  often  a  result  of  proctitis.  It  also  occurs 
with  cancer,  intestinal  ulcers,  and  other  structural  diseases  which  may  in- 


304  DISEASES   OF   THE   DIGESTIVE   SYSTEM. 

volve  the  rectal  mucous  membrane.  It  may  be  traumatic  in  origin.  It  is 
especially  liable  to  develop  in  phthisical  subjects  at  a  point  remote  from  the 
rectum,  and  it  may  be  one  of  the  changes  in  metastatic  pyemic"  inflamma- 
tion. 

Symptoms. — The  existence  of  periproctitis  is  determined  by  a  physical 
examination.  There  is  local  pain,  heat,  and  tenderness  ;  a  tumor  develops, 
which  soon  fluctuates  and  either  gradually  disappears  or  opens  externally. 
If  extensive,  the  formation  of  the  pus-cavity  will  be  attended  by  hectic, 
rigors  and  irregular  sweats.  There  maiy  be  a  well-marked  febrile  move- 
ment, with  nausea  and  vomiting.  If  a  recto-vesical  fistula  form,  then  the 
urine  will  infiltrate  the  adjacent  tissues,  and  septic  symptoms  will  be  de- 
veloped. In  all  cases,  defecation  causes  intense  suffering.  The  tumor  pro- 
duced by  the  abscess  has  been,  in  some  cases,  so  prominent  and  resistant 
that  symptoms  of  intestinal  obstruction  have  resulted.  These  patients  can- 
not sit  erect ;  and  all  pressure  about  the  pelvic  region  is  attended  by  pain. 
When  the  abscess  opens  internally,  foul-smelling,  purulent  masses  will  be 
mixed  with  the  fgecal  discharges,  and  the  tumor  gradually  diminishes. 

DjiFerential  Diagnosis. — Periproctitis  may  be  mistaken  for  any  of  those 
affections  of  the  mucous  membrane  of  the  rectum  which  cause  constipa- 
tion, local  pain,  and  tenesmus ;  but  a  careful  examination  of  the  parts  will 
show  disease  of  the  mucous  membrane,  and  palpation  with  one  finger  ovei 
the  rectal  region  will  discover  a  fluctuating  tumor  that  is  found  in  no  other 
disease. 

Prognosis. — When  occurring  with  structural  and  malignant  disease  of  the 
rectum,  the  prognosis  is  determined  by  the  primary  disease.  Its  prognosis 
is  often  unfavorable,  on  account  of  its  painful  and  annoying  sequelae,  such 
Si&fistulce  and  stricture.  Fistulous  openings  communicating  with  any  other 
parts  than  the  skin  or  intestine,  are  very  grave  results  ;  when  they  occur  in 
phthisical  or  enfeebled  anaemic  subjects  the  prognosis  is  always  unfavora- 
ble. In  idiopathic  and  traumatic  periproctitis,  the  prognosis  is  good.  The 
lower  down  the  suppurative  process,  the  better  is  the  prognosis. 

Treatment. — Before  fluctuation  occurs,  the  rules  of  treatment  are  the 
same  as  in  perityphlitis — rest  and  opium.  When  fluctuation  occurs,  the 
abscess  must  be  opened  at  its  most  prominent  point ;  subsequent  fistulse 
should  be  freely  opened.  The  abscess  should  be  opened  early,  to  prevent 
its  being  discharged  into  the  bladder,  rectum,  or  vagina. 

HEMOEEHOIDS. 

Hemorrhoids,  or  piles,  are  tumors  formed  at  or  near  the  anus  by  dis- 
tended hemorrhoidal  veins,  or  by  connective-tissue  and  skin,  which  have 
been  distended  by  blood  and  indurated  by  local  inflammation.  The  anas- 
tomoses of  the  superior,  middle,  and  inferior  hemorrhoidal  veins  about  the 
anus  form  a  channel  through  which  venous  blood  flows,  either  to  the 
liver  or  to  the  cava  ascendens.  Hence  any  obstruction  in  the  liver,  or 
cava,  may  cause  distention  of  these  veins. 

Morbid  Anatomy. — Hemorrhoids  are  internal  or  external  ;  the  former  are 


HEMOKRHOIDS.  305 

within  the  rectum,  the  latter  are  at  its  anal  margin.  Piles  are  *'  dry  "  or 
*' bleeding  ; "  internal  piles  are  usually  bleeding.  External  piles  are  usu- 
ally dry  ;  they  may  be  large,  smooth,  tense,  dark  blue  tumors,  congested 
and  painful,  or  smaller,  shriveled  tabs  of  skin,  quiescent  and  usually  pain- 
less. The  latter  represent  a  later  form  of  the  former  after  partial  spontane- 
ous cure. 

On  section  these  tumors  exhibit  a  congeries  of  dilated  veins,  sometimes  a 
central  cyst  containing  a  blood  clot,  and  sometimes  free  extravasated  blood. 
Their  size  varies  from  that  of  a  pea  to  that  of  a  walnut.  Internal  hemor- 
rhoids are  sometimes  merely  flat  patches  of  the  mucous  membrane  with 
dilated  capillaries,  and  bleed  at  the  slightest  touch.  Any  internal  pile 
may  be  extruded  during  defecation,  and,  if  not  directly  replaced,  become 
congested  and  inflamed  through  partial  strangulation  by  constriction  of  the 
sphincter.  Thrombi  forming  in  the  large  varicose  tumors  may  lead  to 
ulceration  and  obliteration.  A  strangulated  hemorrhoidal  tumor  may 
slough,  and  pyemic  symptoms  may  follow,  or  a  hemorrhoidal  ulcer  may 
form.  Again,  the  process  may  cause  periproctitis,  abscess,  or  a  rectal  fis- 
tula.' 

Etiology.— Hemorrhoids  are  oftenest  met  with  after  the  fiftieth  year. 
There  is  often  an  hereditary  tendency  to  their  development.  A  sedentary 
mode  of  life,  luxurious  living,  and  a  tropical  climate  are  predisposing  causes. 
Any  thing  retarding  blood-return  from  the  rectum,  such  as  impacted  faces, 
habitual  constipation,  a  gravid  uterus,  or  pelvic  tumor,  leads  to  their  devel- 
opment. Cirrhosis,  atrophy,  and  passive  hyperaemia  of  the  liver,  or  ob- 
structive hepatic  disease  will  cause  hemorrlioids.  In  diseases  of  the  heart 
or  lungs,  causing  obstruction  in  the  venae  cavee,  hemorrhoids  will  develop. 
Proctitis,  cancer,  ulceration  about  the  rectum,  and  the  excessive  use  of  drastic 
purges  are  causes  of  hemorrhoids.  They  may  be  produced  by  prolonged 
attacks  of  diarrhoea  or  dysentery.  Excess  in  venery  is  a  frequent  cause, 
and  they  often  develop  just  after  the  menopause. 

Symptoms. — The  symptoms  of  hemorrhoids  vary  with  the  size,  number, 
stage,  and  seat  of  the  tumors.  At  first  there  is  a  feeling  of  weight  and  ful- 
ness in  the  rectum,  or  a  sensation  as  if  a  foreign  body  were  present.  Dur- 
ing and  after  a  hard  stool,  there  is  a  throbbing,  aching  or  burning  pain,  ra- 
diating to  the  loins  or  down  the  limbs.  There  is  heat,  soreness  and  tingling 
about  the  anus,  and  as  the  tumor  increases  in  size,  sitting  becomes  uncom- 
fortable, and  the  individual  grows  restless,  depressed,  and  anxious.  The 
pain  soon  becomes  constant,  and  is  always  more  severe  after  a  passage  or 
after  a  moderate  walk. 

Internal  hemorrhoids  have,  as  their  chief  symptom,  Needing,  when  the 
bowels  are  evacuated.  Prom  this  symptom  the  name  is  derived.  Slight 
internal  piles  may  exist  for  years  and  only  produce  local  itching  and  heat. 
Large  internal  piles  are  almost  always  extruded  during  a  passage,  but  at 
first  are  easily  replaced.     Later  on,  standing  or  walking  may  cause  thejn  to- 

1  Among  pathological  sequences  of  hemorrhoids,  are  anal  fissureg,  prolapsus  ani,  and  changes  in  the^ 
WMcmiH  mc.rnhrarie.  described  by  Virchow  as  relaxation,  with  the  formatif)n  of  puffs  or  folds,  slightly  thick- 
ened and  grayish  white.    The  submucous  tissue  is  increased  and  relaxed  and  very  vascular.    The  mem- 
brane is  usually  covered  with  a  tough,  whitish  mucus. 
20 


306  DISEASES    OF   THE    DIGESTIVE    SYSTEM. 

protrude.  When  they  are  congested  and  protrude,  they  appear  as  dark  pur- 
ple, soft,  vascular  tumors.  The  amount  of  blood  lost  in  internal  hemor- 
rhoids varies  from  a  couple  of  drachms  to  a  quart ;  in  the  latter  case  there 
is  marked  exhaustion  and  anaemia.  Bleeding  may  be  venous  or  arterial, 
regular,  irregular,  or  periodical.  The  latter  relieves  renal  and  hepatic  con- 
gestion, and  may  ward  olf  gouty  and  apoplectic  seizures.  Many  '*  reflex 
symptoms "  accompany  hemorrhoids  ;  such  as  irritable  bladder,  urethra, 
and  vagina.  This  class  of  patients  are  usually  low-spirited,  irritable,  sal- 
low and  anaemic.     They  may  become  subjects  of  melancholia. 

DiiFerential  Diagnosis. — Hemorrhoids  may  be  mistaken  for  proctitis,  can- 
cer of  the  rectum,  stricture  of  the  rectum,  prolapsus  ani,  venereal  ex- 
crescences, or  intestinal  liemorrhages.  The  points  in  the  differential  diag- 
nosis of  the  first  three  have  been  given.  A  careful  examination  of  the  everted 
but  normal  mucous  membrane  in  prolapse  readily  distinguishes  it  from 
hemorrhoids.  Venereal  growths  are  hard,  have  well-defined  borders,  a 
cauliflower-like  surface,  are  exceedingly  slow  in  their  development,  and  are 
accompanied  by  other  evidences  of  syphilis.  Intestinal  hemorrhage  is  dis- 
tinguished from  bleeding  hemorrhoids  by  an  ocular  examination  of  the  rec- 
tum. Internal  hemorrhoids  may  be  distinguished  from  rectal  polypus  by 
the  fact  that  rectal  polypus  occurs  chiefly  in  the  young,  as  a  large  solitary 
Mifipale  colored  tumor,  having  a  well-marked  pedicle. 

Prognosis. — The  prognosis  in  uncomplicated  hemorrhoids  is  good  ;  long- 
standing piles  in  the  aged  are  rarely  permanently  cured.  Copious  bleed- 
ings from  internal  hemorrhoids  often  hasten  a  fatal  termination  in  chronic 
diseases  of  the  liver  and  lungs. 

Treatment. — Those  who  have  hemorrhoids  should  never  allow  themselves 
to  become  constipated.  The  diet  should  be  nutritious,  and  so  regulated 
as  to  induce  free  daily  evacuations  from  the  bowels.  Violent  exercise,  espe- 
cially lifting  heavy  weights,  long  walks,  sitting  on  damp,  warm  seats,  alco- 
holic stimulants,  and  highly  seasoned  food  should  be  avoided.  The  best 
cathartics  for  this  class  are  rhubarb,  senna,  sulphur,  glycerine,  and  aloes. 
The  careful  use  of  mineral  water  is  of  service  in  those  who  are  the  subjects  of 
liepatic  disease.  In  external  piles,  a  cold  sitz-bath  should  precede  the  use 
of  astringents,  and  these,  combined  with  opium  and  chloroform,  will  often 
give  marked  relief.  Inflamed  external  piles  call  for  the  application  of  leeches 
and  poultices  about  the  anus.  Eecently,  the  topical  application  of  iodoform, 
and  the  injection  into  the  hemorrhoidal  tumors  of  carbolic  acid  has  been 
recommended.     A  surgical  procedure  is  the  only  sure  and  permanent  relief. 

INTESTESTAL    PAKASITES. 

(Worms.) 

The  history  of  intestinal  worms  dates  from  the  earliest  medical  writings. 
In  the  middle  ages  the  history  of  the  tape-worm  was  closely  associated  with 
the  doctrine  of  spontaneous  generation.  It  is  within  the  last  fifty  years 
that  the  doctrines  of  metamorphosis  and  migration  have  been  established. 
There  was  a  time  when  nearly  every  malady  was  attributed  to  worms, — while 


INTESTINAL   PAEASITES. 


307 


a  reaction  of  sentiment  ascribed  the  utmost  benefit  to  their  presence.  Every 
year  discovers  some  new  parasite ;  of  the  fifty  or  sixty  now  known,  only 
about  ten  per  cent,  are  common  in,  or  peculiar  to  man.  The  worms  which 
have  their  habitat  within  the  intestinal  canal  of  the  human  subject  are 
comparatively  few.  I  shall  only  give  a  brief  history  of  those  which  are  of 
frequent  occurrence. 

Tcenia  Solium,  or  tape-worm,  is  the  final  development  of  an  embryo, 
usually  lodged  in  the  flesh  of  some  animal.  It  is  from  seven  to  thirty  feet 
long,  has  a  globular  head,  connected  by  a  slender  neck  to  its  numerous 
flat  segments  or  joints.  The  neck  is  an  inch  in  length,  and  gradually  widens 
into  a  joint.  The  head  measures  about  l-40th  of  an  inch  ;  around  its 
convexity  is  arranged  a  double  coro- 
net of  booklets, — the  ''armed  tape- 
worm,"— and  it  is  provided  with 
some  two  or  four  suckers.  The  flat, 
thin  joints  vary  from  one-half  to  one- 
eighth  inch  in  length,  being  smallest 
near  the  neck.  The  lower  border  of 
each  segment  is  larger  than  the  upper. 
Each  mature  joint  contains  both  male 
and  female  sexual  organs  (hermaphro- 
dite). The  uterus  is  a  long  tube,  with 
seven  or  ten  branches  on  either  side, 
in  which  the  ova  develop.  An  ordi- 
nary-sized tape-worm  contains  five 
millions  of  ripe  ova.  These  ova, 
l-1700th  inch  in  diameter,  become  in 
the  pig  cysticerciis  celhdoscB  (measly  pork).  From  one 
js.  Lovue  row  of  hooks,  to  forty  T.  solium  may  be  present  in  the  same  intestinal 
B.  Commencing  segments  tract ;  their  liooklcts  and  suckcrs  are  firmly  embedded  in 

below  the  neck.  ,  i  i  »    ,  i  77    •    j     j  •  j  i 

the  mucous  membrane  oi  the  small  intestine — they  are 
almost  exclusively  confined  to  its  upper  third.  The  pro- 
glottides sometimes  hang  far  down  into  the  large  intestine ;  the  terminal 
ripe  oaes  are  constantly  falling  off,  and  are  discharged  with  the  faeces.  T. 
solium  is  the  development  of  the  C.  cellulosus  from  measly  pork,  the  em- 
bryo being  swallowed,  and  its  vesicular  annex  removed  by  the  stomach 
juices,  the  booklets  become  fixed  just  below  the  pylorus,  and  in  a  few 
months  the  tape-worm  reaches  considerable  size. 

Tmnia  saginata,  or  T.  medio-cannellata,- 2l?,o  called  "unarmed  tape- 
worm,"' is  larger,  stronger,  and  thicker  than  T.  solium.  The  segments  are 
broader,  far  more  opaque,  and  harder  than  those  of  T.  solium  ;  the  head 
has  no  booklets,  measures  about  1-lOth  inch,  and  has  four  strong  and  prom- 
inent suckers.  The  uterus  is  more  finely  divided,  and  there  are  from  fifteen 
to  twenty  dichotomous  branches.  The  head  of  the  medio-cannellata  is  more 
club-shaped  than  that  of  the  T.  solium.  The  neck  is  very  short.  The 
larval  form  of  this  worm  is  the  cysticercus  T.  saginata,  or  cysticercus  bovis, 
the  embryo  being  found  in  deef.     The  ova  of  T.  saginata  are  oval,  and 


Fig.  64. 
Head  of  Tasnia  Solium. 
A.  The  Rostelluni. 


Fig  65. 

Mature  Segment  of  Taenia 
Solium. 

A.  Genital  pore. 

B,  B.  Uterus. 

C,  C.  Lateral  branches  of 

the  uterus,    x  30. 


308  DISEASES.   OF   THE    DIGESTIVE    SYSTEM. 

larger  than  those  of  T.  solium.  In  their  larval  state  they  occur  not  only 
in  beef,  but  in  the  sheep,  goat  and  giraffe.  Its  mode  of  entrance,  locality, 
and  development  are  precisely  the  sa7jie  as  the  T.  solium. 
It  occurs  far  more  frequentl}^,  and  more  extensively  than 
T.  solium,  which  formerly  was  the  variety  always  meant 
when  tape- worm  was  mentioned. 

The  Bothrioceplialus  latus  is  the  largest  worm  infesting 
man  ;  the  head  of  this  tape-worm  is  club-shaped,  deeply 
grooved  on  either  side,  and  is  "^  unarmed."  The  head  is 
shaped  like  an  egg,  1-lOth  of  an  inch  long  and  ]-26th  of  an 
inch  wide.  The  neck  is  very  short  and  thread-like  ;  the 
joints  are  about  three  times  as  broad  as  they  are  long, 
but  toward  the  end  of  the  worm  they  are  square.  The 
genital  pores  look  like  a  small  rosette,  and  are  situated 
Fig.  66.  about  the  centre  of  the  segment,  and,  being  all  placed  on 

^iiata°^o?*unamld    *^®  ^^'^^  ^^^®  ^^  *^^®  worm,  this  ccstoid  Can  be  said  to  have 
Tape-worm.  a  bclly  and  a  back.     The  eggs  are  oval,  from  l-350th  to 

B  i'Fmf discs  x  8  I'^SOth  inch,  brown  in  color  and  at  first  ciliated.  They 
possess  six  booklets.  This  worm  sometimes  reaches  sixty 
feet  in  length  ;  its  color,  unlike  the  others,  is  a  dull  bluish-gray.  The  seg- 
ments do  not  drop  off  when  ripe,  and  have  not  an  independent  life.  It  is 
estimated  that  ten  feet  of  this  worm  can  produce  twelve  million  ova.  The 
development  of  this  worm  is  unknown  ;  some  suppose  its  embryo  to  be 
found  in  a  fish  or  mollusk.  It  is  found  in  the  small  intestine  singly,  or 
with  the  other  two  varieties  ;  several  may  inhabit  the  same  individual. 

Round  worms,  or  the  hematoids,  are  more  highly  organized  than  the  ces- 
toids; the  common  round  worm,  or  A  scar  is  lumbricoides,  is  of  a  brown 
color,  with  a  cylindrical  body,  10  x  1-8  inch  in  length  and  breadth  in  the 
male,  and  15x1-4  in  the  female.  The  head  terminates  in  three  thick 
semilunar  lips,  each  lip  having  about  200  teeth.  The  mouth  opens  into 
the  alimentary  canal,  which  can  be  seen  through  the  transparent  body. 
The  tail  is  curved  strongly  toward  the  abdomen  in  the  male,  this,  with  its 
small  size,  distinguishing  it  from  the  female.  The  female  contains  two 
long  coils  of  ovary  and  oviduct,  the  length  of  the  generative  tubes  being 
eleven  times  the  length  of  the  animal.  At  the  end  of  the  tail,  in  the  male, 
two  projecting  spiculae  can  be  seen  connected  with  the  generative  organs, 
which  are  coils  of  tubes  eight  times  as  long  as  the  worm.  The  ova  are  oval 
in  shape  (1-340  to  1-440),  are  produced  in  immense  numbers  (sixty  millions 
in  a  mature  female),  and  are  discharged  with  the  f^ces.  The  vitality  of 
these  ova  is  wonderful.  How  they  obtain  entrance  into  man  is  not  known, 
but  it  is  probable  that  they  previously  pass  through  an  intermediate  state, 
and  that  they  attain  their  full  development  after  entrance.  The  worms; 
inhabit  the  small  intestine,  and  vary  in  numbers  from  one  to  thousands. 
They  wander,  however,  through  the  tract,  may  pass  through  the  nose  or 
mouth,  or  may  enter  the  hepatic,  gall  or  pancreatic  duct,  into  the  gall- 
bladder, or  into  any  fistulous  channel,  and  reach  the  kidneys,  spleen,  lung, 
larynx,  etc.     The  round  worm  occurs  in  the  ox  and  pig  as  well  as  in  man. 


INTESTIN'AL   PARASITES. 


309 


The  ''thread  worm,"  ''maw-worm,"  Oxy^ins  vermicularis,  looks  like  an 
ordinary  piece  of  thread  ;  the  male  (like  the 
round  worm)  is  smaller  than  the  female,  and 
is  ahout  one-sixth  of  an  inch  long.  The  fe- 
male is  from  one-third  to  one-half  an  inch 
long.  The  body  is  cylindrical, the  tail  is  much 
sharper  than  the  head.  The  head  terminates 
in  a  mouth  surrounded  by  three  lips,  from 
which  extends  the  alimentary  tract.  The  end 
of  the  tail,  in  the  male,  is  curved  up  toward 
the  abdomen.  The  eggs  are  oval,  1-100  to 
1-500  inch,  each  female  containing  about  ten 
thousand.  They  are  very  hardy,  having  a 
stout  envelope.  All  their  stages  of  develop- 
ment take  place  within  the  intestinal  canal. 

The  "seat-zvorm,"  as  its  name  indicates, 
has  its  habitat  in  the  large  intestine,  especial- 
ly about  the  rectum,  whence  it  may  pass  into 
the  vagina  or  insinuate  itself  into  narrow 
folds  of  skin  in  the  anal  region.  Mature 
females  especially  inhabit  the  csecp.m.  They 
vary  in  number :  sometimes  'the  mucous 
membrane  is  completely  covered  with  them. 
The  ova  enter  by  means  of  the  food  or  di- 
rectly through  personal  contamination  ;  they 
die  in  a  few  hours  aftei*  they  are  placed  in 
water. 

The  Trichocephdlus  dispar,  or  " loMp-icorm,'"  is  a  small  worm  about  one 
and  one-half  to  two  inches  in  length,  the  female  being  the  larger.  It  has 
heen  called  the  "  hair -headed '^  worm  because  its  head,  which  constitutes 
about  two-thirds  of  its  "length,  is  thread-like.  The  thick  body  contains  the 
genitals  and  the  intestinal  canal ;  the  body  of  the  male  is  curved  into  a 
spiral.  The  male  organ  presents  a  spicula  projecting  from  the  cloaca  ;  it  is 
set  with  numerous  aharp  points,  and  is  surrounded  by  a  sheath.  The  uterus, 
when  distended  with  eggs  (60  ova),  fills  nearly  the  whole  posterior  part  of 
the  body.  The  eggs  are  brown  and  oval  (1-5,000 — 1-12,000  inch)  with  a 
nipple-like  appearance  at  either  pole.  Its  mode  of  entrance  into  the  body  is 
unknown.  There  is  probably  no  intermediate  state  of  the  ova  of  T.  dispar. 
The  embryos  are  probably  liberated  in  the  stomach,  and,  developing  as  they 
travel  onwards,  reach  the  large  intestine.  Their  numbers  vary  from  fifty 
to  one  thousand.  The  T.  dispar  is  found  in  some  varieties  of  apes  ;  and 
the  T.  crenatus  of  the  pig  is  probably  the  same  as  this  worm. 

Trichina  spiralis  belongs  to  general  diseases,  and  will  not  be  considered 
here. 

The  Ancliylostomum  duodonale,  or  dochmius  duodenalis,  is  a  small  cylin- 
drical worin,  the  females  being  seven-tenths  and  the  males  four-tenths  inch 
in  length.    It  is  thicker  than  the  seat-worm,  almost  as  thick  as  the  body  of 


Pig.  67. 
A.  Oxyvris  vermicvlaris,  or  thread  worm, 
female.    B,  Same,  male— both  natu- 
ral  size. 

C.  Female  of  same,  magnified  about  ten 

times,  containing  ova.    a,  anus ;  b, 
vulva. 

D.  Mature  egg  of  the  thread  worm,   x  250. 

E.  Ascaris   luriibricoidefi,    male,    natural 

size.    F,  head,  and  6-',  tail  of  same, 
magnified  about  four  diameters. 


310  DISEASES   OF   THE    DIGESTIVE    SYSTEM. 

the  whip-worm.  The  mouth  is  furnished  with  eight  teeth.  The  armature 
of  the  mouth,  and  the  capsule  about  the  head  are  very  complex.  The  male 
terminates  in  a  lobate  enlargement,  but  the  female  is  pointed.  The  eggs 
are  oval  (1-350  to  1-1000  inch),  have  a  very  thin  shell,  but  regarding  their 
development  little  is  known.  It  inhabits  the  lower  part  of  the  duodenum 
and  the  upper  part  of  the  jejunum.  It  probably  has  no  intermediate 
bearer,  but  as  soon  as  developed  attaches  itself  to  the  villi  and  may  become 
encysted  between  the  mucous  and  muscular  coats.  It  may  cause  intestinal 
hemorrhage. 

Etiology. — Worms  develop  in  the  intestines  6f  man,  either  by  the  en- 
trance of  ova  which  grow  into  the  mother  parasite ;  or  by  the  entrance 
of  what  are  called  "intermediate  parasites."  Their  entrance  into  the 
intestinal  tract  is  only  effected  through  food  and  drink.  Butchers,  and 
those  who  handle  raw  meat,  are  more  subject  to  them  than  others.  Filthy 
surroundings,  squalor,  and  personal  uncleanliness  are  conditions  which 
favor  their  development. 

Cestoids  occur  at  all  ages  ;  tape-worm  has  been  found  in  a  five-day-old 
infant.  Bothriocephalus  latus  is  found  chiefly  in  Scandinavia,  Eussia,  and 
Poland.  T.  solium  occurs  wherever  the  pig  is  domesticated.  T.  saginata 
is  found  wherever  raw  beef  is  used  for  food.  The  Tcenia  are  not  found 
among  Jews  and  those  who  eat  no  pork.  The  monks  of  the  Carthusian 
order,  who  eat  only  fish,  are  free  from  worms.  Iceland  is  the  only  country 
in  which  the  hsematoids  are  not  found.  The  round  worm  occurs  in  warm 
climates  oftener  than  in  cold.  Their  number  and  extent  are  in  direct  pro- 
portion to  the  filth  of  the  surroundings.  They  are  more  common  in  women 
and  children  than  in  men  ;  in  those  who  live  in  the  country  than  in  those 
who  live  in  cities.  The  oxyuris  vermicularis  is  everywhere  prevalent.  It 
occurs  especially  in  young  children,  but  is  not  uncommon  in  adults.  The 
itching  which  these  worms  cause,  especially  at  night  in  a  warm  bed,  induces 
so  much  scratching,  that  when  two  or  more  children  sleep  together  the 
worms  may  be  carried  from  one  to  another  by  the  hands.  Those  who  have 
charge  of  children,  nurses,  etc.,  often  become  infected  in  this  way. 

T.  dispar  abounds  in  this  country,  Europe,  Syria,  and  Egypt ;  it  is 
present  at  all  ages,  but,  strangely  enough,  in  the  first  and  second  years  of 
life  it  is  rare.  The  whip-worm  produces  so  few  symptoms,  and  can  be  so 
readily  overlooked  at  a  post-mortem,  that  its  etiology  is  obscure.  The 
Anchylostomum  duodenale  (or  the  dochmius  or  strongylus  duodenalis)  was 
discovered  by  Dubini  in  1838,  in  Northern  Italy.  It  prevails  in  Brazil  and 
Egypt.  The  negro  is  oftener  subject  to  it  than  the  white  ;  but  it  can  be 
shown  that  bad  food  and  drink  are  of  more  importance  in  causing  it  than 
race.  Women  are  affected  oftener  than  men.  The  conditions  known  as 
cachexia  Africana,  mal  d'estomac,  etc.,  are  due  to  the  presence  of  this 
parasite. 

Symptoms. — The  only  symptom  which  gives  positive  evidence  of  the  ex- 
istence of  intestinal  worms  or  their  ova  is  their  discovery  in  the  stools  or 
about  the  anus.  Taenia  produces  no  constant  symptoms.  The  bowels  are 
usually  irregular.     There  may  be  colicky  pains  in  the  abdomen  ;  the  appe- 


IN-TESTIliTAL   PARASITES.  3U 

tite  is  capricious,  the  face  may  be  pale  and  the  mouth  drawn.  Often  the 
stomach  feels  weak,  and  there  is  nausea,  perhaps  vomiting.  In  some  in- 
stances these  stomach  symptoms,  with  colic,  occur  after  certain  articles  of 
food  ;  in  others,  certain  kinds  of  food  relieve  thpm.  Among  the  reflex 
symptoms  are  headache,  dizziness,  ringing  in  the  ears,  sudden  sweatings, 
irregular  attacks  of  palpitation,  depression  of  spirits,  lassitude,  ocular  spec- 
tra, sudden  salivation,  and  itching  about  the  nose  and  anus.  Chorea, 
grinding  the  teeth,  hysteria,  anomalies  in  menstruation,  epileptiform  and 
maniacal  actions  have  occurred  in  those  in  whom  tape-worms  were  found 
to  be  present.  The  special  senses  may  be  temporarily  involved  :— deafness, 
blindness  and  loss  of  speech  have  occasionally  occurred.  All  the  senses  are 
enfeebled  to  a  marked  degree.  These  symptoms  are  more  those  of  hypo- 
chondria and  hysteria  than  of  taenia.  The  subjective  sensations  which  one 
who  believes  he  has  tajnia  may  describe  are  innumerable,  and  each  jDatient 
will  have  his  own  peculiar  group  of  special  notions.  Often  patients  with 
one  large  or  several  small  taenias  enjoy  perfect  health  so  long  as  their  exist- 
ence is  not  suspected.  The  diagnosis  can  only  be  made  by  the  discovery  of 
detached  joints  or  segments  of  the  worms  in  the  faeces. 

The  ascaris  lumhricoides  or  round  worm  may  be  present  in  large  num- 
bers, and  yet  give  no  symptoms  of  its  presence.  Usually,  however,  there 
are  certain  symptoms  which  are  regarded  as  ''  signs  of  worms,"  such  as 
itching  and  picking  at  the  nose,  foul  breath,  colicky  pains,  especially 
about  the  umbilicus,  bloody  mucous  diarrhoea,  perverted  appetite,  restless- 
ness, disturbed  sleep  in  which  the  child  grinds  its  teeth,  with  nausea  and 
vomiting,  which  is  regarded  as  evidence  that  the  "  worms  have  passed  into 
the  stomach."  The  vomiting,  however,  is  reflex.  The  abdomen  is  usually 
tumid,  distended,  and  doughy  to  the  feel.  The  urine  looks  somewhat  like 
rice-water,  the  lower  eyelid  is  of  a  dark  purple  color,  or  there  may  be  rings 
about  the  eyes  ;  the  pupils  are  often  unequal.  Later  there  are  hysterical 
convulsions,  with  choreal  movements,  and  the  child  becomes  emaciated. 
These  worms,  by  coiling  themselves  into  a  bundle,  have  caused  intestinal 
obstruction.  They  have  entered  the  larynx  and  induced  death  by  suffoca- 
tion, have  reached  the  ductus  communis  and  caused  jaundice  and  heiDatic 
abscess,  and  they  may  take  their  way  through  any  artificial  opening  into 
the  peritoneal  cavity  or  bladder,  but  they  cannot  cause  intestinal  perfora- 
tion. It  is  a  question  if  lumbrici  can  induce  catarrh  and  ulceration  of  the 
intestine.  At  an  autopsy,  where  large  colonies  of  lumbrici  have  been  found, 
the  intestine  has  been  intensely  congested  in  the  neighborhood,  leaving  no 
doubt  as  to  the  cause.  Attacks  of  laryngismus  stridulus  are  sometimes 
induced  by  lumbrici  in  highly  nervous  children.  While  the  existence  of 
these  worms  may  be  suspected,  their  diagnosis  can  only  be  made  by  their 
discharge  from  the  stomach  or  intestine. 

The  seat-worm,  or  oxyuris  vermicularis,  when  present  in  small  numbers, 
produces  few  symptoms.  When  they  are  numerous  in  nervous  and  suscep- 
tible patients,  there  is  intense  itching  about  the  anus,  especially  on  retiring, 
when  the  increased  warmth  causes  them  to  be  very  active,  and  by  this  sleep 
is  more  or  less  disturbed.     They  often  cause  a  frequent  desire  to  go  to  stool. 


312  DISEASES    OF   THE   DIGESTIVE    SYSTEM. 

and  sometimes  there  is  an  abnormal  amount  of  mucus  mixed  with  thefaecea 
showing  that  they  have  produced  extensive  local  irritation.  In  such  cases^^ 
there  will  be  punctate  redness  about  the  anus,  and  in  female  children,  where 
the  worm  wanders  into  the  vagina,  there  will  be  irritation  of  the  vulva, 
which  leads  to  vulvitis.  Sometimes  with  the  itching  there  will  be  pain  and 
tenesmus,  and  the  fetid  stools  will  be  bloody  and  streaked.  The  genito- 
urinary disturbance  may  cause  such  abnormal  excitement  of  the  sexual 
organs,  that  it  may  lead  to  onanism,  seminal  loss,  and  nymphomania.  Hys- 
terical, epileptiform,  choreal,  and  cataleptic  symptoms  have  been  induced 
by  the  irritation  produced  by  these  worms.  On  account  of  the  local  irrita- 
tion which  they  produce  and  their  easy  detection  on  careful  examination, 
their  diagnosis  is  not  difficult,  for  their  ova  or  the  parasites  themselves 
will  be  found  in  the  faeces,  or  in  the  folds  at  the  margin  of  the  anus.  A 
careful  inspection  of  the  rectum  in  those  who  suppose  they  are  suffering 
from  hemorrhoids  will  often  disclose  the  presence  of  the  seat-worm  as  the 
cause  of  the  anal  irritation. 

Trichocephalus  dispar  produces  no  symptoms.  Either  the  worms  or  their 
eggs  must  be  found  in  the  faeces  to  establish  a  diagnosis. 

Anchylostomum  duodenale  induces  a  chlorosis-like  anaemia ;  the  skin  and 
mucous  membranes  are  pale,  and  the  cardiac  and  venous  murmurs  of  anae- 
mia are  well  marked.  The  loss  of  flesh  and  strength  is  constant  and  pro- 
gressive. Dyspepsia  and  anorexia,  alternating  with  bulimia,  and  an  appe- 
tite for  certain  and  peculiar  articles  of  food,  are  early  symptoms.  In  most 
cases  there  is  a  sense  of  weight  or  pain  in  the  abdomen  ;  the  stools  are  fre- 
quently colorless,  and  the  urine  is  pale  and  abundant.  Sometimes  slight 
intestinal  hemorrhage  will  occur. 

Differential  Diagnosis. — The  diagnosis  of  the  presence  of  intestinal  para- 
sites is  made  by  the  discovery  of  the  parasites  or  their  ova  in  the  stools  or 
the  matters  vomited.  Acute  liydrocepTialus  may  be  mistaken  for  worms, 
but  in  hydrocephalus  the  projectile  vomiting,  the  slowed  pulse,  the  fever 
with  irregular  exacerbations  and  remissions,  the  constipation,  the  hydro- 
cephalic cry,  and  the  retracted  abdomen,  all  stand  in  marked  contrast  to 
the  symptoms  of  intestinal  parasites. 

Prognosis. — Intestinal  parasites  may  cause  death,  first  by  their  entrance 
into  the  larynx,  the  ductus  communis  (causing  abscess  of  the  liver),  or  when 
they  collect  in  masses  and  cause  fatal  intestinal  obstruction ;  secondly, 
when  extreme  anaemia  and  exhaustion  are  produced  by  anchylostomum 
duodenale.  The  prognosis  in  taenia  is  good,  except  in  very  young  children, 
and  in  the  enfeebled.  When  parasites  have  resided  a  long  time  in  the  in- 
testines, some  of  the  reflex  symptoms  may  remain  after  their  removal.  It 
is  thought  that  the  ascaris  lumbricoides  does  not  remain  longer  than  a  year 
in  the  human  body,  unless  there  is  an  exposure  to  new  sources  of  infection. 
Death  occurs  with  symptoms  of  exhaustion,  greatly  increased  by  the  intes- 
tinal hemorrhage,  profuse  diarrhoea,  and  persistent  vomiting. 

Treatment. — Prophylaxis  demands  that  all  raw  or  '' underdone"  meat 
shall  be  avoided.  Measly  pork  should  not  be  allowed  to  be  sold  in  the 
markets,  and  wells  and  springs  from  which  drinking  water  is  obtained 


INTESTIKAL   PARASITES.  313 

should  be  removed  from  the  neighborhood  of  stockyards.  A  point  in  prophy- 
laxis that  has  never  been  mentioned  is  the  washing  of  green  vegetables,  such 
as  lettuce,  as  the  Swiss  and  Germans  sprinkle  their  growing  vegetables  with 
the  water  drained  from  liuman  excrements. 

The  means  to  be  employed  for  the  expulsion  of  the  tape-worm  have  for 
their  object  the  dislodgment  of  its  head  ;  so  long  as  this  remains,  it  is  use- 
less to  hope  for  cessation  of  the  symptoms.  Whatever  anthelmintic  is 
administered  for  this  purpose,  the  bowels  must  be  thoroughly  evacuated. 
This  can  be  effected  by  some  of  the  saline  purges,  or  by  a  copious  draught 
of  some  purgative  mineral  water.  The  diet  should  be  restricted  for  two  or 
three  days  before  its  administration,  and  then  either  pomegranate,  Kousso, 
male  fern,  or  pumpkin-seeds  may  be  given  in  full  doses.  As  the  adminis- 
tration of  anthelmintics  may  induce  vomiting,  a  cup  of  black  coffee  may  be 
given  a  few  minutes  before  they  are  taken.  The  cortex  radicis  punicce 
granati  is  used  in  the  form  of  a  decoction  (three  ounces  to  a  pint  and  a 
haK  of  water).  When  boiled  down  one-half,  it  should  be  given  in  three 
divided  doses.  To  this  may  be  added  filix  mas,  gamboge,  or  tansy ;  and  in 
case  the  worm  is  not  dislodged,  a  dose  of  castor-oil  should  follow.  Kousso, 
the  flower  of  the  Br  ay  era  anthelmintica,  is  given  in  one-half  oz.  doses 
mixed  with  water  ;  or  in  an  infusion  (one-quarter  oz.  to  four  oz.  of  water). 
The  odor  of  the  Kousso  is  very  offensive. 

The  male  fern  (aspidium  filix  mas)  is  one  of  the  oldest  and  best  known 
vermifuges.  The  ethereal  extract — oleoresin — is  given  in  capsules  ;  dose, 
one- half  drachm.  It  may  be  given  as  the  powder  of  the  rhizome,  60  to  100 
grains.  It  should  also  be  followed  by  a  dose  of  castor-oil,  gamboge,  or  cal- 
omel. Oil  of  turpentine,  in  one-half  or  one-ounce  doses,  is  very  effective ; 
it  may  produce  headache,  giddiness,  or  a  kind  of  intoxication.  Petroleum, 
in  20  to  30-drop  doses,  has  been  used  in  Egypt.  Kameela  {Rottlera  tinc- 
tqria)  is  to  be  given  in  one-third  drachm  doses  every  three  hours.  Carbolic 
acid  (5  grains)  and  salicylic  acid  (12  grains)  have  also  been  found  eflBcacious. 
An  emulsion  of  pumpkin-seeds  frequently  acts  efficiently.  The  active  prin- 
ciple of  pomegranate-root  bark,  pelletierine,  is  thought  by  some  to  possess 
all  the  powers  of  the  root.  All  the  above-named  drugs  are  efficacious,  and 
when  they  fail  it  is  usually  because  they  are  not  properly  administered. 

For  round  worms,  besides  the  vermicides  mentioned,  santonin,  spigelia,  cal- 
omel, and  chenopodium  may  be  used.  Santonin  is  by  far  the  most  reliable, 
but  it  requires  care  in  its  use,  on  account  of  the  severe  gastric  and  nervous 
symptoms  which  it  causes  ;  one-half  grain  for  a  child  and  three  to  six  grains 
for  an  adult  is  a  maximum  dose.  The  oil  of  chonopodium  is  recommended, 
— dose,  five  to  ten  drops  ;  and  the  fluid  extract  of  senna  and  spigelia  is  often 
effective. 

The  thread  or  seat-worm  may  be  destroyed  and  washed  away  by  enemata 
of  quassia,  oak-bark,  alum,  salt  and  water,  or  carbolic  acid.  At  the 
same  time  the  vermifuges  should  be  given,  and  the  bowels  gently  moved 
by  castor-oil.  Thoroughly  washing  the  anus  and  the  parts  around  it  with 
a  one  per  cent,  solution  of  carbolic  acid,  and  subsequent  attention  to  clean- 
liness, suffice  in  the  majority  of  instances.     It  is  said  that  turpentine  and 


314  DISEASES   OF   THE   DIGESTIVE   SYSTEM. 

calomel  are  the  best  means  of  getting  rid  of  the  A.  duodenale.  Following 
the  expulsion,  tonics  should  be  used.  For  either  the  round,  seat,  or  whip- 
worm, santonin  is  the  best  remedy  ;  and  for  the  last  two  varieties,  thorough 
local  treatment  and  absolute  cleanliness  will  generally  suffice. 

FUNCTIOKAL  DISEASES  OF  THE  INTESTINES. 

The  principal  functional  diseases  of  the  intestines  are  constipation  and 
colic  or  enteralgia. 

CONSTIPATION. 

Constipation  is  a  relative  term,  for  some  perfectly  healthy  persons  have 
only  one  movement  from  the  bowels  every  seconder  third  day,  while  others 
have  two  stools  daily.'  It  is  difficult  to  explain  these  differences,  and  to 
say  what  constitutes  constipation  in  an  individual  unless  his  habit  is  known. 
No  standard  can  be  applied  indiscriminately  to  all  persons.  Those  who 
suffer  from  constipation  are  always  able  to  make  their  own  diagnosis.  In 
the  majority  of  instances  constipation  is  due  to  a  deficiency  in  the  peristal- 
sis of  the  large  intestine. 

Morbid  Anatomy. — There  are  no  lesions  which  are  constant  in  functional 
constipation,  but  if  it  has  been  of  long  standing  it  may  cause  changes  which 
after  a  time  become  an  additional  cause,  such  as  dilatation  of  the  intestine 
and  hypertrophy  of  its  walls.  The  colon  may  become  so  dilated  as  to  meas- 
ure from  twelve  to  fifteen  inches  in  circumference.  If  hypertrophy  occurs 
it  is  usually  most  marked  at  the  upper  part  of  the  rectum  and  at  the  sig- 
moid flexure  of  the  colon.  More  or  less  paralysis  of  the  muscular  coat  pre- 
cedes and  accompanies  dilatation,  and  pouches  may  form  along  the  colon 
containing  masses  of  mucus  and  fsecal  matter.  These  pouches  occur  most 
frequently  at  the  sigmoid  flexure,  and  may  be  arranged  in  rows.  Ulcera- 
tion and  perforation  of  the  dilated  and  weakened  intestinal  wall  may  cause 
fatal  peritonitis.  Sometimes  the  intestines  rupture  without  ulceration  from 
prolonged  and  severe  peristalsis  at  the  seat  of  the  faecal  obstruction.  Typh- 
litis and  perityphlitis  may  be  a  result  of  fsecal  impaction  due  to  habitual 
constipation.  Many  diseases  of  the  rectum  and  adjacent  viscera  are  also 
among  its  results,  such  as  haematuria,  rectal  abscess,  fistulae,  anal  fissures, 
prolapsus  ani,  and  passive  hyperaemia  of  the  pelvic  viscera.  Hemorrhoids 
usually  complicate  long-standing  constipation. 

Etiology. — Constipation  often  results  from  the  same  habits  and  mode  of 
life  which  cause  dyspepsia,  and  it  is  a  very  frequent  accompaniment  of  it. 
It  may  arise  from  the  prolonged  use  of  opium  and  the  abuse  of  laxatives. 
It  occurs  with  certain  diseases  of  the  brain  and  spinal  cord.  In  those  who 
have  what  is  called  a  "  costive  habit "  collections  of  pills  which  have  been 
taken  for  its  relief  sometimes  form  a  nucleus  about  which  masses  of  im- 
pacted faeces  collect.  A  change  in  habits  of  life  or  diet  is  frequently 
followed  by  temporary  constipation.  Those  who  lead  a  sedentary  life,  the 
feeble,  infirm,  the  bed-ridden,  and  child-bearing  women  are  predisposed  to 

'  Cases  are  recorded  where  periods  of  three  months  have  elapsed  between  two  snccessive  movements, 
and  yet  the  individual  was  apparently  in  good  health. 


CONSTIPATION.  315 

constipation.  Loss  in  the  contractile  power  of  the  abdominal  muscles  from 
any  cause  may  induce  constipation.  Abnormalities  in  the  intestinal  se- 
cretion, as  in  chronic  alcoholismus,  and.  organic  or  functional  disturbances 
of  the  liver  lead  to  constipation;  heart  disease,  bronchitis,  emphysema,  and 
asthma  are  included  in  this  list.  It  may  also  result  from  unnatural  dry- 
ness of  the  faeces,  such  as  occurs  in  diabetes,  where  large  quantities  of  fluid 
are  carried  off  by  the  kidneys.  This  dryness  may  also  occur  in  those  whose 
occupations  cause  profuse  perspiration.  General  anaemia  and  chlorosis 
cause  it. 

One  of  its  most  frequent  causes  is  anxiety  and  prolonged  mental  labor, 
especially  in  those  leading  a  sedentary  life.  It  is  common  in  melan- 
cholia and  insanity,  and  may  occur  with  hysteria.  The  long-continued  use 
of  cathartics  is  a  frequent  cause  of  obstinate  constipation.  Hereditary  pre- 
disposition may  be  classed  as  a  cause.  Old  age  is  always  a  predisposing 
cause.  Cases  are  on  record  where  from  boyhood  until  the  seventieth  year 
the  bowels  did  not  move  more  than  once  a  week,  and  yet  the  individual  en- 
joyed perfect  health.  In  those  accustomed  to  large  doses  of  opium  the 
bowels  have  been  known  to  move  only  four  times  in  the  year.  Departure 
from  the  standard  natural  to  each  individual  will  determine  the  existence 
or  non-existence  of  constipation. 

Symptoms. — Usually  when  a  person  whose  bowels  have  been  accustomed 
to  move  daily  habitually  passes  two  or  three  days  without  defecation  he 
complains  of  a  sense  of  fulness  in  the  rectum,  with  flatulence,  headache, 
vertigo,  a  foul  breath,  anorexia,  and  well-marked  dyspeptic  symptoms. 
Nervous  subjects  become  hypochondriacal,  'and  there  is  mental  inactivity 
with  insomnia,  or  the  individual  awakes  unrefreshed  from  a  broken  sleep. 
The  skin  becomes  parched,  shrivelled,  sallow  and  pasty.  Eruptions  such  as 
psoriasis,  eczema,  prurigo,  erythema  and  urticaria  often  appear  upon  the 
surface.  There  are  frequent  flushings  of  the  face,  and  the  eyes  are  sur- 
rounded by  deep  purplish  rings.  The  tongue  is  flaccid,  often  indented  by 
the  teeth.  The  breath  and  the  perspiration  have  an  offensive  odor,  and 
frequent  attacks  of  cardiac  palpitation  cause  the  patient  to  become  anxious 
about  himself.  Those  who  are  habitually  constipated  are  subject  to  fits  of 
vertigo  and  temporary  loss  of  consciousness. 

Besides  the  subjective  symptoms  of  constipation  there  are  those  produced  by 
the  mechanical  interference  caused  by  the  hard  faecal  masses.  If  the  colon  is 
distended  there  is  more  or  less  pain,  which  is  nearly  always  located  in  "  the 
chest."  A  distended  transverse  colon  may  cause  such  pressure  upon  the 
duodenum  as  to  interfere  with  its  function  and  give  rise  to  dyspeptic  symp- 
toms. The  pressure  of  large  faecal  collections  in  the  descending  colon  and 
caecum  sometimes  causes  irritation  along  the  genito-urinary  tract,  irrita- 
bility of  the  bladder,  and  neuralgic  pains  in  the  groins,  ovaries,  testicles, 
loins  and  lower  extremities.  At  any  time  the  symptoms  of  intestinal  ob- 
struction may  occur.  Diarrhoea  may  follow  prolonged  constipation,  from 
the  catarrh  excited  by  the  irritation  of  the  mucous  membrane  produced  by 
the  faecal  mass,  and  pressure  on  the  biliary  duct  may  cause  an  obstructive 
jaundice. 


316  DISEASES   OF  THE   DIGESTIVE   SYSTEM. 

The  impacted  fgecal  masses  may  give  rise  to  one  large  tumor,  or  to 
several  small  yet  distinct  masses  which  can  easily  be  detected  along  the 
line  of  the  large  intestine  ;  they  may  be  felt  often  in  the  transverse  or 
ascending  colon  as  movable  tumors,  but  generally  the  largest  accumula- 
tions collect  in  the  sigmoid  flexure  and  caecum.  These  tumors  are  often  so 
large  that  they  cause  tenesmus.  In  the  aged,  torpor  of  the  rectum  is  often 
marked  by  spurious  diarrhoea,  acute  pain  in  the  lower  part  of  the  abdomen, 
great  tenesmus  and  bearing  down  at  stool,  accompanied  by  dysuria,  and, 
often,  retention  of  the  urine. 

Differential  Diagnosis. — The  method  of  the  diagnosis  of  impacted  faecal 
masses  Las  been  given  under  the  head  of  "Intestinal  Obstruction."  Im- 
pacted faeces  in  the  rectum  may  be  mistaken  for  cancer;  a  digital  examina- 
tion of  the  rectum  will  establish  the  diagnosis. 

Prognosis.,^ When  the  constipation  is  functional,  and  not  the  result  of 
malignant  growths,  or  intestinal  obstruction  other  than  faecal,  the  progno- 
sis is  good.  In  very  old  people  it  is  almost  impossible  to  overcome  habitual 
constipation,  on  account  of  their  constant  indolence  and  apathy.  Inflam- 
matory complications  always  render  the  prognosis  unfavorable ;  and  after 
long-continued  constipation  the  symptoms  of  intestinal  obstruction  are 
apt  to  be  followed  by  peritonitis  of  a  low  type,  which  may  not  be  suspected 
during  life. 

Treatment. — The  treatment  of  temporary  constipation  consists  in  the  ad- 
ministration of  a  dose  of  Epsom  or  Rochelle  salts,  or  a  tumbler  of  any  one 
of  the  many  efficient  natural  waters ;  or,  if  indicated,  a  mercurial  purge 
followed  by  a  saline.  It  is  not  often  that  a  physician  is  consulted  for  sim- 
ple constipation  ;  care,  diet,  and  exercise,  with  an  occasional  cold  water 
enema,  are  usually  all  that  is  required  to  keep  the  bowels  open. 

Habitual  constipation,  however,  frequently  attains  the  dignity  of  a  disease, 
and  it  requires  much  care  and  patience,  both  on  the  part  of  the  physician  and 
patient,  to  overcome  it.  One  who  suffers  from  habitual  constipation  should 
endeavor  to  establish  a  regular  hour  for  the  evacuation  of  the  bowels.  Strain- 
ing at  stool  should  be  avoided.  Eegular  habits  in  this  respect  are  most  effi- 
cient for  overcoming  obstinate  constipation  ;  the  success  of  any  plan  of 
treatment  will  depend  largely  upon  the  perseverance  of  the  individual. 
The  dietetic  measures  consist  in  partaking  freely  of  those  articles  of  food 
which  leave  a  bulky  residue,  such  as  the  coarser  vegetables,  cracked  wheat, 
oatmeal,  etc.  Fruits  which  have  fine  seeds  (figs,  strawberries)  that  will  stim- 
ulate the  intestinal  mucous  membrane,  are  of  service  if  they  do  not  cause 
indigestion.  Prunes  sweetened  with  molasses  are  sometimes  very  efficient. 
Great  care  should  be  exercised  not  to  overload  the  stomach  with  food  difficult 
of  digestion,  and  each  individual  is  a  law  unto  himself  in  this  matter.  A 
goblet  of  cold  or  hot  water  Just  before  retiring  and  on  rising  will  often  over- 
come a  long-standing  constipation,  while  the  daily  use  of  saline  waters  is  to 
be  avoided,  for  such  use  often  makes  the  constipated  habit  more  inveterate. 
Daily  exercise  in  walking  or  horseback  riding,  is  a  most  efficient  means  for 
overcoming  constipation  in  those  who  are  strong  and  vigorous.  Water 
should  be  taken  freely  before  and  after  the  exercise.     The  tonic  effects  of  ti 


INTESTIKAL  COLIC.  317 

cold  sponge  or  shower-bath  on  rising  are  often  of  great  service.  The  mechan- 
ical means  consist  in  friction  and  kneading  of  the  abdomen.  In  the  old 
and  bed-ridden,  bending  the  body  backward  and  forward  will  be  found  to 
provoke  and  aid  defecation.  The  galvanic  current  is  especially  beneficial  in 
the  aged  and  paralyzed.  Included  in  the  list  of  mechanical  means  are  ene- 
mata  and  suppositories.  Cold  water,  salt  water,  soap  and  water,  castor-oil, 
etc.,  are  at  first  very  efiicient  as  enemata,  but  the  rectum  very  soon  becomes 
accustomed  to  them  and  ceases  to  respond  to  their  stimulus. 

If  mechanical  means,  diet  and  change  of  habits  fail  to  overcome  the  con- 
stipation, recourse  must  be  had  to  medicinal  agents.  These  are  very 
numerous  ;  the  rule  is  to  begin  with  the  mildest.  Cases  are  often  met  with 
where  an  individual  has  taken  stronger  and  stronger  cathartics  without 
avail,  and  until  the  great  object  of  his  life  seems  to  be  to  get  a  movement 
from  the  bowels.  It  will  generally  be  found  in  such  cases  that  reliance  has 
been  placed  wholly  on  drugs  ;  by  changing  to  the  milder  cathartics,  regulat- 
ing the  diet,  and  insisting  upon  daily  exercise,  the  constipation  is  easily 
overcome.  It  is  always  to  be  borne  in  mind  that  drugs  are  only  aids  to 
other  measures.  Tonics  should  always  be  combined  with  laxatives ;  gen- 
tian, strychnine  and  quinine,  combined  with  aloes,  will  often  effect  more 
than  the  most  drastic  purgatives.  Favorite  cathartic  combinations  are  : — 
(1)  aloes,  myrrh,  colocynth,  gentian,  and  quinine  ; — (2)  aloes,  rhubarb 
and  strychnia  ; — (3)  strychnia  and  aloin  ; — (4)  nux  vomica,  aloes,  bella- 
donna, and  podophyllum.  In  all  combinations  for  constipation  in  females, 
belladonna  and  hyoscyamus  are  very  active  agents.  Podophyllum  produces 
slow  and  painless  evacuations,  and  acts  efficiently  for  a  long  time.  In  very 
obstinate  cases,  colocynth,  scammony,  or  one-sixth  of  a  drop  of  croton-oil 
may  be  required  until  the  habit  of  daily  evacuation  is  established.  Ehu- 
barb  and  magnesia  is  a  favorite  cathartic  in  children  and  young  girls.  In 
old  age  and  in  children,  drastic  cathartics  are  always  to  be  avoided.  If  a 
large  faecal  mass  becomes  impacted  in  the  lower  part  of  the  colon,  it 
will  often  have  to  be  scooped  out  with  the  finger  or  rectal  scoop.  If 
the  mass  is  exceedingly  hard,  it  is  best  to  throw  a  steady  stream  of  moder- 
ately hot  water  and  glycerine  against  it  before  attempting  to  remove  it. 
Enemata  are  adjuvants  to  all  plans  of  treating  constipation,  where  there 
is  evidence  of  a  large  faecal  accumulation  in  the  lower  bowel. 

n^TESTINAL    COLIC. 

The  term  intestinal  colic,  in  its  wider  sense,  includes  all  painful  affec- 
tions of  the  intestines  which  are  not  caused  by  structural  changes  in  the  in- 
testinal walls.  Its  varieties  are  flatulent,  Ulious,  lead,  copper,  gouty  and 
rheumatic  colic.  It  belongs  to  the  class  of  neuroses,  and  is  purely  func- 
tional in  its  nature.  It  is  attended  by  irregular  spasmodic  contraction  of 
the  muscular  coat  of  the  intestine. 

Etiology.— It  occurs  most  frequently  in  the  young,  the  liability  to  it  stead- 
ily decreasing  with  advancing  years,  and  in  females  oftener  than  in  males. 
Neurotic  temperaments  and  a  sedentary  mode  of  life,  rheumatism,  chronic 


318  DISEASES    OF   THE   DIGESTIVE   SYSTEM. 

alcoholismus,  and  gout  predispose  to  it.  Its  most  frequent  direct  cause  is 
excessive  distention  of  a  portion  of  the  intestinal  canal.  It  is  apt  to  occur 
in  the  hysterical  and  hypochondriacal,  and  in  those  who  are  the  subjects  of 
malarial  and  syphilitic  cachexia.  Hepatic  and  biliary  derangements  induce 
it.  Cold,  especially  cold  to  the  feet,  is  often  its  exciting  cause.  Direct 
irritation  of  the  bowels  by  undigested  food,  certain  articles  of  food,  as  cu- 
cumbers, shell-fish,  strawberries,  etc.,  will  cause  colic  in  some  persons. 
Gaseous  collections  and  distention  of  the  intestine  by  faeces,  or  by  bundles 
of  worms,  sometimes  excite  it.  Lead  and  the  copper  salts  cause  coUca  pic- 
tonum  and  copper  colic.  All  metallic  colics  seem  to  result  from  hyperaes- 
thesia  of  the  terminal  nerves. 

Symptoms. — An  attack  of  intestinal  colic  may  be  preceded  by  a  sense  of 
distention  in  the  abdomen,  slight  nausea  and  belching,  languor,  numb- 
ness, irritability  of  temper,  or  apathy.  The  attack  itself  comes  on  sud- 
denly. 

In  flatulent  colic,  there  is  a  severe  twisting,  paroxysmal  pain  around 
the  umbilicus,  ar  in  the  region  of  the  colon.  The  abdomen  becomes  dis- 
tended with  the  flatus,  the  bowels  are  constipated,  eructations  and  borbo- 
rygmi  are  present,  and  there  may  be  vomiting.  The  escape  of  flatus,  change 
of  position,  and  steady  pressure  over  the  abdomen  relieve  the  pain  ;  rarely 
is  the  abdomen  tender.  There  is  no  rise  of  temperature,  the  surface,  if  the 
pain  is  severe,  is  cold  and  covered  with  clammy  perspiration.  The  pulse  is 
small  and  feeble.  At  the  height  of  the  attack  the  patient  groans  and  rolls 
about,  frequently  throwing  himself  across  some  hard  substance,  so  as  to " 
cause  pressure  on  the  abdomen.  In  children,  convulsions,  projectile  vom- 
iting, syncope,  strangury,  priapism,  and  cardiac  palpitation  are  not  infre- 
quent. A  large  quantity  of  limpid  urine  is  usually  secreted,  and  there  is  a 
frequent  desire  to  urinate.  After  several  hours,  during  which  many  spasms 
of  the  colic  have  occurred,  large  discharges  of  flatus,  rumbling  of  the  bow- 
els and  milder  paroxysms  of  pain,  mark  the  termination  of  the  attack.  In 
the  weak  and  nervous,  the  expression  of  the  countenance,  the  condition  of 
the  pulse,  and  the  signs  of  collapse  may  cause  one  to  suspect  intestinal  per- 
foration. On  palpation  during  a  spasm,  the  intestine  at  points  may  be 
felt, rigid  and  hard;  the  symptoms   disappear  as  the  paroxysm  subsides. 

Flatulent  colic  is  often  called  crapulous,  when  it  follows  a  too  hearty  meal 
or  the  ingestion  of  indigestible  articles  of  food.  In  crapulous  colic,  the 
tongue  is  either  covered  with  a  white  fur,  is  enlarged,  showing  the  red 
papillse  through  it,  or  it  is  bright  red  at  the  tip  and  edge.  Crapulous  colic 
is  accompanied  by  pains  in  the  head  and  dimness  of  sight ;  and  sometimes 
urticaria  and  roseola,  strophulus,  and  other  lichenous  eruptions  appear  on 
the  skin.  Flatulent  colic  is  most  frequently  met  with  in  infants,  and  the 
picture  presented  by  a  child  with  wind  colic  is  too  familiar  to  need  further' 
description.  In  adults,  flatulent  colic  may  be  due  to  malarial  influence, 
and  then  the  attacks  will  be  periodical. 

Bilious  colic  is  accompanied  by  nausea  and  vomiting,  the  vomited 
matters  being  greenish  and  yellow.  It  is  preceded  by  nausea,  anorexia  and 
a  coated  tongue.     It  sometimes  begins  with  a  chill.     The  bowels  are  ob' 


INTESTINAL   COLIC.  319 

stinately  constipated,  there  is  slight  fever,  the  abdomen  is  tender  and 
sligMly  distended,  or  it  may  be  retracted.  When  prolonged,  bilious  colic 
may  be  accompanied  by  janndice.  Bilious  colic  occurs  in  summer  and 
autumn,  chiefly  in  malarial  districts.  A  form  of  colic  which  is  often  a 
distinct  "  cramp,"  is  obviously  due  to  a  gouty  or  rheumatic  diathesis ; 
beyond  its  etiology,  it  does  not  differ  from  flatulent  colic.  It  may  be 
metastatic. 

Of  the  metallic  colics,  lead  colic,  "  colica  pictonum,"  is  far  the  most  fre- 
quent ;  it  is  a  true  colic,  no  lesions  being  found  in  the  intestines  of  those 
who  have  died  of  it.  The  metallic  colics  are  produced  by  the  primary  ac- 
tion of  the  metal  on  the  nervous  system,  and  are  preceded  by  the  general 
symptoms  of  the  poisoning.  Lead  colic  comes  on  with  moderately  se- 
vere paroxysms  of  pain,  which  gradually  increase  in  severity  until  a  series 
of  intense  paroxysms  rapidly  follow  each  other.  The  pain  is  located  about 
the  umbilicus,  and  is  twisting  or  grinding  in  character.  With  the  colic 
there  may  be  cramps  and  pains  in  the  extremities.  The  abdomen  is  con- 
tracted and  hard  ;  knots  of  rigid  intestine  can  sometimes  be  felt.  The 
abdomen  is  not  tender,  and  forcible  pressure  markedly  relieves  the  pain. 
The  bowels  are  obstinately  constipated,  but  as  the  attack  passes  ofE  diarrhoea 
often  occurs.  After  the  subsidence  of  the  pain  another  attack  may  be  ex- 
cited by  taking  food,  or  one  may  return  without  any  apparent  cause.  The 
pulse  is  slow  during  an  attack,  and  there  is  no  rise  of  temperature.  An 
individual  suffering  from  lead  poison  is  sallow,  anaemic,  and  more  or  less 
enfeebled.  The  extensors  of  the  fore-arm  are  often  paralyzed  (drop-wrist), 
and  there  may  be  amaurosis  (due  to  optic  neuritis)  and  epileptiform  con- 
vulsions. Along  the  edge  of  the  gums  is  a  deep  blue  dotted  line  composed 
of  lead,  formed  by  the  sulphuretted  hydrogen  produced  by  decomposing 
food  lodged  between  the  teeth  reacting  on  the  lead  which  circulates  in  the 
capillaries.  This  is  the  distinctive  sign  of  lead  poisoning.  The  pain  in 
lead  colic  radiates  in  all  directions,  and  its  point  of  maximum  intensity  is 
located  at  different  times  in  different  regions  of  the  abdomen. 

Copper  colic  may  be  distinguished  from  lead  colic  by  the  fact  that  the 
pain  is  increased  by  pressure,  the  abdomen  is  distended  instead  of  retracted, 
and  in  place  of  obstinate  constipation  there  is  diarrhoea  with  greenish  stools  ; 
there  is  a  purplish  line  about  the  gums,  and  there  may  be  attacks  of  dysp- 
noea from  laryngeal  and  bronchial  spasm. 

Differential  Diagnosis.— Intestinal  colic  may  be  confounded  with  peritoni- 
tis, intestinal  ohstruction,  gall-stone  colic,  intestinal  perforation,  spinal 
disease,  aneurism,  lahor-pains,  hernia  and  muscular  rheumatism. 

In  peritonitis  there  is  usually  a  distinct  febrile  movement,  the  pulse 
is  accelerated  and  is  tense  and  wiry  m  character.  In  colic  there  is  no 
fever  or  increase  in  pulse-rate,  the  rule  being  rather  a  slowed  pulse.  In 
peritonitis  the  patient  avoids  the  slightest  motion  of  the  body,  and  firm 
pressure  over  the  abdomen  increases  the  pain,  while  in  colic  the  patient 
tosses  from  one  side  to  the  other,  and  firm  pressure  over  the  abdomen 
relieves  the  pain.  The  pain  of  peritonitis  is  constant,  that  of  colic 
is  paroxysmal. 


320  DISEASES   OF  THE   DIGESTIVE   SYSTEM. 

Perforation  of  the  intestine  is  to  be  distinguished  by  the  intensity  and 
rapidly  increasing  severity  of  the  pain,  rapidity  of  the  pulse,  rapidly  de- 
veloping tympanitis  and  collapse. 

In  spinal  disease  the  pain  is  along  the  course  of  the  nerves  and  all  the 
intestinal  symptoms  of  colic  are  absent. 

Aneurism  of  the  abdominal  aorta  is  distinguished  by  the  physical  signs 
of  aneurismal  tumor,  by  the  change  in  the  femoral  pulse,  and  by  constant 
localized  pain  in  the  back. 

Hernia  has  an  external  tumor,  there  is  stercoraceous  vomiting,  and  only 
great  carelessness  in  the  examination  will  allow  of  error  in  the  diagnosis. 

Lahor-pains  may  simulate  colic,  and  there  are  cases  on  record  where — 
in  concealed  pregnancy — the  true  state  of  affairs  was  not  recognized  until 
labor  was  completed. 

Muscular  rheumatism  is  attended  by  intense  and  constant  pain,  aggra- 
vated by  motion  and  pressure,  having  its  maximum  intensity  at  the  origin 
and  insertion  of  the  muscles.  There  will  be  a  history  of  exposure,  and  also 
of  frequent  rheumatic  attacks  in  other  parts  of  the  body. 

Prognosis. — The  prognosis  is  always  favorable.  Death  has  occurred  from 
rupture  of  the  intestine  from  excessive  gaseous  distention,  and  from  con- 
vulsions in  very  young  children. 

Treatment. — The  indications  for  treatment  are  to  be  found  in  the  etiology 
of  each  attack.  In  flatulent  colic,  and  in  that  from  impacted  faeces  and 
undigested  food,  evacuants  are  indicated.  The  internal  administration  of 
castor-oil  and  an  aperient  enema  generally  give  relief.  If  the  colic  is  due 
to  exposure  of  the  feet  or  abdomen  to  cold,  hot  aromatic  teas  and  diapho- 
retics are  indicated.  In  all  forms,  opium,  chloroform,  hydrate  of  chloral, 
or  ether  may  be  given  to  relieve  the  pain  and  spasm.  In  hysterical  and 
nervous  subjects,  at  the  onset  of  the  attack,  Hoffman's  anodyne,  musk, 
asafoetida,  valerian,  and  the  essential  oils  often  quickly  relieve  the  pain  and 
remove  the  flatus.  In  children,  bromide  of  potassium  in  carminative 
waters,  often  affords  speedy  relief.  In  some  cases  it  will  be  necessary  to  re- 
lieve an  overloaded  stomach  by  administering  an  emetic.  Malarial  colics 
demand  for  their  relief  quinine  combined  with  calomel.  Grouty  colic  is  best 
treated  with  oil  of  cajeput,  Warner's  cordial,  and  carminatives.  The  feet 
are  to  be  placed  \\\  a  mustard  bath,  and  a  mustard  plaster  is  to  be  placed 
on  the  abdomen.  Anti-gout  remedies  are  to  be  given  as  soon  as  the  sever- 
ity of  the  colic  is  relieved. 

In  lead  colic,  opium  is  the  most  efficient  remedy.  It  will  often  relieve 
the  constipation.  My  rule  is  to  combine  it  with  belladonna  and  croton 
oil  (1  grain  of  opium,  l-6th  grain  of  the  extract  of  belladonna,  and  1  drop 
of  croton  oil),  every  two  hours,  until  relief  is  obtained.  Sulphate  of  mag- 
nesia is  preferred  by  some  to  the  croton  oil ;  a  warm  bath  will  often  give 
immediate  relief  and  hasten  the  action  of  the  croton  oil.  As  soon  as  the 
bowels  are  acted  upon  the  pain  disappears.  Faradic  electricity  and  pilo- 
carpin  are  advocated  by  some  German  authorities.  A  milk  diet  acts  as  a 
prophylactic  and  curative  agent,  and  workmen  in  lead  factories  should 
drink  large  quantities  of  i;^.     It  is  claimed  by  some,  that  sulphuric-acid 


PEEITONITIS.  321 

lemonade  is  a  good  preventive,  as  it  forms  insoluble  lead  sulphate.     A  long 
time  elapses  before  all  the  lead  is  removed  from  the  system. 

In  copper  colic  sulphur  baths,  turpentine  stupes  or  sinapisms,  ether  and 
opium,  and  a  milk  diet,  with  the  casual  indications,  are  all  that  is  ne- 
cessary for  its  successful  management.  In  all  forms  there  are  two  prom- 
inent indications  for  treatment,  viz. :  to  relieve  pain  with  opium,  and  to 
evacuate  the  bowels.  Warm  fomentations  and  sinapisms  to  the  abdomen 
are  always  of  service.  Cold  applications  are  contra-indicated.  Always 
seek  for,  and,  if  possible,  find  the  cause  before  cathartics  are  given. 

PERITONITIS. 

Peritonitis  is  an  inflammation  of  the  whole  or  a  j)art  of  the  serous  mem- 
brane which  lines  the  abdominal  wall  and  covers  the  viscera  contained  in 
the  abdominal  cavity.  It  may  be  ac^^^e  or  chronic;  local  (circumscribed) 
or  general.  The  acute  form  usually  begins  at  one  point  and  rapidly  spreads 
over  the  entire  membrane.  The  chronic  may  result  from  the  acute,  or  it 
may  be  interstitial,  hemorrhagic,  tubercular  or  cancerous. 

Morbid  Anatomy. — Acute,  general  (or  diffused)  peritonitis  begins  with  an 
intense  injection  of  the  capillaries  of  some  portion  of  the  visceral  or  parietal 
layer  of  the  peritoneum.  Sometimes  the  injection  is  so  intense  that  the 
capillaries  rupture  at  points  and  cause  small  blood  extravasations.  The  in- 
flamed portion  at  first  presents  a  mottled  appearance  ;  the  redness  is  most 
intense  at  the  starting  point  of  the  inflammation.  With  the  capillary 
hypersemia  there  is  desquamation  of  the  endothelial  cells,  and  the  perito- 
neum loses  its  natural  glistening  appearance,  becomes  dry  and  lustreless, 
and  there  is  swelling  and  an  increase  in  the  number  of  its  fixed  connective- 
tissue  cells.  Following  this,  a  more  or  less  abundant  exudation  takes  place 
upon  its  free  surface,  into  its  substance  and  underneath  it.  This  exudation 
may  be  fibrinous,  sero-fibrinous,  or  purulent.  The  changes  in  general  peri- 
tonitis are  usually  most  marked  in  the  parietal  portion  of  the  peritoneum, 
in  layers  of  the  omentum,  and  in  the  meso-colon. 

With  the  advance  of  the  disease,  the  fibrinous  exudation  increases  in 
amount,  and  assumes  a  distinctly  yellowish  tinge  ;  as  it  increases  in  thick- 
ness it  presents  the  appearance  of  a  roughened  false  membrane,  which  may- 
vary  in  thickness  from  a  mere  film  to  a  quarter  of  an  inch  or  more ;  its 
consistency  varies  from  a  pulpy  mass  to  a  coherent,  elastic  membrane.  It 
may  form  a  continuous  layer  over  the  visceral  or  parietal  portion  of  the 
peritoneum,  and  agglutinate  its  opposing  surfaces  more  or  less  firmly  to  each 
other.  If  a  serous  effusion  occurs  at  the  same  time,  it  tends  to  gravitate  to^ 
the  most  dependent  portion  of  the  peritoneal  cavity  ;  it  is  usually  small  in 
quantity.  After  a  time  cells  appear  in  the  layer  of  fibrinous  exudation, 
probably  derived  from  the  connective-tissue  of  the  peritoneum,  which 
cause  the  development  of  a  layer  of  new  connective-tissue,  which  may  give 
rise  to  permanent  thickenings  and  adhesions  between  the  surfaces.  Pap- 
illary connective-tissue  growths  may  also  form  and  cause  adhesions  j 
these  adhesions  are  usually  in  patches.  The  new  connective-tissue  is  most 
21 


322  DISEASES   OF   THE    DIGESTIVE   SYSTEM, 

extensive  and  thickest  over  the  solid  viscera,  as  the  uterus,  liver  and 
spleen. 

The  bands  of  adhesion  may  bind  down  a  portion  of  the  intestine  and 
cause  fatal  obstruction,  or  they  may  form  tense  cords  underneath  which  a 
loop  of  intestine  may  be  suddenly  incarcerated.  On  the  surface  of  the  solid 
viscera  the  new  tissue  gradually  becomes  indurated,  resembling  cicatricial 
tissue.  Sometimes  the  new  connective-tissue  bands  are  so  slight  that  the 
peristaltic  motion  of  the  intestines  causes  them  to  disappear.  Firmer  adhe- 
sions may  cause  displacement  of  the  viscera  or  twisting  of  the  intestines,  or 
the  whole  contents  of  the  abdominal  cavity  maybe  matted  into  one  globular 
mass.  Acute  peritonitis  may  cause  a  general  thickening  of  the  peritoneum 
without  adhesions,  its  tissue  becoming  dense,  white  and  fibrous.  In  these 
cases  the  fibro-cellular  developments  are  chiefly  in  the  substance  of  the 
peritoneum — not  on  its  surface. 

The  changes  in  the  intestines  vary:  at  first,  vascular  lines  are  seen  running 
along  their  long  axis,  and  in  very  acute  cases  their  whole  surface  is  red- 
dened. Interstitial  cell-growth  of  the  sub-peritoneal  coat,  accompanied  by 
inflammatory  oedema,  causes  their  peritoneal  surface  to  present  an  opaque 
appearance.  The  muscular  coat  loses  its.  contractile  power,  and  they  become 
distended  with  gas,  so  that  when  the  abdomen  is  opened  they  protrude 
through  the  incision.  The  abdominal  muscles  and  the  surface  of  the  vis- 
cera, especially  the  liver  and  spleen,  are  paler  than  normal.  The  intestinal 
mucous  membrane  is  sometimes  paler  than  normal,-  sometimes  intensely 
hyperasmic. 

In  non-adhesive  or  sero-fibrinous  peritonitis,  with  the  plastic  exudation 
there  is  a  more  abundant  effusion  of  fluid,  containing  flocculi  of  lymph 
and  cells  which  are  most  abundant  in  the  most  dependent  portions  of 
the  abdominal  cavity.  Its  color  varies  from  a  delicate  straw  color  to  a 
grayish  red.  Underneath  the  fluid  on  the  surface  of  the  peritoneum  there 
is  a  layer  of  exudation  which  in  its  anatomical  arrangement  is  the  same  as 
that  in  adhesive  peritonitis,  and  it  undergoes  similar  changes.  Displace- 
ments of  the  abdominal  and  thoracic  organs  often  occur  from  the  pressure 
of  a  large  fluid  effusion.  The  fluid  effusion  may  undergo  absorption,  and, 
the  two  plastic  layers  coming  in  contact,  adhesions  will  form  as  in  the 
adhesive  variety. 

Acute  suppurative  peritonitis  may  have  for  its  product  a  fibre-  or  sero- 
purulent  exudation.  In  this  variety,  the  parietal  and  visceral  layers  of 
the  peritoneum  are  partially  or  completely  covered  and  infiltrated  with 
a  gray,  opaque,  soft,  fibrous  exudation,  which  is  infiltrated  with  pus 
cells.  The  effusion  varies  in  color  and  consistency;  it  may  be  thick, 
creamy,  and  viscid,  or  turbid,  thin  and  watery.  It  collects  in  the  de- 
pendent portions  of  the  pelvic  cavity.  The  purulent  exudation  may  be 
spread  out  over  the  entire  surface  of  the  membrane,  or  it  may  be  associated 
with  adhesions  when  it  occurs  in  distinct  collections  ;  it  is  bounded  by  or- 
ganized septa,  and  appears  as  if  there  were  numerous  separate  abscesses.  An 
ulcerative  process  may  be  established,  and  the  purulent  accumulation  may 
be  discharged  through  the  abdominal  walls  into  the  intestinal  canal,  blad- 


PEEITOKITIS.  323 

der,  vagina,  or  even  into  the  thoracic  cavity.  The  purulent  accumulation 
may  find  exit,  in  rare  instances,  along  the  plane  of  the  psoas  muscle.  In 
"puerperal  peritonitis,"  the  uterus  and  its  appendages  are  thickly  covered 
and  infiltrated  with  pus.  Sometimes  the  ovaries  and  the  Fallopian  tubes 
contain  pus.  In  nearly  every  instance  of  acute  suppurative  peritonitis  the 
surfaces  of  the  viscera  present  evidences  of  lymphangitis,  phlebitis,  or  super- 
ficial abscesses.  If  recovery  takes  place  without  a  discharge  of  the  purulent 
accumulation,  a  part  of  it  is  absorbed,  and  the  remainder  becomes  cheesy 
and  encysted. 

If  acute  local  peritonitis  is  secondary  to  visceral  inflammation,  the  in- 
flammatory process  in  the  viscus  reaches  its  surface  and  involves  the  peri- 
toneum covering  it.  These  inflammations  have  received  various  names, 
as  perihepatitis,  perisplenitis,  perimetritis,  etc.  ;  the  inflamed  peritoneum 
in  this  variety  is  usually  sharply  defined.  Adhesions  are  quickly  formed, 
and  encysted  purulent  effusions  frequently  result.  By  the  establishment 
of  local  peritonitis,  ulcers  of  the  stomach  or  intestine  and  abscesses  of 
the  liver  are  prevented  from  penetrating  the  abdominal  cavity  and  causing 
a  rapidly  fatal  general  peritonitis. 

General  Chronic  Peritonitis. — An  acute  general  peritonitis  may  run  a 
protracted  course,  become  chronic,  and  cause  sero-j)urulent  collections, 
or  it  may  be  chronic  from  the  onset.  An  extensive  adhesive  or  sero- 
fibrinous peritonitis  may  become  chronic,  causing  numerous  adhesions 
and  thickenings  of  the  peritoneum,  and  a  more  or  less  abundant 
collection  of  fluid  contained  in  the  spaces  formed  by  the  adhe- 
sions. The  fluid  after  a  time  usually  becomes  sero-purulent  or  puru- 
lent, and  in  the  latter  case  may  be  converted  into  a  cheesy  mass.  Coils  of 
intestine  are  matted  together,  or  very  firm  adhesions  with  organs  or  with 
the  abdominal  parietes  occur.  In  all  cases  of  chronic  peritonitis  there  are 
extensive  peritoneal  adhesions  and  thickenings.  When  a  considerable  quantity 
of  pus  is  circumscribed  by  fibrous  septa,  either  an  external  opening  takes 
place  or  it  becomes  encapsulated.  In  some  cases  of  chronic  general  perito- 
nitis, there  is  a  gradual  ascitic  accumulation.  In  most  cases,  pigmented 
and  hemorrhagic  spots  stud  the  thickened  peritoneum.  Local  or  circum- 
scribed chronic  peritonitis  may  be  developed  over  an  enlarged  spleen,  or  a 
cirrhotic  liver,  or  in  connection  with  chronic  intestinal  diseases.  Its  ana- 
tomical changes  are  similar  to  those  of  general  chronic  peritonitis. 

In  Jieynorrliagic  sub-acute  peritonitis,  the  new  tissue  formations  are  exceed- 
ingly vascular,  and  the  thin  walls  of  the  vessels  may  rupture.  The  new  mem- 
brane may  consist  of  one  thin  layer,  or  of  several  strata  with  effused  blood 
between  them.  Sometimes  the  new  tissue  is  infiltrated,  and  the  entire  sur- 
face of  the  peritoneum  may  assume  a  dark  brown  color,  the  fluid  in  its 
cavity  having  a  distinct  chocolate  hue.  This  form  of  peritonitis  is  especially 
liable  to  occur  with  hypertrophic  cirrhosis. 

In  tubercular  peritonitis  there  may  be  only  a  few  tubercular 
nodules  on  the  surface  of  the  peritoneum,  or  there  may  be  a  gran- 
ular infiltration  of  the  entire  membrane.  In  its  milder  form  only 
a  few  gray,   semi-transparent   tubercles  will   be  found  in  that  portion 


324  DISEASES   OF   THE   DIGESTIVE    SYSTEM. 

of  the  peritoneum  which  overlies  intestinal  ulcerations.  In  severe  or 
extensive  tubercular  peritonitis,  the  surface  of  the  peritoneum  is  studded 
with  tubercular  granulations,  which"  are  also  disseminated  through  the  new 
tissue  formation,  and  in  the  subjacent  peritoneal  and  subperitoneal  tissue. 
The  mesentery  and  omentum  are  also  studded  with  granules.  Robin  states 
that  these  tubercles  are  secondary  to  the  peritonitis.  The  adhesions  formed 
in  tubercular  peritonitis  divide  the  cavity  into  compartments,  which  con- 
tain the  effusion.  The  effusion  may  be  sero-fibrinous  or  purulent ;  in  some 
instances  it  is  hemorrhagic,  and  varies  in  color  from  a  light  pink  to  a  deep 
chocolate.  In  very  severe  cases,  tubercular  peritonitis  is  always  hemorrhagic. 
Ecchymotic  spots  and  petechige  are  frequently  present  in  the  new  mem- 
brane. ISTo  form  of  diffuse  peritonitis,  except  cancerous,  causes  such  ex- 
tensive thickenings,  adhesions  and  distortions  as  tubercular. 

Cancerous  Peritonitis. — Cancer  of  the  peritoneum  is  rarely  primary,  but 
is  propagated  to  the  peritoneum  from  adjacent  organs.  When  peritonitis  is 
the  result  of  cancer  in  the  peritoneum,  it  commences  with  the  primary  cancer- 
ous developments,  or  is  established  when  cancer  of  the  abdominal  or  pelvic  vis- 
cera reaches  their  surface  and  involves  the  peritoneum  covering  them.  The 
cancerous  developments  may  begin  in  the  omentum  and  gradually  involve 
the  entire  peritoneum.  Cancerous  peritonitis  may  begin  as  a  diffused  sup- 
purative peritonitis,  in  connection  with  rapid  cancerous  developments  in 
some  of  the  abdominal  viscera,  especially  in  the  uterus.  Sometimes,  in 
cancerous  peritonitis,  the  peritoneum  may  be  distended  with  a  serous,  lemon- 
colored  or  whey-like  fluid,  accompanied  by  a  more  or  less  abundant  plastic 
exudation  with  hemorrhages  into  the  exudation.  The  hemorrhage  into  the 
effusion  colors  it  as  well  as  the  cancerous  nodules  on  the  surface  of  the  per- 
itoneum. Adhesions  are  formed  as  in  the  other  varieties  of  peritonitis,  and 
collections  of  fluid  may  thus  become  encapsulated.  This  variety  of  peri- 
tonitis is  not  only  attended  by  the  development  of  tough,  leathery  mem- 
hranes,  but  entire  organs  may  be  enveloped  by  the  new  tissue  formations  ; 
in  these  cases  the  mucous  membrane  of  the  intestinal  tract  is  usually  the 
seat  of  chronic  enteritis. 

Etiology. — Peritonitis  may  occur  at  any  age,  in  the  strong  and  robust  as 
well  as  in  the  weak  and  feeble.  It  is  met  with  more  frequently  in  females 
than  in  males  ;  certain  localities  predispose  to  it,  and  the  tendency  to  it  is 
greater  in  those  suffering  from  chronic  diseases.  Earely,  if  ever,  is  acute 
peritonitis  of  spontaneous  origin.  But  the  discovery  of  its  cause  during 
life  is  often  very  difficult,  yet  very  important,  for  on  the  cause  depends  the 
prognosis  and  to  some  extent  the  treatment. 

The  exciting  causes  of  acute  peritonitis  are  :  first,  intestinal  obstruc- 
tions and  perforations.  Under  this  head  may  be  included  typhlitis 
and  perityphlitis,  with  ulceration;  rupture  of  hepatic  and  other 
abscesses ;  ulceration  and  rupture  of  the  stomach,  the  gall  or  urinary 
bladder;  rupture  of  hydatid  and  ovarian  cysts;  ulceration  and  per- 
foration of  the  intestines  in  typhoid  fever,  syphilitic  or  tubercular  in- 
testinal ulcers ;  and  the  rupture  of  an  abdominal  aneurism.  In  rare 
instances,  hydatids   of  the   lung  or  purulent  pleural  accumulations  open 


PERITONITIS.  325 

into  the  cavity  of  the  abdomen  and  set  up  a  diffuse  peritonitis.  Injections 
into  the  uterus  may  pass  through  the  Fallopian  tubes  into  the  peritoneal 
cavity  and  cause  peritonitis.  Rupture  of  an  organ  from  a  blow  or  fall,  and 
penetrating  wouuds  of  the  abdomen,  are  causes  of  traumatic  peritonitis. 
Abscesses  of  the  abdominal  parietes,  of  the  vesiculge  seminales,  or  psoas  and 
lumbar  abscesses  from  caries  and  necrosis  of  the  spine,  ribs  or  pelvic  bones, 
may  open  into  the  peritoneal  cavity  and  cause  general  peritonitis. 

Secondly,  the  extension  to  the  peritoneum  of  inflammation  of  organs 
covered  by  peritoneum  is  a  common  cause  of  local  peritonitis.  In  this 
class  of  cases  the  peritonitis  is  first  local,  and  then  it  may  become  general. 
Inflammation  of  the  stomach  or  intestines  may,  by  extension,  involve  the 
peritoneum  covering  them.  Peritonitis  may  result  from  extension  of  in- 
flammation from  the  uterus  and  its  appendages,  liver,  spleen  and  kidneys. 
In  typhlitis,  perityphlitis,  proctitis,  periproctitis  and  chronic  ulcer  of  the 
rectum,  peritonitis  may  occur  by  extension  of  inflammation  without  per- 
foration. Venous  thrombi,  especially  lymphangitis  and  phlebitis  of  the 
uterus,  or  severe  contusions  of  the  abdomen  may  cause  peritonitis  by  exten- 
sion. Intestinal  intussusceptions,  volvuli,  hernise,  etc. ,  quickly  induce  per- 
itonitis even  when  no  rupture  has  occurred.  Gangrenous  and  inflammatory 
processes  in  the  umbilical  vessels  often  give  rise  to  peritonitis  in  the  new- 
born. In  the  very  young,  incomplete  descent  of  the  testicle  may  cause 
it.  Diverticula  from  hernia  of  the  mucous  membrane  of  the  lower  bowel 
through  the  muscular  coat,  may  become  filled  with  faeces  and  excite  peri- 
tonitis.' 

Tliirdly,  in  many  instances  acute  general  peritonitis  is  the  immediate  re- 
sult of  infection  ;  pyaemia,  septicaemia,  and  puerperal  fever  are  the  condi- 
tions in  which  infectious  peritonitis  is  most  likely  to  occur.  Puerperal  peri- 
tonitis may  occur  with  or  without  pyaemia.  Intra-uterine  peritonitis  can 
often  be  traced  to  a  syphilitic  taint,  and  to  puerperal  sepsis  in  the  mother. 
Exposure  to  cold  and  wet  rarely,  if  ever,  directly  causes  peritonitis.  Serous 
inflammations  of  a  rheumatic  character  are  very  interesting  in  their  com- 
binations ;  we  may  find  peritonitis  with  pericarditis  and  pleurisy,  or  with 
pneumonia  and  dysentery.  Erysipelas  has  been  complicated  by  peritonitis. 
Chronic  general  peritonitis  may  result  from  acute  diffuse,  or  from  acute 
local  peritonitis,  or  from  tubercle  and  cancer.  It  may  be  caused  by  long- 
standing ascites,  in  connection  with  cirrhosis  of  the  liver  and  chronic 
splenitis.  Chronic  local  peritonitis  follows  inflammatory  conditions  in  or- 
gans which  have  a  serous  covering,  by  simple  contiguity  of  tissue,  as  in 
hepatitis,  hobnailed  liver,  enlarged  spleen,  chronic  dysenteric  ulcers, 
chronic  typhlitis,  etc.,  etc.  Tumors  may  excite  local  chronic  peritonitis 
when  they  are  in  contact  with  the  peritoneum,  as  ovarian  tumors.  Chronic 
peritonitis  has  occurred,  according  to  Virchow,  in  intra-uterine  life.  Ex- 
tra-uterine pregnancy  without  rupture,  when  the  foetus  undergoes  degen- 
eration, may  lead  to  chronic  peritonitis.  Hemorrhagic  peritonitis  occurs 
most  frequently  with  hypertrophic  cirrhosis  of  the  liver,  Bright's  disease, 
general  tuberculosis,  and  acute  articular  rheumatism.     Tubercular  peri- 

>  American  Clinical  Lectures,  page  221. 


326  DISEASES   OF  THE   DIGESTIVE   SYSTEM. 

tonitis  is  met  with  most  frequently  in  early  life,  and  cancerous  peritonitis 
between  the  ages  of  forty  and  sixty-five. 

Symptoms. — The  symptoms  of  acute  peritonitis  vary  with  its  extent, 
severity,  and  the  causes  which  produce  it.  If  it  is  the  result  of  intestinal 
perforation,  its  onset  will  be  marked  by  excessive  pain  over  the  whole  ab- 
domen. In  infectious  peritonitis,  the  first  symptom  will  be  a  severe  chill. 
Peritonitis  resulting  from  the  extension  of  an  already  existing  visceral  in- 
flammation begins  with  local  and  gradually  increasing  pain.  All  varieties 
of  acute  peritonitis  from  whatever  cause  are  ushered  in  hj  pain  as  one  of 
the  earliest  symptoms.  The  pain  may  be  local  or  diffuse.  In  severe  cases, 
if  local  at  first,  it  becomes  diffuse  in  a  few  hours.  It  is  described  as  a. 
cutting,  burning  pain,  aggravated  by  pressure  and  by  movements  of  the 
abdomen.  The  more  sudden  the  onset,  the  more  intense  the  pain.  In  some 
cases,  the  weight  of  the  bedclothes  cannot  be  borne.  The  pain  causes  the 
patient  to  remain  motionless,  he  lies  on  his  back,  with  the  knees  drawn 
up,  the  breathing  is  wholly  thoracic,  the  respirations  are  rapid  and  super- 
ficial, and  the  face,  by  its  pallid,  drawn  and  anxious  look,  is  almost 
diagnostic  of  the  disease.  In  most  cases,  the  pain  is  at  first  paroxys- 
mal. 

If  the  peritonitis  is  general  the  abdomen  soon  becomes  distended  and  tym- 
panitic, the  tympanitis  increasing  as  the  disease  advances.  At  the  onset  of 
acute  peritonitis,  the  abdominal  muscles  are  rigid  and  contracted  ;  after 
this  tonic  rigidity  they  relax  and  allow  of  abdominal  •  distention.  Some- 
times the  distention  is  so  great  that  the  diaphragm  is  pushed  up  as  far  as 
the  third  or  fourth  rib,  the  lungs  are  compressed,  and  the  heart,  liver  and 
spleen  are  displaced.  In  local  acute  peritonitis,  the  tympanitis  is  usually 
slight ;  in  diffused  it  is  excessive  and  increases  the  pain  and  causes  dysp- 
noea, the  respirations  often  being  increased  to  forty  or  sixty  per  minute. 
As  the  intestines  become  distended  with  gas,  percussion  elicits  a  tympa- 
nitic note  over  the  whole  abdominal  cavity.  If  there  is  a  rapid  effusion  of 
serum,  it  will  gravitate  to  the  most  dependent  portion  of  the  peritoneal 
cavity  and  an  abnormal  area  of  dulness  will  mark  its  position,  the  line  of 
which  will  change  with  a  change  in  the  position  of  the  patient.  If  a  large 
amount  of  coagulable  lymph  is  poured  out  over  that  portion  of  the  perito- 
neum which  covers  the  liver  or  spleen,  a  distinct  fremitus  may  be  com- 
municated to  the  hand  as  it  passes  over  the  hepatic  and  splenic  regions, 
accompanied  by  distinctly  audible  friction  sounds. 

The  temperature  in  acute  peritonitis  has  no  typical  range ;  it  may  not 
rise  above  the  normal.  In  most  cases  it  ranges  from  102  to  103°  F.  ;  it  is 
of  the  remittent  type,  being  lowest  in  the  morning.  If  recovery  takes 
place,  it  gradually  falls  to  normal.  In  fatal  cases  it  may  fall  below  the 
normal  during  the  period  of  collapse.  The  pulse  is  accelerated,  often  reach- 
ing 140  per  minute.  For  hours  before  a  fatal  issue  it  may  beat  200  per 
minute.  It  is  small,  hard  and  wiry  in  character,  and  when  very  rapid  is' 
hardly  perceptible  at  the  wrist.  In  exceptional  cases  it  is  tolerably  full  and 
strong,  and  does  not  rise  to  more  than  90  beats  per  minute. 

Vomiting  is  a  prominent  symptom ;  if  that  portion  of  the  i)eritoneum 


PERiToisriTis.  327 

coTering  the  stomach  is  first  involved,  it  precedes  all  other  symptoms.  It 
usually  comes  on  about  the  second  day  ;  the  vomited  matters  at  first  con- 
sist of  the  contents  of  the  stomach,  later  they  are  a  mucus  mingled  with 
a  spinach-green  material,  which  by  some  is  regarded  as  characteristic. 
Whenever  stercoraceous  vomiting  occurs  in  peritonitis,  it  is  evidence  of 
intestinal  obstruction,  such  an  obstruction  being  the  cause  or  the  result  of 
the  peritonitis.  Total  paresis  of  the  lower  bowel  in  rare  instances  may 
cause  stercoraceous  vomiting  when  the  muscular  wall  of  the  intestine 
above  is  still  active.  Sometimes  there  is  constant  nausea  without  vomit- 
ing ;  hiccough  and  gaseous  eructations  indicate  that  the  diaphragmatic 
portion  of  the  peritoneum  is  involved.  The  tongue  is  covered  with  a 
thick  coating,  and  anorexia  is  present  from  the  onset.  Constipation  due 
to  paralysis  of  the  muscular  coat  of  the  intestine  is  the  rule,  especially 
in  the  early  stage  of  peritonitis.  Yet  diarrhoea  may  not  only  occur  during 
the  later  stages  of  the  disease,  but  it  may  exist  throughout  its  entire  course. 
In  puerperal  peritonitis  there  is  usually  watery  diarrhoea,  and  diarrhoea  is 
often  present  in  the  peritonitis  of  children. 

The  tirine  is,  scanty  and  deposits  urates  ;  "  scalding  "  frequently  occurs, 
and  if  the  peritoneal  covering  of  tlie  bladder  is  involved  there  may  be 
retention  of  urine  or  painful  micturition.  The  tendency  to  heart  failure 
and  to  collapse  is  one  of  the  most  striking  characteristics  of  acute  peritonitis. 
In  all  varieties  it  must  be  remembered  that  the  disease  rarely  runs  a  typical 
course  ;  even  pain  may  be  absent.  A  sudden  collapse  attended  by  a  soft, 
feeble  pulse  and  brown  tongue,  quickly  terminating  in  death,  may  be  fol- 
lowed by  an  autopsy  which  shows  the  intestines  matted  together  by  recent 
inflammatory  products.  When  peritonitis  follows  intestinal  perforation,  all 
the  symptoms  from  the  onset  are  severe.  The  face  quickly  becomes  haggard, 
drawn,  and  dejected;  the  eyes  are  sunken  and  surrounded  by  dark 
purple  rings ;  the  nose  and  cheeks  are  pinched,  the  lips  are  blue, 
the  upper  one  being  lifted  and  tightly  drawn  across  the  teeth, 
the  voice  becomes  feeble,  or  the  patient  speaks  in  a  husky  whisper, 
the  extremities  are  cold  and  covered  with  a  clammy  perspiration,  the 
radial  pulse  is  hardly  perceptible,  the  respirations  assume  the  type  known 
as  ''  Cheyne-Stokes  "  respiration,  general  cyanosis  supervenes  and  death  is 
reached  within  forty-eight  hours.  Sometimes  death  occurs  within  three 
or  four  hours  from  the  shock  of  the  perforation.  The  mind  is  usually 
clear  throughout  the  entire  course  of  the  disease  ;  in  infectious  peritonitis 
loss  of  consciousness,  apathy,  or  delirium  may  precede  death  by  a  few 
hours.  The  pulse  and  the  amount  of  cyanosis  are  measures  of  the  heart 
failure.  In  cases  where  there  is  a  large  amount  of  fluid  effusion  the  j^ain 
subsides  with  the  occurrence  of  the  effusion,  and  this  sometimes  leads  to  a 
mistake  in  prognosis  on  account  of  the  supposed  subsidence  of  the  peri- 
tonitis. In  suppurative  peritonitis  the  pain  is  not  infrequently  absent,  but 
typhoid  symptoms  are  present  from  the  onset,  delirium  is  the  rule  rather 
than  the  exception,  recurring  rigors  are  common,  the  fever  increases 
toward  evening,  and  the  pulse  becomes  very  rapid.  Occasionally  in  typhli- 
tis, gastric  ulcer,  and  intestinal  perforation,  the  shock  of  the  perforation, 


328  DISEASES   OP   THE   DIGESTIVE   SYSTEM. 

or  the  feeling  as  if  something  had  suddenly  burst,  or  been  torn  within  the 
abdomen,  is  distinctly  appreciated  by  the  patient. 

Local  or  circumscribed  peritonitis  usually  pursues  a  sub-acute  rather  than 
an  acute  course.  Chronic  peritonitis  (non-tubercular  and  non-cancerous) 
is  usually  the  sequela  of  an  acute  attack.  If  convalescence  is  not  established 
during  the  first  week  of  an  acute  general  peritonitis,  the  character  of  the 
inflammation  changes  and  it  becomes  chronic.  Rigors  alternate  with  irregu- 
lar sweats,  and  a  steady  increase  in  the  size  of  the  abdomen  marks  the  pas- 
sage from  an  acute  to  a  chronic  peritonitis.  There  is  rapid  loss  of  flesh  and 
strength,  and  a  marked  diminution  in  the  general  vital  powers.  The  face 
assumes  the  haggard,  drawn  look  so  often  found  with  chronic  abdominal 
disease.  The  intense  pain  of  the  acute  attack  subsides,  and  a  "  dull  ache  " 
with  more  or  less  tenderness  remains.  The  pain  assumes  a  colicky  character 
and  not  infrequently  is  increased  by  taking  food.  The  abdominal  muscles 
remain  rigid  and  tense.  The  temperature  ranges  from  99°  to  104°  F.  The 
pulse  continues  rapid  and  feeble.  There  is  anorexia  and  progressive  ex- 
haustion ;  diarrhoea  alternates  with  constipation.  Fluid  accumulates  in 
the  peritoneal  cavity,  sufficient  in  some  cases  to  cause  dyspnoea.  The 
thickenings  and  adhesions  which  develop  may  so  interfere  with  the  ve- 
nous return  that  oedema,  thrombosis  and  albuminuria  may  result.  In 
latent  general  chronic  peritonitis  there  may  be  large  ascitic  accumulations 
accompanied  by  abdominal  tenderness,  loss  of  appetite  and  progressive 
ansemia.  The  pulse  is  small  and  rapid,  the  vomiting  is  persistent,  and  with 
the  accompanying  diarrhoea  exhausts  the  patient.  Eecurring  attacks  oi 
acute  local  peritonitis  hasten  the  fatal  issue. 

In  tubercular  peritonitis  the  pain  is  paroxysmal  in  character.  Its  onset 
is  often  sudden,  attended  by  fever  and  well-marked  constitutional  disturb- 
ance, the  pulse  is  rapid  and  feeble,  there  is  nausea,  vomiting  and  diarrhoea. 
The  tongue  is  heavily  coated,  thirst  is  intense,  and  there  is  rapid  loss  of  flesh 
and  strength.  The  skin  becomes  harsh  and  dry.  Typhoid  symptoms  appear 
early,  fluids  gradually  accumulate  in  the  peritoneal  cavity  and  the  patient 
dies  of  asthenia.  Redness  and  oedema  about  the  umbilicus  are  regarded  as 
characteristic  of  tubercular  peritonitis.  In  some  cases  the  pain  is  so  slight 
as  to  amount  only  to  a  sense  of  tension  and  fulness  in  the  abdomen  ;  and 
yet  there  may  be  a  large  effusion  into  the  peritoneal  cavity.  The  tongue 
becomes  red  and  shining,  the  stomach  is  irritable ;  hectic  fever  is  accom- 
panied by  prof nse  sweats  during  sleep,  and  the  abdomen  has  a  doughy  feel. 
Some  cases  are  unattended  by  ascites,  and  knots  of  intestine  embedded  in 
firm  hard  masses  are  felt  in  the  region  of  the  umbilicus.  Friction  sounds 
may  be  heard  over  these  masses.  Tubercular  peritonitis  may  have  for  its 
chief  and  only  symptoms,  ascites,  anasmia,  and  the  evidences  of  geneial 
tuberculosis  ;  its  progress  is  interrupted,  now  there  is  marked  improvement 
and  cessation  of  all  the  abdominal  symptoms,  and  then  there  follows  a  period 
when  death  seems  imminent.  As  a  rule,  there  is  moderate  fever  and  slight 
pain,  with  considerable  ascites.  The  mesenteric  glands  are  usually  en- 
larged. 

Cancerous  peritonitis  is  attended  by  the  same  local  symptoms  as  tuber- 


PERiToisriTis.  329 

cular.  Sometimes  a  tumor  may  be  felt,  especially  in  the  region  of  the  omen- 
tum and  mesentery.  There  is  always  ascites  ;  the  fluid  collects  giadually, 
and  often  in  very  large  quantities  ;  constipation  is  more  frequent  than  diar- 
rhoea, and  death  is  often  the  result  of  intestinal  obstruction.  In  some  cases 
the  abdomen  is  very  sensitive,  and  paroxysms  of  colicky  pains  are  not  in- 
frequent. The  temperature  rarely  reaches  100°  F.  If  the  i)eritonitis  has 
extended  from  the  stomach,  liver  or  intestine,  the  symptoms  of  the  primary 
disease  will  have  been  well  defined  before  the  develojjment  of  the  peritoni- 
tis. At  any  period  in  the  course  of  cancerous  peritonitis  all  the  symptoms 
of  acute  general  peritonitis  are  liable  to  be  developed.  The  diagnosis  rests 
on  the  presence  of  a  gradually  increasing  tumor  and  the  cancerous  cachexia. 

Differential  Diagnosis. — Peritonitis  may  be  mistaken  for  colic,  intestinal 
obstruction  (without  peritonitis),  enteritis,  abdominal  neuralgia,  hysteria, 
rheumatism  of  the  abdominal  muscles,  renal  and  biliary  colics,  and  supjM- 
rative  cellulitis  of  the  abdominal  walls.  The  ascites  of  chronic  peritonitis 
may  be  mistaken  for  that  of  the  last  stages  of  cirrhosis  of  the  liver.  The 
differential  diagnosis  of  colic,  intestinal  obstruction,  and  enteritis  has  al- 
ready been  given. 

The  pain  in  abdominal  neuralgia  simulates  that  produced  by  a 
tightly  drawn  cord  about  the  abdomen,  and  follows  the  course  of 
the  genito-crural  nerve.  There  is  tenderness  on  pressure  only  at  the 
point  of  exit  of  the  nerve  from  the  spine.  There  is  no  tympanitis,  no  asci- 
tes, no  rise  of  temperature,  or  acceleration  of  the  pulse,  and  no  signs  of 
collapse.     The  muscular  rigidity  of  commencing  peritonitis  is  absent. 

In  hysteria,  the  patient  is  ready  to  complain  of  increased  pain  before  the 
hand  touches  the  abdomen,  yet  the  firmest  pressure  does  not  increase  the 
pain  if  the  attention  of  the  patient  is  engaged.  The  pulse,  temperature,  and 
signs  of  collapse  of  peritonitis  are  absent,  the  countenance  is  not  that  of  peri- 
tonitis, and  there  is  present  the  globus  hystericus,  and  the  attack  is  followed 
by  the  passage  of  a  large  quantity  of  watery,  straw-colored  urine. 

In  rheumatism  of  the  abdominal  muscles,  the  pain  and  tenderness  are 
most  intense  at  the  origin  and  insertion  of  the  muscles.  There  is  no  rise  of 
temperature,  no  vomiting,  and  no  signs  of  collapse ;  the  pulse  is  normal, 
and  there  will  be  a  history  of  acute  or  sub-acute  articular  rheumatism. 

In  the  passage  of  a  gall-stone,  and  in  renal  colic,  the  patient  throws  him- 
self about  in  excruciating  agony,  and  the  pain  is  referred  to  the  region  of  the 
common  bile-duct,  or  to  the  course  of  the  ureter.  In  the  passage  of  a  gall- 
stone, it  is  paroxysmal  in  character,  and  will  shoot  back  from  the  margin  of 
the  ribs  over  the  gall-bladder  to  the  spinal  column.  If  it  continues  twenty- 
four  hours,  the  patient  becomes  jaundiced.  In  renal  colic  the  pain  radiates 
from  the  kidney  along  the  ureter  to  the  testicle,  which  is  retracted.  Both 
are  accompanied  by  characteristic  changes  in  the  urine  or  fgeces,  neither  is 
attended  by  rise  of  temperature  or  great  acceleration  of  pulse,  and  there  is  no 
tympanitis  or  tenderness  on  firm  pressure  in  either. 

Suppuration  of  the  abdominal  parietes  is  at  first  difficult  to  distinguish 
from  peritonitis,  but  after  the  first  two  days  the  superficial  swelling  and  the 
absence  of  the  constitutional  symptoms  of  peritonitis  establish  the  diagnosis. 


330  DISEASES    OF   THE    DIGESTIVE    SYSTEM, 

Prognosis. — Acute  general  peritonitis  is  a  very  fatal  disease.  Its  average- 
duration  is  from  four  to  eight  days  ;  death  may  occur  in  a  few  hours,  or  be 
delayed  two  or  three  weeks.  The  prognosis  in  any  case  is  to  a  great  extent 
determined  by  its  cause  ;  it  is  most  unfavorable  when  it  results  from  perfora- 
tion, intestinal  obstruction,  or  sepsis.  General  puerperal  peritonitis  is  almost 
always  fatal.  The  presence  of  typhoid  symptoms,  a  very  rapid  and  feeble 
pulse,  cold  extremities,  with  the  other  symptoms  of  impending  collapse,  in- 
dicate an  unfavorable  termination.  Peritonitis  from  rupture  of  an  organ  is  al- 
ways fatal.  The  prognosis  is  favorable  when  the  peritonitis  is  due  to  extension 
of  inflammation  from  a  viscus.  When  the  pain  and  vomiting  cease,  the  tym- 
panitis subsides,  the  pulse  diminishes  in  frequency,  the  temperature  reaches 
the  normal,  and  the  patient  is  able  to  turn  in  bed,  a  favorable  termination 
is  to  be  expected.  Chronic  diffuse  peritonitis  in  children,  unless  purulent, 
usually  terminates  in  recovery.  Tubercular  peritonitis,  after  weeks  and 
months  of  anaemia  and  exhaustion,  terminates  in  death.  The  same  is  true 
of  carcinomatous  peritonitis.  Death  in  acute  peritonitis  may  result  from 
shock,  from  asthenia  with  typhoid  symptoms,  and  from  exhaustion.  Among 
its  sequelae  are  collections  of  pus,  stenosis  or  complete  obstruction  of  the- 
intestine,  pyaemia,  and  septicsemia.  Permanent  Jaundice  may  result  from 
narrowing  of  the  bile  duct  by  the  contraction  of  new  tissue  formations  in 
the  transverse  fissure. 

Treatment. — Acute  peritonitis  is  a  severe,  rapidly  progressive,  and  dan- 
gerous inflammation,  and  on  this  account  has  always  been  treated  heroic- 
ally. Formerly  patients  with  acute  peritonitis  were  subjected  to  excessive 
bleedings,  tartar  emetic  was  administered  in  nauseating  doses,  and  to  prolong 
the  effects  of  the  bleeding,  and  as  an  adjunct  to  these  calomel  was  given 
for  its  specific  effect.  At  the  same  time  many  physicians  of  recog- 
nized authority  were  eager  to  obtain  the  purgative  effects  of  cathartics,  and 
for  this  purpose  recommended  and  administered  large  doses  of  drastic  pur- 
gatives. Local  bleeding  by  leeches  is  often  of  great  service  in  local  perito- 
nitis, but  it  should  be  resorted  to  only  at  the  very  onset  of  the  attack  in  the 
strong  and  robust.  Tartar  emetic  and  calomel,  so  highly  regarded  as  anti- 
plastics,  have  fallen  into  disuse.  While  acute  peritonitis  is  progressing  the 
bowels  cannot  be  moved,  and  no  benefit  would  result  if  they  were  ;  so  that 
under  no  circumstance  should  there  be  an  attempt  at  purgation. 

The  plan  of  treatment  which  I  have  followed  for  years — a  plan  which 
gains  in  favor  with  me  with  every  new  experience — is  the  opium  plan.  Prof. 
Alonzo  Clark  first  developed  this  plan  and  brought  it  to  the  notice  of  the 
profession.  The  details  of  it  are  as  follows  : — as  soon  as  the  unmistak- 
able symptoins  of  peritonitis  are  developed,  administer  at  one  dose  from 
two  to  five  grains  of  opium  or  one-half  to  one  grain  of  morphine.  The  exact 
quantity  in  each  case  is  to  be  determined  by  the  condition  of  the  patient ;  the 
rule  is  to  bring  the  patient  as  soon  as  possible  fully  under  the  influence  of  the 
drug.  In  the  treatment  of  this  disease,  it  will  be  observed  how  greatly  pain 
and  inflammation  modify  the  effects  of  this  powerful  drug.  I  have  adminis- 
tered to  patients  with  peritonitis  four  grains  of  opium  every  two  hours  for 
twenty-four  hours,  and  then  have  obtained  only  a  moderate  effect  of  the 


PERITONITIS.  331 

drug.  The  point  wliicli  must  be  reached  in  its  administration  is  moderate 
narcotism,  in  whicli  stale  the  patient  must  be  kept,  not  only  until  all  pain 
and  tenderness  have  subsided,  but  until  the  pulse  has  reached  its  normal 
standard  and  the  tympanitis  has  entirely  subsided.  The  question  arises  : 
what  are  the  indications  which  are  to  govern  the  administration  of  each 
dose  of  opium  ?  One  must  be  prepared  at  the  commencement  of  the  treat- 
ment of  a  case  of  peritonitis,  according  to  this  plan,  to  be  present  and  de- 
cide upon  the  quantity  of  opium  to  be  given  at  each  dose,  until  the  patient 
has  fully  convalesced.  It  cannot  be  trusted  to  attendants,  however  intelli- 
gent they  may  be.  As  the  patient  is  brought  fully  under  the  influence  of  the 
opiate,  it  will  be  noticed  that  the  entire  surface  of  the  body  becomes  bathed 
in  a  profuse  perspiration.  In  twenty-four  hours  a  rash,  due  to  the  opium, 
will  make  its  appearance  on  the  surface  and  neck  ;  this  is  accompanied  by 
an  itching  of  the  surface  and  a  constant  disposition  to  rub  the  nose.  The 
pupils  become  contracted,  the  eyes  suffused,  the  countenance  assumes  a  dull 
expression,  and  there  is  a  constant  irresistible  disposition  to  sleep.  The 
pulse  becomes  lessened  in  frequency  and  force,  and  the  respirations,  which, 
before  the  administration  of  the  opium,  may  have  ranged  from  40  to  60 
in  a  minute,  become  less  and  less  frequent  as  the  patient  comes  fully  under 
its  influence,  until  they  are  only  twelve  in  a  minute.  Xow  the  greatest  care 
is  to  be  exercised  in  the  administration  of  the  opium  ;  the  patient  is  in  the 
condition  in  which  it  is  desirable  to  keep  him.  By  holding  him  in  this 
state  of  semi-narcotism,  all  will  be  accomplished  that  can  be  by  the  opium 
plan  of  treatment,  and  with  the  respiration  at  twelve  per  minute  the  patient 
is  perfectly  safe.  The  amount  of  sleep  is  not  to  be  taken  into  account,  but 
the  profoundness  of  the  slumber  is  of  great  importance.  If  it  is  found  dif- 
ficult to  arouse  the  patient,  the  administration  of  the  opium  must  be  stopped 
until  he  can  be  easily  aroused.  If  by  mistake  or  negligence  the  patient  be- 
comes fully  narcotized,  the  respirations  will  sometimes  diminish  in  fre- 
quency to  seven  or  even  five  in  a  minute.  In  this  extremity,  if  the  admin- 
istration of  opium  be  stopped,  the  patient  will  usually  rally  from  its  effects 
after  a  few  hours ;  but  avoid  extremes,  endeavor  to  keep  the  patient  in  a 
quiet  sleep,  not  profound,  but  one  from  which  he  can  be  easily  aroused. 
When  the  pulse  begins  to  diminish  in  frequency  and  becomes  fuller,  one 
may  be  certain  that  he  is  controlling  the  peritonitis,  and  as  it  is  controlled 
the  patient  will  become  more  and  more  susceptible  to  the  influence  of  the 
opium.  Slowness  of  respiration  and  absence  of  pain  cannot  be  relied  on  as 
sure  indications  that  the  opium  is  controlling  the  inflammatory  action  ;  but 
a  diminution  in  the  frequency  of  the  pulse,  and  a  subsidence  of  the  tympa- 
nitis are  sure  indications  that  the  peritonitis  is  arrested,  and  that  ultimate 
recovery  is  probable.  In  most  cases,  if  an  acute  peritonitis  does  not  depend 
for  its  exciting  cause  upon  the  escape  of  intestinal  gases  into  the  peritoneal 
cavity,  or  upon  complete  intestinal  obstruction,  the  inflammatory  action 
can  be  controlled  within  forty-eight  hours  from  the  commencement  of  the 
attack  by  adopting,  within  twelve  hours,  this  plan  of  treatment.  It  must, 
however,  be  continued  four  or  five  days  longer,  for  there  is  still  danger  of 
a  renewal  of  the  inflammation.     As  the  condition  of  the  j)atient  demands 


333  DISEASES   OF   THE    DIGESTIVE   SYSTEM. 

less  opium,  the  dose  may  be  diminished,  or  the  interval  between  the  doses 
lengthened.  A  safe  rule  by  which  to  be  guided  is  that,  so  long  as  any 
tympanitis  exists,  the  opium  should  be  continued. 

When  convalescence  is  fully  established,  one  should  not  be  too  anxious  to 
overcome  the  constipation  which  usually  exists,  for  a  free,  spontaneous 
movement  of  the  bowels  generally  follows  a  complete  subsidence  of  the 
peritonitis.  Wait  at  least  a  week  for  this  result  before  administering  a  ca- 
thartic, and  then,  if  necessary,  employ  one  mild  in  its  action,  such  as  cas- 
tor-oil. Warm  poultices  over  the  abdomen  are  usually  the  only  local  appli- 
cation which  I  have  employed.  It  is  claimed  by  some  that  cold  compresses 
have  a  much  more  beneficial  effect  than  warm  applications.  My  experience 
leads  me  to  doubt  the  utility  of  the  former,  while  the  latter  are  far  safer, 
and  I  believe  equally  efficacious.  It  has  been  stated  that  when  the  peritoni- 
tis becomes  general,  excessive  gaseous  distention  of  the  intestines  occurs, 
and  this  distention  greatly  increases  the  danger  to  the  patient ;  under  such 
circumstances  I  have  recently  resorted  to  minute  puncturing  of  the  dis- 
tended intestine  with  a  hypodermic  or  a  very  small  aspirating  needle,  and 
have  thus  relieved  the  intestinal  distention  by  allowing  the  gas  to  escape. 
By  so  doing,  not  only  is  the  tension  of  the  peritoneum  (which  becomes  an 
exciting  cause  of  the  peritonitis)  relieved,  but  the  principal  obstruction  to 
the  respiration  is  removed,  and  thus  cyanosis  is  diminished.  Immediate 
and  marked  relief  is  afforded  by  such  a  procedure,  and  as  thus  far  I  have 
had  no  bad  results  follow,  I  am  disposed  to  resort  to  it  in  all  cases  where  the 
abdomen  becomes  excessively  distended  and  tympanitic.  I  remember  one 
case  in  which  the  gaseous  distention  was  excessive,  and  the  peritonitis  was 
supposed  to  be  due  to  strangulation  of  a  portion  of  intestine  from  old  peri- 
toneal adhesions,  where  the  relief  of  the  distended  intestine  by  puncture 
was  soon  followed  by  a  removal  of  the  intestinal  obstruction  and  the  rapid 
recovery  of  the  patient.  From  this  circumstance  I  can  readily  understand 
how  a  portion  of  intestine  that  was  partially  constricted  by  a  band  of  ad- 
hesion might  become  completely  obstructed  at  the  point  of  stricture  by  a 
rapid  gaseous  distention  of  the  intestine  above  the  point  of  constriction,  and 
the  relief  of  the  intestinal  distention  by  puncture  would  very  likely  liberate 
the  constricted  portion  and  thus  overcome  the  strangulation,  and  so,  per- 
haps, save  the  life  of  the  patient. 

The  necessity  of  absolute  quiet,  and  of  the  frequent  administration  of  nour- 
ishment and  sometimes  of  stimulants,  in  small  quantities,  to  this  class  of 
patients,  is  apparent.  Preceding  and  during  the  stage  of  plastic  exudation, 
large  doses  of  quinine  are  beneficial ;  but  little  nutriment  should  be  admin- 
istered, and  that  only  in  a  fluid  and  a  highly  condensed  form.  Cracked  ice 
may  be  given  to  relieve  the  thirst,  and,  if  there  are  signs  of  asthenia,  iced 
champagne  or  brandy  should  be  given  in  small  doses.  If  hiccough  is  dis- 
tressing, it  should  be  relieved  temporarily  by  the  inhalation  of  chloroform. 
Vomiting  is  sometimes  allayed  by  carbonated  water,  cracked  ice  and  cham- 
pagne, or  hydrocyanic  acid.  Turpentine,  as  an  injection  and  employed  lo- 
cally as  an  embrocation,  will  sometimes  relieve  the  tympanitis.  With  the 
asthenic  form  of  peritonitis,  a  stimulating  plan  of  treatment  should  be  em- 


ASCITES.  333 

ployed  with  the  opium.  In  puerperal  peritonitis,  great  attention  should  be 
paid  to  the  condition  of  the  uterus  and  its  aj^pendages.  Chronic  peritonitis 
is  treated  by  local  applications  of  iodine  and  mercury,  and  by  the  internal 
use  of  iodide  of  potassium.  Its  products  may  be  removed  by  tapi3ing.  The 
nutrition  of  the  patient  must  be  carried  to  the  highest  point.  Tubercular 
peritonitis  demands  small  doses  of  opium,  warm  anodyne  applications,  and 
the  administration  of  tonics,  cod-liver  oil  especially.  The  treatment  of  can- 
cerous peritonitis  is  purely  symptomatic  ;  nausea  and  attacks  of  diarrhoea 
and  constipation  must  be  promptly  relieved.  Narcotics  may  be  given  for 
the  sleeplessness.  Concerning  the  prophylactic  and  sanitary  treatment  of 
puerperal  peritonitis,  the  reader  is  referred  to  obstetrical  works. 


ASCITES. 
(Abdominal  Dropsy.) 

Ascites  is  a  local  dropsy, — an  accumulation  of  serum  in  the  peritoneal 
cavity.  It  has  also  been  called  peritoneal  dropsy,  dropsy  of  the  abdomen, 
and  hydro-peritoneum.  The  circumstances  under  which  it  occurs  are 
similar  to  those  which  allow  of  general  dropsy — viz.  :  obstruction  to  the 
capillary  or  lymphatic  circulation  of  the  peritoneum,  a  diminished  amount 
of  albumen  in  the  blood,  and  degenerations  of  the  peritoneum.  Those 
hydrsemic  conditions  which  accompany  exhausting  chronic  diseases,  espe- 
cially diseases  of  the  kidneys,  will  induce  it.  One  or  several  of  these  con- 
ditions may  be  present  in  the  same  case. 

Morbid  Anatomy. — The  amount  of  fluid  present  in  ascites  may  vary  from 
a  few  ounces  to  four  or  five  gallons.  In  consistency  it  may  be  viscid  or 
watery.  It  is  usually  of  a  liglit  straw  color,  having  a  faint  greenish  opal- 
escent tint.  It  may  be  opaque  and  dark,  from  admixture  of  blood.  With 
disease  of  the  lymphatics  it  is  milky  and  opalescent.  Sometimes  it  does  not 
differ  in  appearance  from  pure  water.  It  is  alkaline  in  reaction,  and  may 
contain  albumen,  blood,  fibrin,  fibrinogen,  bile-pigments,  kreatin,  kreatin- 
in,  lymph  flocculi,  and  bile  acids.  Albuminate  of  soda,  leucocytes  and  pus 
cells  are  its  occasional  ingredients.  The  endothelia  of  the  peritoneum  are 
turbid,  thick,  and  in  vai-ious  stages  of  fatty  degeneration.  The  sub-serous 
tissue  is  thickened,  and  the  whole  membrane  has  the  look  and  feel  of  being 
water-logged.  The  blood  changes  that  cause  it  consist  chiefly  in  a  diminu- 
tion of  albumen  and  an  increase  of  water.  Compression,  dislocation,  and 
diminished  function  of  the  abdominal  viscera  are  the  results  of  the  ascitic 
accumulation. 

Etiology. — Ascites  may  be  a  late  symptom  of  general  dropsy.  In  most 
other  instances  it  results  from  damming  back  of  the  blood  in  the  portal 
tributaries,  from  pressure  on  the  portal  vein — either  from  hepatic  and 
abdominal  tumors,  or  from  a  diseased  condition  of  the  liver  substance — 
as  in  cirrhosis,  waxy  degeneration,  abscess,  hepatic  atrophy,  portal  throm- 
bosis, enlarged  lymphatics  in  the  transverse  fissure,  and  the  constrictions 
due  to  perihepatitis.     These  all  mechanically  impede  the  blood  current  in 


334  DISEASES    OP   THE    DIGESTIVE    SYSTEM, 

the  portal  vessels.  Diseases  of  the  heart  or  lungs  which  interfere  with  the 
normal  flow  of  the  blood  from  the  cavae  will  induce  it  in  connection  with 
genera]  dropsy ; — under  this  head  are  included  tricuspid  obstruction  and 
insufficiency,  chronic  bronchitis  and  emphysema,  fibrous  phthisis,  and  cer- 
tain forms  of  mediastinal  tumors.  Anaemia,  hydraemia,  chlorosis,  malarial 
cachexia,  purpura,  chronic  arsenical  poisoning,  scurvy  and  chronic  Bright's 
disease,  j)roducing  hydraemia— and  old  age  or  great  exhaustion  without 
structural  disease — lead  to  what  is  often  called  asthenic  ascites  or  cachectic 
dropsy.  Peritoneal  dropsy  not  infrequently  accompanies  extensive  degen- 
eration of  the  peritoneum,  such  as  tubercle  and  carcinoma.  Finally,  ascites 
may  occur  from  unknown  causes — from  taking  cold,  after  suppression  of  the 
menses,  after  the  sudden  disappearance  of  acute  and  chronic  cutaneous 
eruptions  and  ulcers,  and  perhaps  from  atmospheric  causes.'  It  has  been 
suggested  that  malignant  disease  of  the  ovaries  and  other  pelvic  organs,  and 
of  the  mesenteric  and  retro-peritoneal  glands,  obstructs  the  capillaries  and 
the  lymphatic  orifices,  increasing  the  functional  activity  of  the  endothelia, 
and  thus  induces  ascites.^ 

Symptoms. — The  first  sign  of  ascites  is  a  gradual  increase  in  the  size  of 
the  abdomen.  The  enlargement  in  simple  ascites  takes  place  without  pain, 
tenderness,  or  local  subjective  symptoms.  There  is  a  feeling  of  fulness, 
and  the  patient  is  rendered  uncomfortable  by  pressure  of  the  fluid.  The 
respiratory  movements  are  interfered  with,  and  dyspnoea  soon  results. 
The  functions  of  the  stomach  may  be  disturbed,  and  there  may  be  vomit- 
ing, anorexia,  and  perhaps  hsematemesis.  Flatulence  and  diarrhoea  are 
frequently  present,  but  when  the  accumulation  of  fluid  is  large  it  produces 
colicky  pains,  and  often  obstinate  constipation.  All  these  symptoms  are 
relieved  as  soon  as  the  fluid  is  removed.  Gradually  the  dyspnoea  increases, 
the  patient  walks  with  difficulty,  with  the  legs  spread  widely  apart ;  the 
urinary  secretion  is  diminished  from  the  pressure  on  the  kidneys  and  renal 
"vessels.  The  recumbent  posture  greatly  aggravates  the  dyspnoea.  The 
skin  and  mucous  membranes  become  dry  ;  the  liver  and  pelvic  viscera  are 
displaced  ;  the  heart  and  lungs  are  pushed  upward,  and  the  skin  over  the 
abdomen  becomes  tense  and  shining.  The  umbilicus  is  bulged  out  in  the 
form  of  a  globular  tumor.  The  superficial  veins  are  enlarged  and  tortuous. 
If  the  inguinal  canal  is  open,  fluid  may  pass  into  the  scrotum  ;  and  ex- 
cessive ascites,  by  pressure  on  the  vena  cava,  causes  oedema  of  the  feet  and 
legs.  In  hepatic  diseases  the  fluid  is  chiefly  confined  to  the  abdomen,  but 
in  cardiac  and  pulmonary  dropsies  the  fluid  accumulates  first  about  the  feet 
and  extends  upward,  and  the  abdominal  dropsy  is  then  a  part  of  a  general 
anasarca.  In  hepatic  dropsies  the  extremities  emaciate  while  the  abdomen 
enlarges ;  the  skin  has  a  muddy  jaundiced  hue,  and  the  patient  becomes 
exhausted  and  apathetic.  Jaundice,  uraemia,  delirium,  convulsions,  coma, 
and  cholaemia  are  prominent  symptoms  as  death  approaches. 

Physical  Signs. — The  physical  examination  of  the  abdomen  is  most  im- 
portant in  the  diagnosis  of  ascites. 

Inspection. — The  abdomen,  if  distended  with  fluid,  presents  the  appear- 

1  Wagner,  Gen.  Path.,  pp.  234-5.  ^  Oppolzer. 


ASCITES.  335 

ance  of  a  globular  or  dome-like  tumor,  the  false  ribs  are  elevated  and 
pressed  out,  and  the  superficial  veins  are  visible  and  prominent.  The  cir- 
cumferential measurement  of  the  abdomen  will  often  be  three  times  as 
great  as  normal.  If  the  effusion  is  moderate,  the  shape  of  the  abdomen 
changes  with  a  change  of  the  position  of  the  patient :  it  broadens  when  he 
lies  on  his  back,  and  when  he  stands  the  enlargement  will  be  confined  to 
the  lower  portion.  The  fluid  always  gravitates  to  the  most  dependent 
portion. 

Palpation. — Fluctuation  is  obtained  when  the  level  of  the  fluid  is  above 
the  pelvic  brim.  To  obtain  the  wave  most  distinctly  place  the  patient  on 
his  back,  place  the  flat  of  the  hand  on  one  side  of  the  broadened  abdomen, 
and  with  the  other  hand  give  one  smart  tap  at  a  point  opposite  ;  che  im- 
pulse of  the  blow  will  be  felt  by  the  palm  of  the  hand. 

Percussion. — There  "will  be  flatness  below  the  level  of  the  fluid,  and 
tympanitic  resonance  above.  The  line  of  dulness  changes  with  the 
change  of  position,  and  accurately  measures  the  amount  of  fluid.  When 
only  a  small  amount  of  fluid  is  present  the  physical  signs  of  its  presence  are 
commonly  obtained  by  placing  the  patient  in  the  "  knee-elbow  "  position. 

Differential  Diagnosis. — Ascites  may  be  mistaken  for  ovarian  dropsy,  dis- 
tended bladder,  pregnancy,  hydatid  cysts  of  the  liver,  and  enlargement  of 
the  spleen.  It  is  imjDortant  in  making  a  differential  diagnosis  between 
ascites  and  ovarian  dropsy  to  have  a  perfect  history  of  the  case.  The  ab- 
dominal enlargement  in  ascites  is  uniform,  in  ovarian  dropsy  it  is  irregu- 
lar. Ascites,  however  slight,  begins  at  the  most  dependent  portion  of  the 
abdomen,  while  ovarian  dropsy  begins  in  one  of  the  iliac  fossae  and  gradu- 
allv  extends  upwards  toward  the  umbilicus.  With  every  change  of  posi- 
tion, in  ascites,  the  line  of  dulness  changes  ;  a  large  ovarian  cyst  is  to  be 
recognized  by  its  fixed  position  and  non-gravitation  of  its  fluid.  In  ascites 
there  is  fluctuation  on  palpation  ;  in  ovarian  dropsy,  fluctuation  is  absent 
or  localized.  The  abdomen  is  usually  tympanitic  above  the  level  of  the 
fluid  and  flat  below  in  ascites,  while  in  ovarian  tumor  there  is  often  a  tym- 
panitic percussion  sound  at  the  most  dependent  portion  of  the  abdominal 
cavity.  In  ovarian  dropsy  the  outline  of  the  cyst  is  generally  appreciable, 
except  in  very  large  tumors  where  the  peculiar  form  of  the  cyst  may  be 
lost,  but  a  rectal  or  vaginal  exploration  will  generally  at  once  remove  all 
doubts.  In  ascites  there  will  generally  be  a  history  of  liver,  heart,  or 
kidney  disease,  and  the  uterine  organs  and  functions  will  be  normal.  On 
tapping  the  abdomen  a  serous  fluid  will  be  withdrawn  in  ascites  ;  in  ovarian 
tumors,  it  will  be  a  dark,  highly  albuminous  fluid  and  contain  granular 
non-nucleated  cells,  supposed  to  be  characteristic. 

A  distended  and  sacculated  bladder  may  be  mistaken  for  dropsy,  but  the 
introduction  of' the  catheter  will  decide  the  question. 

Pregnancy  will  afford  ballottement,  placental  bruit,  the  sounds  of  the 
foetal  heart,  and  will  be  accompanied  by  distinct  mammary  changes.  The 
uterine  tumor  can  be  distinctly  mapped  out,  and  a  vaginal  examination 
combined  with  external  palpation  will  rarely  fail  to  make  a  differential 
diagnosis  between  it  and  ascites. 


336  DISEASES    OF   THE    DIGESTIVE   SYSTEM. 

An  hydatid  cyst  of  the  liver  produces  flatness  undeviating  in  area,  which 
gradually  extends  from  above  downwards,  and  seldom  reaches  the  pelvic 
brim.  Hydatids  produce  hydatid  fremitus  on  percussion,  which  is  charac- 
teristic. Again,  on  withdrawal  of  the  fluid,  a  miscroscopical  examination 
will  often  discover  the  booklets  of  the  echinococci. 

Enlargement  of  the  spleen  is  unsymmetrical  ;  the  tumor  is  fixed,  there  is 
no  tympanitis,  no  fluctuation,  and  the  boundaries  of  the  enlarged  organ 
can  be  mapped  out  on  palpation  and  percussion.  Usually  the  nofch  at  the 
anterior  border  of  the  spleen  is  so  distinct  that  it  at  once  indicates  the 
gland. 

Prognosis. — The  prognosis  depends  upon  the  conditions  under  which  the 
ascites  occurs ;  if  it  is  dependent  upon  organic  disease  of  the  liver,  heart, 
or  kidney,  the  prognosis  is  unfavorable,  but  when  it  is  not  dependent  upon 
structural  visceral  lesions,  e.g.,  idiopathic  and  anaemic  ascites,  the  prog- 
nosis is  good.  The  ascitic  accumulation  may  take  place  rapidly,  or  weeks 
or  months  may  elapse  before  the  cavity  of  the  abdomen  ia  distended.  The 
average  duration  of  hepatic  ascites  is  about  six  months.  So  long  as  the 
cause  remains,  the  fluid  will  accumulate.  Ascites  may  terminate  in  re- 
covery by  the  spontaneous  or  mechanical  removal  of  the  fluid,  or  by  the 
removal  of  its  cause,  or  it  may  terminate  in  death,  from  complications,  as 
peritonitis,  albuminuria  or  heart-failure,  or  from  pure  slow  asthenia. 

Treatment. — The  first  and  most  important  thing  in  the  treatment  of 
ascites  is  to  discover  the  cause,  and  either  to  remove  or  palliate  it.  In 
most  cases  the  treatment  merges  into  the  treatment  of  the  diseased  condi- 
tions which  produce  it.  In  all  cases  the  diet  should  be  highly  nutritious 
and  concentrated  ;  as  little  fluid  as  possible  should  be  taken.  The  contin- 
ued use  of  powerful  diuretics  and  hydragogue  cathartics  usually  does  harm. 
They  weaken  the  patient  and  often  favor  rather  than  retard  the 
ascitic  accumulation.  Elaterium  is  the  most  efficient  drastic  cathartic, 
the  potash  salts,  nitre,  squills  and  juniper  are  the  most  efficient  diuretics. 
Jaborandi  has  recently  been  much  employed  for  the  removal  of  dropsical 
accumulations.  In  most  cases  these  accumulations  can  be  rapidly  removed 
by  this  drug,  but  my  own  experience  leads  me  to  the  conclusion  that  it 
hastens  rather  than  retards  the  fatal  issue.  Hot-air  baths  should  never  be 
employed  for  the  removal  of  ascitic  accumulations. 

Paracentesis  abdominis  will  have  to  be  resorted  to  sooner  or  later  in  these 
cases,  but  the  rule  is  to  postpone  it  as  long  as  possible.  I  am,  however, 
in  favor  of  tapping  before  the  accumulated  fluid  has  caused  pressure 
upon  the  viscera.  I  am  convinced  that  whenever  fluid  accumulation  takes 
place  in  the  peritoneal  cavity,  tapping  should  be  promptly  resorted  to, 
unless  the  cause  can  be  removed  by  mild  cathartics  or  non-stimulating 
diuretics ;  and  the  number  of  recoveries  and  the  prolongations  of  life 
which  have  followed  this  course  in  my  experience  cause  me  unequivocally 
to  recommend  it  in  preference  to  the  prolonged  use  of  those  remedial 
measures  which  increase  the  discharges  from  the  skin,  kidneys  and  bowels. 
In  a  large  number  of  cases,  improvement  of  the  patient's  general  health  by 
tonics,  of  which  quinine,  iron  and  cod-liver  oil  are  the  best,  is  followed  by 


ACTIVE   HYPERyEMIA    OF   THE    LIVER.  337 

subsidence  of  the  dropsy,  and  its  return  is  also  prevented  for  a  long  time 
after  its  removal  by  tapping. 

DISEASES    OF   THE   LIVER. 

Diseases  of  the  liver  may  be  classified  under  the  following  heads  : 

I,  Hypercemta  : —  III.  Degenerations  : — 

a.  Active  or  Fluxion,  .     Amyloid  or  Lardaceou8» 

h.  Passive  or  Congestion.  Fatty. 

II.  Inflammations  : —  Pigmentary. 

a.  Interstitial    Hejjatitis  or  Atrophy. 

Cirrhosis.  IV.  iVew  Growths: — 

b.  Circumscrihed  Hepatitis  or  Cancer. 

Abscess.  Giimmata. 

c.  Diffused  HejMtitis  or  Acute  Hydatids. 

Yellow  Atrophy.      ^  Tubercle. 

Perihepatitis,    Local    or    Gen-      V.    Diseases   of  the   Gall  Ducts 

eral.  and  Gall  Bladder. 

Pylephlebitis,  Adhesive  and  Sup-      VI.    Jaundice,  Hepatogenous  and 
purative.  Hematogenous. 

VII.  Functional  Derangements. 


ACTIVE   HYPEREMIA    OF    THE    LIVER. 

Active  hyperaemia  of  the  liver  is  an  abnormal  determination  of  blood 
to  the  organ.     It  may  be  acute  or  chronic. 

Morbid  Anatomy. — A  liver  that  is  the  seat  of  active  hyperaemia  is  more 
or  less  enlarged  in  all  directions.  Its  color  varies  from  a  light  to  a  dark  red'. 
It  has  a  firmer  feel  than  normal,  although  its  consistency  is  really  dimin- 
ished. The  organ  is  heavier  and  smoother  than  normal,  its  surface  present- 
ing a  peculiar  shining  appearance. 

On  section,  its  substance  shows  a  uniform  red  color,  blood  flows  freely 
over  its  cut  surface,  from  the  arteries  and  capillaries  which  are  dilated  and 
sometimes  tortuous.  When  the  hyperemia  is  intense,  the  glandular  sub- 
stance of  the  organ  is  compressed  and  there  may  be  evidences  of  sub-peri- 
toneal effusion.  So  intense  may  be  the  hyperaemia  that  hemorrhagic  soften- 
ing and  apoplectic  extravasation  result,  and  isolated  clots  or  an  unbroken 
layer  of  coagulated  blood  may  be  found  under  its  serous  covering. 

In  chronic  hyper mmia  the  liver  is  often  found  in  a  state  of  partial  fatty 
degeneration,  somewhat  softened,  and  of  a  light  red  or  yellow  color.  In 
rare  instances,  chronic  hyperaemia  may  lead  to  induration  and  incipient 
cirrhosis.  In  the  severer  types  abscesses  may  be  found,  and  the  infiltration 
of  a  substance  resembling  albumen  has  in  some  cases  advanced  so  far  as  to 
give  distinct  colloid  degeneration.  In  syphilitic  new-born  children,  active 
hepatic  hyperaemia  is  sometimes  found  associated  with  a  peculiar  plastic 
23 


338  DISEASES    OF    THE    DIGESTIVE    SYSTEM. 

exudation.  It  is  important  to  remember  that  the  normal  hepatic  hyper- 
semia  temporarily  developed  after  hearty  meals  or  the  free  use  of  stimulants 
may  be  mistaken  for  active  hypersemia.  Both  acute  and  chronic  hyper- 
semia  of  the  liver  may  be  associated  with  catarrh  of  the  bile  ducts. 

Etiology. — There  is  a  normal  functional  hyperaemia  of  the  liver  induced 
by  an  unusually  large  meal,  or  one  very  rich  in  hydrocarbons,  or  by  the 
free  use  of  wines  :  this  hypersemia  is  due  to  increased  blood  pressure  in  the 
vena  portge  ;  it  becomes  abnormal  in  those  who  daily  indulge  in  eating  to 
excess,  especially  if  they  lead  sedentary  lives.  If  the  liver-tissue,  which 
supports  the  walls  of  the  capillary  vessels,  becomes  relaxed,  there  will  be  an 
abnormal  afflux  of  blood  to  the  organ.  This  is  the  case  in  traumatic 
hypergemia,  where  a  blow  over  the  viscus  causes  a  localized  fluxion.  Any 
inflammation  or  growth  causing  softening  of  the  parenchyma  will  induce  it. 
The  action  of  drugs,  spices  and  alcohol  is  best  explained  on  this  basis.  In- 
tense hepatic  hypergemia  may  be  caused  by  miasmatic  influences,  malaria, 
and  other  blood-poisons.  Under  the  latter  head  is  included  a  peculiar 
active  hyperaemia  which  occurs  in  the  livers  of  syphilitic  children,  and  in 
secondary  syphilis  of  adults.  High  temperature  undoubtedly  gives  rise  to 
active  hepatic  hyperfemia,  especially  when  it  is  associated  either  with  acute 
or  chronic  malarial  infection,  Vaso-motor  disturbances  may  undoubtedly 
lead  to  active  hepatic  hyperaemia.  It  sometimes  occurs  during  and  after 
pregnancy  from  some  unknown  cause  ;  also  before  the  establishment  of  the 
menses,  and  during  the  menopause.  Capillary  embolism  may  cause  local- 
ized hepatic  hyperaemia. 

Symptoms. — Active  hypergemia  of  the  liver  is  usually  attended  by  a  sense 
of  weight  and  constriction  in  the  right  hypochondrium,  with  some  tender- 
ness on  pressure  under  the  free  border  of  the  ribs.  In  active  malarial 
hypergemia,  there  is  also  gastro-intestinal  catarrh,  nausea,  vomiting,  diar- 
Thoea,  and  slight  jaundice.  There  is  a  bitter  taste  in  the  mouth,  loss  of 
.■appetite,  coated  tongue,  drowsiness  and  apathy.  Headache  is  frequent,  and 
ihe  patient  complains  of  pain  shooting  up  the  right  side  to  the  right 
;shoulder.  This  pain  is  due  to  pressure  on  the  phrenic  nerve,  and  is  more 
intense  after  meals  and  when  lying  on  the  left  side.  A  sense  of  dizziness 
tcomes  on  when  the  patient  assumes  any  other  position  than  on  the  back  or 
right  side.  It  is  more  or  less  increased  by  pressure  upward  against  the 
liver.  In  severe  cases  of  malarial  hyperaemia,  or  when  it  is  associated  with 
extensive  blood  changes,  such  as  scurvy,  the  symptoms  are  often  masked  by 
those  of  the  condition  with  which  it  occurs. 

Physical  Signs. — Inspection  in    severe   cases  may  show  bulging  of  the 

right  hypochondrium,  and  loss  of  motion  of  the  lower  ribs  on  the  right  side. 

On  jpalpation   the  liver  is    found  enlarged  and  smooth,  and    its   free 

border  is  felt  below  the  ribs  ;  firm  pressure  against  its  under  surface  causes 

pain. 

Percussion. — The  area  of  hepatic  dulness  is  increased  in  every  direction, 
but  more  vertically  than  laterally. 

DiiFerential  Diagnosis. — A  severe  active  hyperaemia  may  be  mistaken  for 
circumscj'ihed  hepatitis  with  abscess.     In  circumscribed  hepatitis  there  is 


PASSIVE   HYPEREMIA    OF   THE    LIVER.  339 

acceleration  of  the  pulse,  rigors  followed  by  a  slight  rise  of  temperature, 
and  localized  pain.  Kecurring  cliills  and  sweats  indicate  the  formation  of 
pus.  In  abscess  the  hepatic  enlargement  is  irregular,  while  in  active 
hypersemia  it  is  uniform.  If  the  case  is  seen  early,  and  the  enlargement  is 
carefully  followed,  in  hyperaemia  it  will  be  seen  to  take  place  rapidly,  while 
in  abscess  it  will  be  slow.  The  hepatic  enlargement  from  active  hyperaemia 
may  be  distinguished  from  displacement  of  the  liver  downwards,  by  the 
fact  that,  although  its  free  border  may  extend  far  below  the  free  border  of 
the  ribs,  the  normal  area  of  hepatic  dulness  is  not  increased. 

Prognosis.— Active  hyperaemia  generally  subsides  as  rapidly  as  it  occurs. 
The  only  danger  is  that  the  causes  which  produce  it  may  be  continued, 
and  lead  to  some  form  of  hepatic  degeneration. 

Treatment. — The  main  indication  in  the  treatment  of  this  condition  is  to 
remove  its  cause.  When  high  living  and  alcoholic  stimulants  cause  it,  re- 
strict the  diet  and  stop  the  alcohol.  When  it  occurs  from  prolonged  high 
temperature,  or  from  malarial  influences,  a  change  of  residence  is  the  only 
remedy.  An  excess  of  blood  in  the  liver  may  be  temporarily  removed  by 
saline  or  mercurial  purges,  by  taraxacum  or  podophyllum  ;  their  action  will 
be  increased  by  the  application  of  one  or  two  leeches  about  the  anus.  In 
active  malarial  hyperemia,  the  mercurial  purges  and  leeches  may  be  followed 
by  full  doses  of  quinine.  Turpentine  stupes  may  be  applied  over  a  very 
tender  liver.  When  there  is  gastro-intestinal  catarrh  with  diarrhoea, 
chloride  of  ammonium  and  ipecacuanha  will  be  found  of  service.  In  those 
who  have  a  predisposition  to  active  hepatic  hyperaemia,  the  daily  use  of 
mineral  waters  will  be  found  of  service. 


PASSIVE   HTPEE^MIA    OF  THE    LIVEK. 

Passive  or  mechanical  hepatic  hyperaemia  (''congestion  of  the  liver") 
consists  in  an  excess  of  blood,  chiefly  in  the  portal  veins,  with  a  slowed 
current. 

Morbid  Anatomy. — A  congested  liver,  in  its  early  stage,  is  larger,  heavier 
and  darker  in  color  than  the  normal  liver,  the  extent  of  the  increase  in  size 
corresponding  to  the  degree  of  the  congestion.  The  capsule  may  be 
stretched  tightly  over  the  enlarged  organ,  and  present  a  shining  appear- 
ance. The  consistency  of  the  organ  is  increased,  frequently  amounting  to 
a  stony  hardness. 

On  section,  the  cut  surface  appears  mottled,  rarely  uniformly  red  in 
color  ;  the  small  dark  spots  seen  upon  its  cut  surface  are  the  enlarged  and 
thickened  veins  in  the  centre  of  the  liver  lobules,  and  as  the  return  of 
blood  by  these  veins  is  impeded,  the  surrounding  cells  undergo  atrophy, 
and  a  granular  pigment  is  deposited  about  the  vence  centrales.  This  change 
in  color  is  made  more  apparent  by  a  deposit  of  fat  globules  in  the  periphery 
of  the  lobules,  which  causes  a  dirty  white  ring  around  the  dark  central 
spot.  Occasionally  there  are  yellowish  spots  about  the  central  vein  due 
either  to  a  catarrh  in,  or  obstruction  of  the  bile  ducts,  or  to  distention 


340 


DISEASES    OF   THE   DIGESTIVE   SYSTEM. 


of  the  minute  ramifications  of  the  portal  vein. 


In  the  advanced  stage  of 
hepatic  congestion, 
the  liver  is  diminish- 
ed in  size  and  has  a 
peculiar  hard  feel. 
On  section,  it  presents 
the  char  acteristic 
''nutmeg"  appear- 
ance, which  has  been 
called  the  red  granu- 
lar liver.  The  proc- 
esses which  were  es- 
tablished in  the  ear- 
lier stage  of  the  con- 
gestion, and  the  new 
conn  ective -tissue 
which  has  been  de- 
veloped in  the  inter- 
lobular spaces,  dimin- 
ish the  parenchyma 
of  the  organ.'  The 
rootlets  of  the  central 
vein  become  dilated 
and  hypertrophied 
and  crowd  upon  the 
liver  cells  ;  thus  the 
central  spot  spreads  nearly  to  the  periphery  of  the  lobules.  Atrophy  of 
the  cells  grouped  around  the  central  vein  occurs,  and  a  soft  pultaceous 
mass,  in  which  appear  new  vessels,  takes  their  place.  The  cells  at  the 
periphery  are  in  a  state  of  fatty  infiltration,  and  connective-tissue  passing 
inward  from  the  interlobular  spaces  produces  the  contracted,  stony  hard 
liver.  In  connection  with  these  changes  in  the  liver,  the  mucous  mem- 
brane of  the  stomach  is  usually  the  seat  of  chronic  catarrh,  and  the  spleen 
is  enlarged. 

Etiology. — The  causes  of  hepatic  congestion  are  mainly  included  under 
the  head  of  impeded  venous  return.  Heart  disease  is  the  most  fre- 
quent cause  of  such  obstruction.  The  damming  back  of  the  blood  in  the 
hepatic  veins  is  the  necessary  result  of  tricuspid  insufficiency,  and  of  right 
heart  failure.  When  right  ventricular  hypertrophy  fails  to  compensate  for 
valvular  lesions  in  the  left  heart,  or  when  disease  of  the  lungs,  as  emphyse- 
ma and  chronic  pleurisy,  obstructs  the  blood  current  in  the  pulmonary  artery 
so  that  the  right  ventricle  is  unable  to  empty  itself,  engorgement  of  the 
hepatic  veins  necessarily  follows.  The  absence  of  valves  in  these  veins, 
and  the  fact  that  they  cannot  collapse,  favor  this  result.  In  the  same 
way  enfeebled  heart  power,  occurring  in  the  course  of  exhausting  diseases, 
causes  congestion   of  the  liver.      Habitual   constipation   and  a  sedentary 

1  Atrophy  is  chronic  congestion  with,  dilatation  of  the  central  vessels  and  their  radicles. 


Pig.  68. 
Passive  Hepatic  Hypersemia. 

Section  of  liver  shoiving  a  single  lobule. 

A.  Central  vein  of  lobule. 

B.  Area  of  congestion. — Vessels  filled  with  blood,  crowding  the  hepatic 

cells. 

C.  Atrophied  liver  cells. 

B.  CommeruAng  fatty  infiltration  of  cells  in  peripheral  zone,     x  350. 


PASSIVE   HYPERiEMIA    OF   THE    LIVER.  341 

mode  of  life,  either  singly  or  combined,  may  produce  it.  The  sudden 
suppression  of  long-continued  hemorrhages,  as  menorrhagia,  or  bleed- 
ing hemorrhoids,  may  lead  to  passive  hypergemia  of  the  liver.  A  large 
mediastinal  tumor,  such  as  a  thoracic  aneurism,  may  also  produce  it  by 
pressure  on  the  cava. 

Symptoms. — As  there  is  usually  some  derangement  in  the  circulation  of 
the  thoracic  organs,  the  early  symptoms  are  very  apt  to  be  confounded  with 
those  of  cardiac  or  pulmonary  disease.  But  soon  slight  jaundice  follows 
the  headache,  drowsiness  and  apathy,  and  it  lacks  the  i^eculiar  greenish 
hue  of  that  which  sometimes  accompanies  the  cyanosis  of  long-standing 
heart  disease.  Gastric  catarrh  will  usually  attend  these  symptoms,  marked 
by  loss  of  appetite,  nausea,  and  vomiting.  In  the  "India  Liver"  there  is 
anaemia,  and  soon  a  cachexia  is  developed.  The  skin  is  dry  and  harsh. 
Later,  hemorrhoids  appear,  and  after  a  paroxysm  of  dyspnoea  and  cyanosis 
the  hepatic  dulness  is  markedly  increased.  In  severe  cases  haematemesis 
may  occur.  If  congestion  has  reached  the  stage  of  induration,  the  gastric 
symptoms  become  greatly  aggravated,  and  tympanitis,  gastric  hemorrhage, 
and  general  dropsy  occur,  'i'he  bowels  become  constipated,  and  the  faeces 
clay-colored.  The  urine  is  scanty,  high-colored,  and  usually  presents  traces 
of  albumen ;  it  is  loaded  with  lithates.  These  patients  finally  become 
irritable,  and  are  subject  to  fits  of  palpitation  and  irregularities  of  the 
pulse. 

Physical  Signs. — Inspection  may  show  slight  bulging  of  the  right  hypo- 
chondrium  and  some  restriction  in  the  movements  of  the  lower  portion  of 
the  right  thoracic  walls. 

Palpation. — In  its  early  stage,  the  free  border  of  the  liver  is  readily  felt 
below  the  margin  of  the  ribs  ;  it  is  smooth  and  tender.  Later  the  organ 
is  diminished  in  size,  but  its  free  margin  can  still  be  felt,  and  is  hard  and 
uneven. 

Percussion. — At  its  commencement  the  normal  hepatic  dulness  is  in- 
creased in  every  direction,  and  firm  percussion  elicits  pain.  In  advanced 
cases  the  area  of  hepatic  dulness  is  uniformly  diminished.  It  is  always 
important  to  subject  the  chest  to  a  thorough  physical  examination  to  deter- 
mine the  presence  or  absence  of  pulmonary  or  cardiac  disease. 

Differential  Diagnosis. — Congestion  of  the  liver  may  be  so  masked  by  the 
primary  disease  which  produces  it,  that  it  will  be  overlooked,  but  it  will 
rarely  be  confounded  with  any  other  form  of  hepatic  disease. 

Prognosis. — The  prognosis  depends  upon  the  condition  which  causes  it. 
If  constipation  and  a  sedentary  life  cause  it,  the  prognosis  is  favorable.  In 
chronic  pleurisy  and  emphysema  it  can  only  partially  be  relieved.  When  it 
is  associated  with  extreme  cardiac  disease,  recovery  is  impossible  and  re- 
lief is  only  temporary. 

Treatment. — When  the  symptoms  which  attend  congestion  of  the  liver 
are  urgent,  a  mercurial  purge  or  a  brisk  saline  cathartic  with  the  applica- 
tion of  a  few  leeches  about  the  anus  will  give  relief.  If  the  symptoms  are 
not  urgent,  a  mild  laxative  followed  by  a  course  of  mineral  waters  will 
be  beneficial.     If  the  gastric  symptoms  are  severe  leeches  may  be  applied 


342  DISEASES   OF   THE    DIGESTIVE   SYSTEM. 

over  the  stomach.  The  diet  must  be  as  free  from  carbo-hydrates  as  is 
compatible  with  nutrition.  Nitro-muriatic  acid  internally  and  externally 
is  recommended  by  English  and  East  Indian  physicians.  Chloride  of  am- 
monium and  iodide  of  potassium  are  often  advantageous,  reducing  the 
enlarged  organs.  In  some  cases  of  extensive  cardiac  disease,  mineral 
waters  are  not  well  home;  and  although  digitalis  will  relieve  the  conges- 
tion, it  is  apt  to  interfere  with  digestion.  Each  case  is  peculiar  and  requires 
its  special  treatment,  which  at  best  is  only  palliative. 

INTERSTITIAL    HEPATITIS. 

Interstitial  hepatitis  is  an  inflammation  of  the  connective-tissue  of  the 
liver.  It  has  been  variously  named  sclerosis  of  the  liver,  cirrhosis,  the 
"gin-drinker's"  liver,  the  "hob-nailed"  liver,  granular,  and  gouty  liver. 
Cirrhosis  of  the  liver,  the  name  most  commonly  used,  was  first  applied  by , 
Laennec.  It  means  yellow,  referring  to  the  color,  and  not  to  the  consis- 
tence of  the  organ. 

Morbid  Anatomy. — The  anatomical  changes  in  interstitial  hepatitis  begin 
in  the  connective-tissue  covering  the  smaller  twigs  of  the  vena  portae,  and 
gradually  extend  to  its  larger  branches.  The  hyperplastic  process  consists 
in  the  formation  of  a  soft,  red,  pulpy  or  gelatinous  mass,  which  makes  its 
appearance  first  in  the  portal  canals.  This  mass  consists  of  an  immense 
number  of  small  round  cells,  which  soon  undergo  fibrilization  and  form 
new  connective-tissue.  The  new  tissue  contracts  ;  this  contraction  may 
be  limited,  or  it  may  involve  the  whole  organ.  In  the  latter  case,  both 
stages — namely,  the  stage  of  enlargement  due  to  the  hyperplasia,  and  the 
stage  of  diminution  in  size,  the  result  of  connective- tissue  contraction — 
may  exist  in  the  same  liver  at  the  same  time.  The  new  tissue,  contract- 
ing, presses  on  the  portal  capillaries  and  liver-cells,  and  gradually  en- 
croaches on  the  intra-lobular  structures,  causing  atrophy  and  disappearance 
of  the  cells  at  the  periphery  of  the  lobules,  while  those  at  the  centre  un- 
dergo fatty  change,  the  result  of  defective  nutrition.  Sometimes  the  cells 
at  the  periphery  undergo  fatty  change  before  they  atrophy.  The  bile-ducts 
and  hepatic  capillaries  suffer  from  compression,  and  the  cells  around  the 
central  vein  are  bile-stained. 

In  the  first  stage  of  cirrhosis,  the  liver  is  slightly  enlarged,  noticeably  in 
the  vertical  direction  ;  it  is  resistant  and  hard  to  the  feel,  the  edges  are 
rounded  and  smooth,  and  the  capsule  becomes  opaque  and  thickened.  Upon 
the  capsule  are  numerous  small  flattened  projections,  which  are,  however, 
not  sufficiently  prominent  to  destroy  the  smoothness.  In  the  first  stage  the 
liver  is  uniformly  enlarged  and  hypersemic.  In  the  second  stage  it  is 
smaller  than  normal,  the  left  lobe  usually  being  but  a  caudal-like  append- 
age to  the  right,  which  is  nearly  globular  in  shape.  The  whole  organ 
presents  a  hob-nailed  appearance,  and  is  hard,  rough,  leathery  and  granu- 
lar. The  serous  covering  assumes  a  dull  gray  color,  and  fibrous  bands  bind 
the  organ  to  the  adjacent  parts,  especially  to  the  diaphragm.  In  syphilitic 
cirrhosis  these  changes  are  in  patches,  which  are  large  and  well  defined. 


INTERSTITIAL   HEPATITIS. 


343 


On  section  the  liver-tissue,  during  the  first  stage,  is  extremely  hyper- 
gemic.  The  new  cell  growth  around  the  branches  of  the  portal  vein  and  be- 
tween the  lobules  has  a  pulpy,  fleshy  look.  In  the  second  stage,  the  liver 
gives  a  cartilaginous  feel  to 
the  knife,  and  the  capsule 
is  thickened  and  resistant. 
The  cut  surface  presents  a 
yellow,  mottled  appearance, 
the  mottling  being  due  to 
three  changes :  first,  the 
non-vascular  fibrinous 
bands,  which  are  of  a  slate 
color  ;  second,  the  obstruc- 
tion of  the  bile  ducts  inter- 
fering with  the  outflow  of 
bile,  and  the  centres  of  the 
atrophied  cells  becoming 
pigmented  ;  third,  the  cells 
at  the  periphery  of  the  lobes 
becoming  the  seat  of  fatty 
degeneration.  The  n  e  w- 
formed  connective-tissue  is 
filled  with  an  abundance  of 
round  cells,  formerly  called 
nuclei ;  they  are  now  known 
as  lymphatic  corpuscles,  and 
are  probably  emigrated  leu- 
cocytes. The  smaller 
branches  of  the  portal  vein 
are  shrunken  and  twisted, 
and  in  extreme  cases  new 
capillaries  are  developed, 
which  communicate  with  both  hepatic  and  portal  vessels.  Again,  a  whole 
lobule  may  have  disappeared  and  its  place  be  occupied  by  connective-tissue. 
The  bile-ducts  have  their  commencing  I'ootlets  destroyed  and  their  mucous 
membrane  tumefied.  In  cases  of  long-standing  cirrhosis,  the  gall-bladder 
will  be  found  bound  to  the  adjacent  parts  by  adhesions,  and  its  walls  are 
thick  and  tough  ;  while  the  spleen  is  enlarged,  softened  and  congested. 
The  gross  appearance  of  the  liver  in  cirrhosis  may  vary  in  different  cases, 
but  the  anatomical  lesions  are  the  same  in  all. 

There  is  a  form  of  this  disease  which  has  been  called  liijpertropliic 
cirrhosis,  because  the  liver  is  markedly  increased  in  size,  sometimes  reach- 
ing six  or  seven  pounds  in  weight  ;  but  the  fibroid  change,  the  yellow 
staining,  the  atrophy  of  liver-cells,  and  the  fatty  change  at  the  periphery  of 
the  lobule,  are  the  same  as  in  the  ordinary  variety,  the  only  difference  being 
a  marked  increase  in  the  size  of  the  liver. 

As  a  result  of  the  compression  and  obliteration  of  the  branches  of  the 


D 

Fig.  69. 

Interstitial  Hepatitis. 

Section  of  liver  in  advanced  cirrhosis,  as  shown .  by  low  mag- 
nifyiiig  power. 

A,  A,  A.  Bands  of  connective-tissue. 

B,  B,  B.  Brunches  of  portal  vein. 

C,  C\  C.  Hepatic  ducts. 
D,  I).  Newly  fanned  connective-tissue. 

E,  E,  E.  Lobules,  separated  by  the  advancing  cirrhosis. 
F,  F.  Lobules  nearly  obliterated,     x  40. 


S4:4 


DISEASES    OF   THE   DIGESTIVE   SYSTEM. 


portal  and  hepatic  vein  from  the  new  connective-tissue  in  the  advanced 
stage  of  cirrhosis,  a  chronic  venous  congestion  occurs  in  those  viscera 
which  empty  their  blood  into  the  portal  vein.     The  spleen,  stomach  and 

intestines  consequently  be- 
come the  seat  of  chronic  ve- 
nous congestion.  The  result 
of  this  is,  that  with  cirrhosis 
of  the  liver  we  find  an  en- 
larged spleen,  and  a  chronic 
gastric  and  intestinal  catarrh. 
If  the  portal  obstruction  is 
very  great,  there  will  be  trans- 
udation of  serum  from  the 
vessels  of  the  peritoneum  into 
the  peritoneal  cavity,  causing 
ascites. 

Etiology. — The  chief  cause 
of  cirrhosis  is  the  intemperate 
use  of  alcohol.  Alcohol  is 
most  rapidly  absorbed  when 
the  stomach  is  empty.  When 
it  is  taken  in  a  concentrated 
form  without  food  it  acts  as 
a  direct  irritant  to  the  hepatic 
circulation.  If  this  irritation 
is  long  continued  interstitial 
hepatitis  is  the  result.  Those 
who  take  alcohol  before  break- 
fast as  well  as  through  the  day  are  almost  certain  to  develop  cirrhosis  of 
the  liver.  Those  who  partake  freely  and  daily  of  highly  seasoned  food, 
even  though  they  may  not  use  alcohol,  are  also  liable  to  develop  this 
disease,  especially  if  they  reside  in  hot  climates.  Syphilis,  gout  and  rheu- 
matism cause  it.  Gout,  especially  starting  from  faulty  liver  digestion,  is 
liable  to  develop  cirrhosis.  Malarial  hyperaemia,  if  long  continued,  may 
lead  to  it.  Extension  of  inflammation  from  the  capsule  of  Glisson  may 
develop  cirrhosis.     It  may  also  occur  without  any  assignable  cause. 

Symptoms. — The  early  symptoms  of  interstitial  hepatitis  are  those  of 
hepatic  congestion.  Following  the  dull  pain  and  tenderness  in  the  hepatic 
region,  the  dyspncBa,  apathy,  headache,  nausea  and  furred  tongue,  there 
is  loss  of  appetite,  especially  for  meats.  The  individual  has  a  desire  for 
food,  but  after  a  few  mouthfuls  the  sense  of  hunger  gives  place  to  loathing; 
this  occurs  most  frequently  at  breakfast.  Diarrhoea  alternates  with  con- 
stipation, and  distressing  attacks  of  retching,  especially  on  waking  in  the 
morning,  are  followed  by  intestinal  pain  and  flatulence.  As  the  dyspepti3 
symptoms  increase,  slight  jaundice  appears,  but  it  is  never  very  marked, 
for  although  the  bile  secretion  is  diminished,  there  is  no  obstruction  to  its 
passage  into  the  intestine.     Hemorrhoids  are  early  signs  of   obstructed 


Pig.  to. 


Interstitial  Hepatitis. 
Same  tissue  as  in  last  illustration,  more  highly  magnified. 
A,  A.  A.  Conrifctive.-tissue  of  ajm'tal  canal,  containing,  B,  B, 
Hepatic  dvcts;    C,  C,  Portal  veins;  and  D,  D,  Hepatic  ar- 

E.  Atrophied  hepatic  cells  in  periphery  of  a  lobtde. 

F.  Infiltration  of  round  cells— the  commencement  of  the  new  con- 

nective-tissue growth,     x  300. 


INTERSTITIAL   HEPATITIS.  345 

portal  circulation  and  are  a  very  constant  accompaniment  of  cirrhosis,  and, 
with  the  gastric  symptoms,  are  the  earliest  indications  of  obstruction  to  the 
portal  circulation.  If  cirrhosis  has  been  induced  by  the  excessive  use  of 
alcohol,  a  craving  for  alcohol  persists.  Attacks  of  vertigo  and  occasional 
slight  elevations  of  temperature  with  emaciation  and  cachexia  mark  the 
end  of  its  first  stage.  The  dingy  hne  of  the  surface,  which  was  early 
present,  disapj)ears,  and  the  skin  gradually  assumes  an  earthy  pallor,  rarely 
tinged  with  yellow.  The  increase  in  the  hepatic  symptoms  and  the  severe 
pain  and  tenderness  over  the  hepatic  region,  which  are  sometimes  present, 
are  due  to  intercurrent  attacks  of  perihepatitis. 

At  the  commencement  of  the  second  stage  gastritis  is  established  as  a 
result  of  the  mechanical  obstruction  to  the  capillary  circulation  of  the 
mucous  membrane  of  the  stomach,  and  is  marked  by  acidity,  nausea,  and 
often  by  vomiting  after  taking  food,  in  consequence  of  which  emaciation, 
weakness,  and  depression  of  spirits  occur  ;  venous  stigni.*/.ta  may  now  appear 
on  the  cheeks.  The  obstruction  of  the  vessels  of  the  gastric  mucous  mem- 
brane is  often  so  great  that  haematemesis  occurs,  and  although  the  patient 
may  experience  temporary  relief  after  the  first  bleeding,  the  hemorrhage 
will  recur,  and  may  be  the  direct  cause  of  death.  Intestinal  hemorrhage 
occasionally  occurs  from  the  same  cause.  If  there  is  persistent  diarrhoea 
during  this  stage,  it  indicates  that  there  is  gastro-intestinal  catarrh.  Tym- 
panitis, as  well  as  intestinal  catarrh,  usually  precedes  the  occurrence  of 
ascites,  which  is  slow  and  insidious  in  its  advent,  and  so  masked  by  the 
preceding  tympanitic  distention  that  it  is  often  difficult  to  determine  the 
exact  time  of  its  occurrence.  It  will  usually  be  noticed  that,  before  the 
appearance  of  the  ascites,  the  abdominal  veins,  especially  of  the  right  side, 
are  distended,  sometimes  enormously. 

Ascites  is  sometimes  absent  in  advanced  stages  of  cirrhosis.  When 
this  happens,  any  or  all  of  the  following  conditions  may  exist  to  ac- 
count for  its  absence  :  first,  during  the  contraction  of  the  new  connective- 
tissue,  the  branches  of  the  vena  portfe  sometimes  remain  patent.  Second, 
the  hemorrhoidal  branches  of  the  inferior  mesenteric  may  inosculate  with 
the  internal  iliac.  Third,  the  veins  of  the  colon  and  duodenum  may 
anastomose  with  the  left  renal  vein.  Fourth,  the  phrenic  vein  may  com- 
municate with  some  of  the  more  superficial  branches  of  the  vena  portge. 
Fifth,  new  vessels  may  be  formed  in  the  adhesions  which  bind  the  liver  to 
the  adjacent  parts,  and  thus  relieve  the  obstructed  portal  circulation. 
Sixth,  the  portal  and  hepatic  vessels  may  anastomose  sufficiently  within 
the  liver  to  relieve  the  portal  obstruction.  Seventh,  branches  of  the  vena 
porta,  which  are  distributed  on  the  under  surface  of  the  diaphragm,  and 
on  the  inner  surface  of  the  abdominal  parietes,  may  anastomose  with  the 
internal  mammary  and  epigastric  veins,  and  thus  assist  in  returning  the 
blood  to  the  right  auricle.  When  the  internal  mammary  in  its  turn  be- 
comes engorged,  there  is  a  dark  bluish  mass  surrounding  the  umbilicus, 
due  to  distention  of  the  cutaneous  veins,  and  called  the  "caput  Medum  " 
When  ascites  is  once  developed  it  progressively  increases.  By  its  pressure 
dyspnoea  and  often  pulmonary  oedema  are  developed,  and  the  gastric  de- 


346  DISEASES    OF   THE    DIGESTIVE    SYSTEM. 

rangements  are  so  increased  that  rapid  emaciation  quickly  follows  its 
accumulation.  (Edema,  beginning  in  the  feet,  gradually  extends  upward. 
Fluid  drawn  from  the  abdominal  cavity  is  of  a  pale  amber  color,  highly 
albuminous,  and  of  a  specific  gravity  varying  from  1.010  to  1.020  ;  it  is  not 
turbid,  and  contains  no  inflammatory  products.  Slight  jaundice  may  ap- 
pear with  the  ascites,  but  if  excessive  is  due  to  pressure  on  the  ducts,  either 
from  connective-tissue  indurations  or  from  enlarged  lymphatics  in  the  trans- 
verse fissure,  which  obstruct  the  outflow  from  the  bile  ducts.  The  mind  is 
usually  clear  to  the  last,  but  sometimes  the  patient  will  pass  into  a  state 
of  complete  stupor,  which  is  preceded  by  delirium  and  active  cerebral 
symptoms.  At  first,  it  seems  plausible  to  ascribe  the  cerebral  symptoms 
to  cholaemia,  but  I  have  found  the  jaundice  in  inverse  proportion  to  the 
cerebral  symptoms.  Cholaemia  may  occur  in  cirrhosis,  and  then,  of  course, 
exhibits  its  peculiar  train  of  symptoms  ;  but  I  think  the  more  reasonable 
view  is  the  one  that  ascribes  the  delirium,  coma,  and  other  cerebral  symp- 
toms which  come  on  late  in  this  disease,  to  alcohol.  The  stools  in  cirrhosis 
are  characteristic.  They  are  clay-colored  in  the  centre  ;  surrounding  this 
there  is  a  dull  pinkish  ring,  and  around  this  a  slaty  gray  ring  tinged  with 
mucus.  The  urine  is  scanty  and  very  dark  colored ;  in  one-third  of  the- 
cases  it  contains  albumen.  Bile  pigment  is  present  in  the  urine  when 
jaundice  exists.  The  urine  is  rich  in  urates,  and  a  pinkish  sediment  of 
lithates  is  very  common. 

Physical  Signs. — Inspectio7i,  in  the  early  stage  of  cirrhosis,  may  show  a 
slight  loss  of  motion  over  the  lower  portion  of  the  right  side.  In  a  few  in- 
stances the  faint  outline  of  the  liver  margin  is  seen  below  the  free  border  of 
the  ribs. 

Palpatio?!. — The  surface  of  the  liver  is  smooth,  or  finely  granular;  the 
edges  are  round  ;  on  firm  pressure  there  is  a  marked  tenderness,  and  more 
or  less  resistance. 

Percussion. — The  area  of  hepatic  dulness  is  somewhat  increased  in  the 
early  stage  (especially  over  the  right  lobe)  in  a  vertical  direction,  and  so, 
too,  is  the  area  of  splenic  dulness. 

Inspection,  in  the  advanced  stage,  shows  enlargement  of  the  superficial 
veins  of  the  abdomen,  chiefly  on  the  right  side,  and  the  caput  Medusm  is 
often  visible.  There  is  usually  more  or  less  ascites,  and  the  face  and  sur- 
face of  the  body  are  clay-colored,  often  tinged  with  yellow. 

Palpation  is  best  performed  when  the  patient  is  lying  on  the  left  side, 
and  if  the  surface  of  the  liver  can  be  felt,  it  will  be  uneven  and  hob-nailed, 
with  sharp,  firm  edges. 

Percussion  gives  a  diminished  area  of  hepatic  dulness,  and  the  left  lobe 
of  the  liver  may  be  so  small  that  the  line  of  hepatic  dulness  will  not  extend 
to  the  left  of  the  median  line.  Persistent  tympanitic  percussion  is  present 
above  the  line  of  the  fluid,  and  flatness  below.  The  spleen  is  markedly  en- 
larged, and  the  splenic  dulness  extends  below  the  free  border  of  the  ribs. 

Differential  Diagnosis. — The  early  stage  of  cirrhosis  may  be  mistaken  for 
fafty  or  waxy  degeneration  of  the  liver.  In  fatty  liver,  the  enlargement  be- 
gins without  localized  pain,  and  there  is  no  sense  of  constriction  or  dys- 


INTERSTITIAL   HEPATITIS.  347 

pepsia,  so  constantly  present  in  the  early  stage  of  cirrhosis.  In  fatty 
liver,  the  skin  is  of  a  light  yellow  color,  is  greasy,  and  has  a  velvety 
feel  ;  in  cirrhosis,  it  is  of  a  dingy  hue,  wrinkled,  and  rough.  There  is  a 
history  of  high  living,  and  of  a  sedentary  life,  or  of  some  phthisical  com- 
plication with  fatty  liver  ;  while  in  cirrhosis,  a  history  of  excessive  spirit- 
drinking,  gout,  rheumatism  or  syphilis  is  elicited.  The  liver  is  doughy  and 
painless  in  fatty  degeneration,  while  it  is  hard,  resistant  and  tender  in  cir- 
rhosis. The  tendency  in  fatty  liver  is  to  obesity,  while  emaciation  is  rarely 
absent  in  cirrhosis.     Ascites  is  never  an  attendant  of  fatty  liver. 

Waxy  liver  is  accompanied  by  a  history  of  syphilis,  prolonged  suppura- 
tion, or  disease  of  bones  ;  the  face  is  pale  and  pufPy,  the  urine  is  increased 
in  quantity  and  of  low  specific  gravity.  Pressure  over  the  liver  gives  no  pain, 
and  the  surface  of  the  organ  is  smooth,  and  its  free  edges  sharp  and  well 
defined.     These  symptoms  readily  distinguish  it  from  cirrhosis. 

The  advanced  stage  of  cirrhosis  may  be  confounded  with  chronic  peri- 
tonitis, of  a  tubercular  or  cancerous  origin,  with  gastric  ulcer,  with  adhe- 
sive pylephlebitis,  chronic  or  brown  atrophy  of  the  liver,  multilocular  hy- 
datids, gummata  and  cancer. 

Gastric  symptoms  are  prominent  in  cirrhosis,  and  absent  \n  peritonitis. 
The  ascitic  fluid  of  cirrhosis  is  albuminous,  while  in  chronic  peritonitis  it 
contains  inflammatory  products.  The  countenance  has  a  clay-colored  or 
jaundiced  hue  in  cirrhosis  ;  in  peritonitis,  it  is  pale  and  anxious.  The  liver 
is  diminished  and  the  spleen  increased  in  size  in  cirrhosis.  The  abdo- 
men is  excessively  tender  in  chronic  peritonitis,  and  the  fluid  accumulates 
more  rapidly  than  in  cirrhosis. 

A  history  of  drinking,  dyspepsia,  haematemesis  and  emaciation  may  sug- 
gest ulcer  of  the  stomach  ;  but  if  it  is  remembered  that  tympanitis,  asci- 
tes, hemorrhoids,  clay-colored  faeces,  dark,  scanty  urine,  a  small  and  hob- 
nailed liver,  and  an  enlarged  spleen  are  present  in  cirrhosis,  and  absent  in 
ulcer  of  the  stomach,  the  differential  diagnosis  is  readily  made. 

In  cancer  of  the  liver,  the  nodules  are  very  much  larger  than  in  cirrho- 
sis. Ascites  and  enlarged  spleen,  if  present  in  cancer,  occur  late,  when  the 
large  size  of  the  liver  leaves  no  doubt  in  the  diagnosis.  The  liver  is  exces- 
sively painful  and  tender  on  pressure,  and  there  are  marked  exacerbations 
of  the  pain.  A  cancerous  cachexia,  with  an  almost  chlorotic  hue,  exists  in 
cancer.  These,  with  the  history  of  the  case,  and  perhaps  the  presence  of 
cancer  in  other  organs,  are  sufficient  for  its  diagnosis. 

Hepatic  phlebitis  may  give  symptoms  identical  with  those  of  cirrhosis. 
The  most  important  diagnostic  point  is,  that  in  hepatic  phlebitis  the  as- 
citic fluid  accumulates  very  rapidly,  and  after  paracentesis  returns  more 
quickly  than  in  cirrhosis.  Jaundice  occurs  early  and  rapidly  deepens,  and 
the  stools  are  dark-brown  and  semi-fluid  in  phlebitis.  The  points  of  dif- 
ferential diagnosis  between  the  other  diseases  which  have  been  named  and 
cirrhosis,  will  be  considered  under  the  head  of  those  diseases. 

Prognosis. — The  prognosis  will  be  determined  by  the  stage  of  the  cirrhosis. 
In  its  early  stage  its  progress  may  be  arrested,  but  Avhen  the  stage  of  contrac- 
tion is  reached,  the  disease  is  progressive,  and  the  prognosis  is  exceedingly 


348  DISEASES    OF   THE    DIGESTIVE    SYSTEM. 

unfavorable.  A  fatal  result  occurs  in  all  cases.  Its  course  is  a  chronic  one, 
and  though  death  has  occurred  in  three  months  from  the  time  the  liver  be- 
gan to  be  diminished  in  size,  I  have  usually  found  a  year  and  a  half  to  be 
its  average  duration.  Complicating  diseases  influence  the  prognosis.  Hem- 
orrhage from  the  intestine  and  from  the  hemorrhoidal  veins  may  be  so  great 
as  to  exhaust  the  patient,  and  render  him  too  feeble  to  resist  the  inroads  of 
the  disease.  This  class  of  patients  are  especially  liable  to  develop  the  cir- 
rhotic form  of  Bright's  disease.  Delirium  tremens,  pleurisy,  and  pneumo- 
nia sometimes  complicate  it.  Death  may  result  from  exhaustion  due  to 
faulty  nutrition,  from  the  large  fluid  accumulation,  from  repeated  and  pro- 
fuse hemorrhages,  and  from  wasting  diarrhrea.  Intercurrent  pulmonary  or 
cardiac  disease,  peritonitis,  or  delirium  tremens  may  be  the  direct  cause  of 
death.  Those  cirrhotic  patients  live  the  longest  who  have  large  dropsical 
accumulations,  the  dropsy  disappearing  and  recurring. 

Treatment— Cirrhosis,  in  its  early  stages,  should  be  treated  in  the  same 
way  as  active  hepatic  hypersemia.  In  alcohol  drinkers,  all  spirituous 
liquors  must  be  abstained  from,  and  the  patients  must  be  placed  on  a  nutri- 
tious, though  restricted  diet,  from  which  all  irritating  ingesta  are  excluded, 
and  alkaline  waters  should  be  freely  taken.  If  the  hepatic  congestion  is 
intense,  leeches  to  the  anus,  mercurial  purges,  and  nitro-muriatie  acid  will 
be  found  of  temporary  service.  The  importance  of  a  restricted  diet,  and 
the  free  use  of  saline  waters  in  this  stage  of  the  disease  cannot  be  over- 
estimated. Cod-liver  oil  is  indicated  in  this  stage.  After  the  stage  of 
contraction  is  reached,  the  treatment  can  only  be  palliative.  The  most 
important  thing  to  be  accomplished  now,  is  to  improve  nutrition,  and  to 
relieve  urgent  and  troublesome  symptoms.  Mineral  acids  combined  with 
vegetable  tonics,  such  as  dilute  nitric  acid  and  calumbo  assist  stomach 
digestion  ;  creosote  and  sulphite  of  sodium  are  of  service  when  acid  fermen- 
tation is  a  distressing  symptom.  Mineral  waters  should  be  discontinued 
during  this  stage.  If  constipation  exists,  the  bowels  may  be  regulated  with 
rhubarb  combined  with  small  doses  of  ipecacuanha.  Cod-liver  oil  should 
be  constantly  taken  by  this  class  of  patients.  Care  must  be  taken  not  to 
suddenly  check  diarrhoea,  or  hemorrhages,  but  if  they  become  exhausting 
opium  may  be  cautiously  given. 

Ascites  and  general  dropsy  are  the  most  troublesome  symptoms  in 
this  stage  of  cirrhosis.  When  it  becomes  imperative  to  remove  the 
dropsy,  it  may  be  attempted  through  the  skin,  kidneys  and  intes- 
tines, or  it  may  be  removed  by  tapping.  If  the  patient  is  too  feeble 
to  employ  drastic  purges  and  hydragogue  cathartics,  diuretics  and  di- 
aphoretics may  be  resorted  to.  The  condition  of  the  intestinal  tract,  as 
well  as  the  strength  of  the  patient,  will  determine  whether  elaterium,  or 
any  of  the  other  drastic  cathartics  can  be  employed.  It  must  be  remem- 
bered that  they  may  excite  acute  gastric  and  intestinal  catarrh.  Diuretics 
(as  squills  and  digitalis)  are  more  efficient  in  this  than  in  any  other  form 
of  dropsy.  If  the  kidneys  and  renal  vessels  are  compressed  by  the  fluid,  diu- 
retics will  have  little  effect.  Its  removal  must  not  be  delayed  too  long,  for 
the  strength  of  the  patient  may  be  so  diminished  that  after  the  removal  of 


CIRCUMSCKIBED    SUPPURATIVE   HEPATITIS.  349 

a  large  quantity  of  fluid  fatal  collapse  may  occur.  When,  however,  reme- 
dial measures  fail  and  dyspncea  becomes  troublesome,  paracentesis  abdo- 
minis should  always  be  resorted  to.  The  mechanical  removal  of  the  fluid 
may  be  effected  either  by  the  aspirator  or  trochar.  After  its  removal,  the 
hob-nailed  surface  of  the  liver  may  cause  peritonitis  by  the  constant  irrita- 
tion produced  by  the  respiratory  movements.  There  are  few  cases  where 
tapping  has  been  frequently  performed,  in  which  after  death  a  moderate 
amount  of  chronic  peritonitis  is  not  found.  The  ascites  will  return  sooner 
or  later  after  paracentesis  ;  but  when  tapping  is  only  required  at  sufficiently 
long  intervals  for  the  patient  to  recuperate  between  the  tappings,  and  the 
amount  of  fluid  gradually  diminishes,  or  becomes  stationary,  the  case  will 
continue  for  years. ' 

CIRCUMSCRIBED    SUPPURATIVE    HEPATITIS. 

Abscess  of  the  liver  is  an  acute  circumscribed  hepatitis  which  results  in 
irregular  areas  of  suppuration,  the  liver-tissue  surrounding  the  points  of 
suppuration  remaining  normal. 

Morbid  Anatomy.  — In  a  certain  proportion  of  cases  circumscribed  hepati- 
tis has  its  origin  in  an  infarction.  The  emboli  which  produce  these  infarc- 
tions are,  in  most  instances,  stamped  with  pyemic  infection  or  are  necro- 
tic ;  they  may  vary  in  number  from  two  or  three  to  a  dozen.  Immedi- 
ately around  the  inflamed  spots  the  liver  substance  is  normal  or  in  a  state 

1  Fatti/  Hypertrophic  Cirrhosis-— In  Le  Progy^es  Medical  [No.  9,  1883,  p.  163,  etc.]  is  an  account  of  a  dis- 
ease whose  name— fatty  hj'pertrophic  cirrhosis— was  given  by  Sabourin.  It  is  claimed  to  be  a  new  variety 
of  hepatic  disease,  which  has  a  special  clinical  history,  that  develops  regularly  and  which  usually  allows  of 
a  positive  diagnosis.  Its  anatomical  changes  were  first  noticed  by  Cornil  ;  and  Hanot,  Lancereaus,  Du- 
pout  and  Renan  have  contributed  to  its  literature.  Autopsical  examinations  first  led  to  clinical  obser- 
vations. At  the  post-mortems  of  many  who  were  supposed  to  liave  hypertrophic  cirrhosis,  the  liver  pre. 
eented  the  yellow  color  of  fatty  degeneration,  and  was  soft  and  flabby.  In  simple  hypertrophic  cirrhosis 
the  liver  is  hard  and  brown,  often  very  dark.  In  fatty  hypertrophic  cirrhosis  the  liver  is  very  thick,  so 
that  the  whole  organ  is  like  a  cube.  Sabourin  dwells  particularly  on  this.  There  are  no  granulations  upon 
its  surface.  Glisson's  capsule,  sometimes  thickened  from  perihepatitis,  is  smooth  and  so  transparent  that 
through  it  can  be  seen  opaline-looking  new  connective-tissue  inclosing  yellow  parenchyma.  It  differs  from 
ordinary  fatty  liver,  in  that  we  find  no  new  tissue  formations  between  the  lobules.  Upon'  section  the 
hepatic  parenchyma  seems  made  up  of  fatty  nodules,  usually  circular,  smaller  or  larger  than  the  normal 
liver  lobules,  and  almost  completely  inclosed  by  new  tissue.  The  latter  has  sometimes  induced  absorption 
of  the  proper  glandular  elements.  With  a  low  power  there  is  an  appearance  like  the  sub-cutaneous  adipose 
tissue;  cirrhotic  bands  inclose  collections  of  fat-cells.  These  groups  of  fat-cells  are  hepatic  lobules.  The 
fatcells  are  merely  enormous  oil-globules.  The  granulo-fatty  degeneration  peculiar  to  typhoid  jaundice  is 
absent.  The  new  growth  originates  in  the  porta!  spaces  ;  the  portal  vessels  and  bile-ducts  being  sur- 
rounded by  compact  fibrous  tissue  whence  radiate  bands  to  the  central  and  sub-lobular  veins.  The  sub- 
lobular  veins  may  undergo  entire  obliteration  ;  but  they  are  always  occluded  more  than  any  other  vessels. 
The  biliary  passages  are  only  secondarily  attacked.  It  is  the  vascular  apparatus  which  is  most  involved  in 
fatty  hypertrophic  cirrhosis.  Sclerotic  renal  chansres  also  coexist.  The  symptoms  are  divisible  into  two 
periods.  The^r.sY,  or  latent  period,  is  often  overlooked  or  misunderstood.  But  when  the  seco?id  stage  sets 
in  there  will  be  abdominal  pain,  weight  in  the  hypochondrinm,  nausea,  vomiting,  anorexia,  attacks  of 
vertigo,  nocturnal  delirium  or  hallucinations,  hyperesthesia  of  the  limbs  and  then  fever.  Now  a  diagnosis 
is  easily  reached.  There  is  oedema  of  the  extremities  and  face,  great  depression,  profuse  sweats,  and 
often  signs  of  a  sub-acute  peritonitis.  Sooner  or  later  there  is  slight  jaundice  or  a  tendency  to  hemorrhages 
This  resembles  "  typhoid  jaundice  '"  (acute  yellow  atrophy).  But  the  jaundice  lasts  longer  and  the  symp- 
toms exacerbate  and  re-unite.  No  flesh  is  lost.  The  patients  are  usually  lat.  The  abdominal  fat  renders 
physical  signs  m^.  Late,  there  maybe  abundant  blood-stained  expectoration.  The  second  period  lasts 
four  to  fi/e  weeks.  There  are,  however,  deceptive  intervals  of  apparent  recovery.  Nearly  all  the  patients 
are  subjects  of  alcoholismus,  and  this,  with  the  frequent  tubercular  complication,  is  a  great  diagnostic 
point.  The  pror/nosis  is  very  bad.  The  treatment  of  this  disease  is  palliative,  expectant— none  of  the 
many  theories  advanced  has,  as  yet,  been  accepted  or  been  free  from  illogical  deductions.  All  we  can  say 
is  that  fatty  hypertrophic  cirrhosis  is  not  an  hybrid  disease— it  lias  a  special  place. 


350 


DISEASES    OF   THE    DIGESTIVE    SYSTEM. 


of  intense  congestion,  and  corresponding  to  them  on  the  surface  of  the 
liver  are  found  brownish-red  elevated  patches  from  an  inch  to  an  inch  and 
a  half  in  diameter,  and  of  firm  consistence.  Their  most  frequent  seat  is 
the  posterior  portion  of  the  right  lobe.  They  may  be  single  or  multiple. 
Soon  after  the  development  of  the  infarction  purulent  inflammation  is  estab- 
lished. In  the  centre  of  the  mass  the  liver  cells  undergo  albuminoid  infil- 
tration, become  larger,  degenerate,  and  pus  is  formed.  As  the  process 
advances  small  cavities  containing  pus  are  developed.  These  may  en- 
large into  one  large  abscess  or  remain  separate.     If  abscesses  result  from 

other  causes  than  pyaemia, 
the  process  does  not  follow 
the  lobular  course,  but  begins 
by  small  exudations  of  lymph 
and  pus,  which  soon  coalesce 
and  become  surrounded  by  a 
membraneous  wall.  The  cavity 
of  the  abscess  varies  in  size 
from  that  of  a  hazel-nut  to 
one  capable  of  containing  two 
or  three  quarts.  Their  con- 
tents are  usually  pale  yellow 
pus  ;  but  when  the  suppu- 
rating process  has  broken 
through  the  wall  of  some 
vessel,  then  the  contents  are  rust  colored  and  have  a  granular  appearance. 
If  the  process  involves  the  bile-ducts  the  pus  has  a  greenish  or  ochre-color. 
Avariety  of  changes  take  place  in  these  purulent  collections  ;  as  they  grow 
older,  their  walls  may  become  smooth,  and  the  encysted  pus  gradually 
become  absorbed,  or  undergo  cheesy  or  calcareous  degeneration.  If  absorp- 
tion takes  place,  a  cicatrix  deeply  indented  on  the  exterior  of  the  liver 
marks  the  place  where  the  abscess  approached  the  surface,  and  within  its 
substance  cicatricial  tissue  indicates  its  exact  seat.  In  other  cases,  no  lining 
membrane  is  produced  around  the  purulent  collection.  As  the  inflamma- 
tion extends,  a  necrotic  process  is  established  which  extends  to  the  surface 
of  the  liver,  and  the  abscess  opens  externally.  This  process  may  pierce  the 
peritoneum,  causing  a  fatal  peritonitis  ;  but  this  is  of  rare  occurrence,  for 
adhesions  are  formed  which  bind  the  diaphragm  and  adjacent  organs  to 
the  liver ;  or  the  abscesses  may  open  into  the  pleural  cavity,  the  right 
lung,  or  the  stomach.  In  rare  instances  the  two  large  venous  trunks,  the 
vena  portse  and  inferior  cava  may  be  pierced.  Frequently  the  abscess 
ruptures  externally,  through  the  adhesions  formed  between  the  surface  of 
the  liver  and  the  abdominal  walls.  The  intestines,  the  gall-bladder, 
or  the  pericardium  may  be  perforated  by  the  abscess.  Again,  the  pus 
may  burrow  in  the  cellular  tissue,  and  discharge  itself  at  some  point  at 
the  lower  part  of  the  trunk.  At  the  autopsy  the  liver  may  be  found  irreg- 
ularly enlarged,  often  attaining  an  immense  size.  The  capsule  is  opaque 
and  thickened,  and  on  its  surface  are  elevated  flat  spots  varying  in  color 


Fig.  n. 
Circumscribed  Suppurative  Hepatitis. 

Sketch  shmving  the  cut  surface  of  a  portion  of  the  left  lobe  of  the 
liver,  the  seat  ofmvltipl'e  abscesses.  The  open  mouths  of  the  di- 
vided hepatic  veins  are  also  shown. 


CIRCUMSCKIBED   SUPPURATIVE   HEPATITIS.  351 

from  dark  red  to  yellow.  Adhesions  generally  exist  between  it  and  the 
adjacent  parts,  and  a  layer  of  lymph  frequently  envelops  the  entire  organ. 
The  whole  liver  is  hypertemic.  Evidences  of  perforation,  in  any  of  the 
directions  which  have  been  mentioned,  may  be  present. 

On  section,  a  dark  fluid  oozes  from  the  congested  surface,  and  the 
interior  of  the  abscess  may  exhibit  any  of  the  changes  above  described. 
Near  an  abscess  the  coats  of  the  veins,  especially  the  portal,  are  thickened, 
and  their  interior  is  often  filled  with  a  shaggy,  fibrinous  deposit. 

Etiology. — Pya^mic  infarction  must  be  regarded  as  a  frequent  cause  of 
hepatic  abscess,  especially  when  associated  with  injuries  to  the  cranial 
bones.  Phlebitis,  with  the  formation  of  thrombi  leading  to  suppurative 
inflammation,  the  result  of  operations  on  the  intestines  (as  for  prolapsus  ani, 
hemorrhoids,  and  strangulated  hernia)  and  any  intestinal  traumatism,  may 
give  rise  to  abscess  of  the  liver.  Hot  climates  and  miasmatic  influences 
favor,  if  they  do  not  cause,  suppurative  hepatitis.  In  hot  climates  dysen- 
tery, particularly  the  epidemic  form,  is  frequently  accompanied  or  followed 
by  hepatic  abscess,  so  that  dysentery  has  come  to  be  regarded  as  one  of  the 
causes  of  abscess  of  the  liver.  Hepatic  abscess  sometimes  accompanies 
ulceration  of  the  stomach  and  of  the  intestine,  especially  of  the  colon. 
Ulceration  of  the  gall-bladder  and  of  the  appendix  vermiformis,  perityphlitis, 
pyelitis,  ulcerative  endocarditis,  and  cancer  of  the  stomach  or  of  the  parts 
near  the  liver  are  often  associated  with  hepatic  abscess.  Worms,  calculi,  or 
other  obstructions  of  the  ductus  communis,  causing  inflammation  of  the 
hepatic  ducts,  sometimes  lead  to  ulceration,  and  this  ulcerative  process  is 
often  followed  by  abscess.  The  prevailing  tendency  of  modern  pathology 
is  to  ascribe  hepatic  abscess  to  an  infective  embolus,  from  a  preceding 
phlebitis,  and  the  attempt  has  been  made  to  trace  back  all  the  causes  above 
named  to  such  a  primary  cause,  though,  in  many,  direct  proof  is  im]3ossi- 
ble.  Abscess  of  the  liver  may  also  be  the  result  of  inflammation  of  the  bile- 
ducts  and  of  the  veins  of  the  liver ;  and,  finally,  it  may  be  developed 
without  any  recognizable  cause. 

Symptoms. — An  abscess  of  the  liver  of  considerable  size  may  exist  with- 
out there  being  local  or  constitutional  symptoms  to  point  to  its  existence. 
A  patient  may  have  fever,  gradually  become  emaciated,  and  finally  die 
from  exhaustion,  without  a  single  objective  symptom  of  abscess,  and  yet  a 
post-mortem  examination  will  reveal  a  large  central  hepatic  abscess.  Again, 
symptoms  of  intermittent  fever,  associated  with  gastric  and  intestinal 
catarrh,  may  be  all  that,  with  the  greatest  care,  can  be  elicited,  when,  in 
fact,  a  large  abscess  is  developing  in  the  liver.  When  abscess  is  associated 
with  dysentery  the  difficulty  is  often  increased  ;  for  chills  and  rigors, 
enlargement  of  the  liver,  and  pain  may  all  be  attendants  of  dysentery  with- 
out abscess.  Again,  in  pyaemia,  when  metastatic  abscesses  in  the  liver  are 
especially  liable  to  develop,  the  recurring  chills,  the  sweats,  the  pyrexia, 
and  the  jaundice,  are  all  part  of  the  history  of  the  pysemia,  so  that  in  many 
cases  we  are  compelled  to  rely  almost  exclusively  on  the'  physical  signs  for 
a  diagnosis  of  abscess  of  the  liver.  Such  cases  of  hepatic  abscess  are  fre- 
quently overlooked.  • 


352  DISEASES    OF   THE    DIGESTIVE    SYSTEM. 

Usually  the  development  of  hepatic  abscess  is  indicated  by  well-de- 
fined symptoms.  A  slight  feeling  of  chilliness,  sometimes  a  distinct  chill, 
is  followed  by  dull  pain  and  weight  in  the  right  hypochondrium,  the  pain 
often  radiating  to  the  tip  of  the  right  shoulder  ;  the  chilly  sensations  recur, 
and  resemble  those  of  a  slight  attack  of  ague.  The  pain  increases,  and 
IS  aggravated  by  position  and  pressure.  The  tongue  is  brown  and 
furred,  there  is  loss  of  appetite,  slight  nausea,  and  often  vomiting,  which 
is  bilious  in  character.  The  bowels  are  at  one  time  constipated,  at  an- 
other there  is  a  bilious  diarrhoea. 

The  respirations  are  hurried  and  shortened,  either  because  of  slight  lo- 
calized pleurisy,  which  so  often  accompanies  hepatic  abscess,  or  because  a 
long  inspiration  increases  the  pressure  on  the  liver,  and  thus  causes  pain. 
With  the  dyspnoea  there  is  a  short  dry  cough  resembling  that  of  pleurisy  ; 
the  skin  rarely  changes  color.  With  the  formation  of  the  abscess  there  is 
a  distinct  exacerbation  of  symptoms  :  hectic,  rigors,  and  recurring  night 
sweats  occur  ;  the  gastric  symptoms  become  urgent,  and  there  is  persistent 
and  profuse  vomiting.  The  pain  becomes  sharp,  lancinating  and  localized, 
and  indicates  the  direction  of  the  future  perforation.  The  temperature 
rises  to  103°  or  104°  F.,  sometimes  reaching  106°  F.  The  pulse  is  accel- 
erated, generally  keeping  pace  with  the  temperature.  Exhaustion  and 
emaciation  are  rapidly  developed,  and  as  the  disease  advances,  typhoid 
symptoms  may  supervene.  If  the  situation  of  the  abscess  is  such  that 
portal  obstruction  results,  hemorrhoids,  ascites  and  oedema  of  the  extremi- 
ties occur,  though  peritonitis  may  be  suspected  in  those  cases  where  there 
is  ascites.  As  the  abscess  advances  toward  the  surface  of  the  liver,  attacks 
of  perihepatitis  are  apt  to  cause  severe  exacerbations  of  pain,  and  the  hepatic 
tenderness  becomes  excessive.  Toward  the  end  delirium.  Jactitation,  som- 
nolence, and  coma  may  develop.  The  urine  is  scanty,  high-colored,  and 
contains  an  abnormal  amount  of  urates,  often  causing  a  considerable  pink- 
ish deposit. 

Hepatic  abscesses  may  be  discharged  (as  has  been  stated)  in  a  variety  of 
ways.  When  an  external  opening  is  to  occur,  the  skin  becomes  tense, 
red,  shining,  and  oedematous  at  some  point  over  the  hepatic  region  ;  fluc- 
tuation can  be  detected,  and  becomes  more  and  more  marked  as  the  ab- 
scess advances  toward  the  surface.  In  some  cases  the  heart  impulse  is 
transmitted  to  the  abdominal  walls  by  the  intervening  tumor.  When  the 
cavity  of  the  peritoneum  is  perforated,  signs  of  local  or  general  peritonitis 
are  developed,  marked  by  rapidly  developed  tympanitis,  intense  and  sud- 
den collapse.  When  an  opening  occurs  into  the  stomach,  severe  gastric 
symptoms  are  developed,  accompanied  by  purulent  vomiting  and  purulent 
stools.  A  sudden  diminution  in  the  size  of  the  hepatic  tumor,  the  sub- 
sidence of  the  pain  and  of  the  urgent  symptoms,  indicate  that  the  intes- 
tine or  biliary  passage  has  suffered  perforation.  Symptoms  of  localized 
pneumonic  inflammation  in  the  right  lower  lobe  precede  the  opening  of 
an  hepatic  abscess  into  a  bronchus.  The  expectoration  suddenly  becomes 
purulent  and  mixed  with  blood,  serum,  and  shreds  of  disintegrated  lung- 
tissue  ;  the  breath  becomes  offensive,  there  is  cessation  of  pain,  and  sub- 


CIKCUMSCRIBED    SUPPURATIVE    HEPATITIS.  353 

sidence  of  the  hepatic  enlargement.  Eecovery  in  such  cases  is  rare  unless 
the  abscess  is  a  small  one,  the  patient  usually  dying  of  exhaustion  from  long- 
continued  suppuration.  When  the  pleural  cavity  communicates  with  the 
abscess,  the  symptoms  of  pleuritic  effusion  and  empyema  are  well  defined, 
and  when,  in  this  case,  an  external  opening  is  to  occur,  the  evidences  of 
it  are  the  same  as  those  of  empyema.  Almost  immediate  death  follows  per- 
foration of  the  pericardial  sac  by  an  hepatic  abscess.  Absorption  of  the 
fluid  contents  of  an  hepatic  abscess,  and  the  development  of  cicatricial  tis- 
sue, followed  by  gradual  diminution  in  the  size  of  the  liver,  are  of  rare 
occurrence. 

Physical  Signs. — Inspection.  If  the  abscess  is  large,  inspection  will  show 
a  bulging  of  the  right  hypochondriac  region,  reaching  nearly  to  the  um- 
bilicus. The  respiratory  movements  on  the  right  side  are  restricted,  and 
the  respirations  are  accelerated.  If  the  abscess  is  to  open  externally,  there 
is  a  flattened,  defined  bulging  near  the  free  border  of  the  ribs,  between 
the  intercostal  spaces. 

Palpation. — The  liver  is  enlarged  and  has  an  uneven  feel,  especially 
when  the  abscesses  are  multiple  and  superficial.  The  pain,  localized  in 
the  case  of  a  single  abscess,  is  increased  and  diffused  in  multiple  abscesses 
by  pressure.  Fluctuation  is  a  valuable  sign,  but  cannot  always  be  de- 
tected. When  it  can  be,  a  ring  of  abnormal  hardness  surrounds  the  spot. 
Palpation  should  be  made  from  before  backward  ;  if  a  single  large  abscess 
exists,  its  outline  may  be  well  defined. 

Percussion. — The  area  of  hepatic  dulness  is  always  more  or  less  in- 
creased. If  the  abscesses  are  multiple,  it  may  be  increased  in  all  direc- 
tions ;  but  if  there  is  only  one  large  abscess,  the  area  of  dulness  will 
correspond  to  the  direction  of  enlargement,  which  may  be  upward  or 
downward ;  by  its  direction  we  are  able  to  determine  the  probable  mode 
of  the  termination  of  the  abscess. 

Differential  Diagnosis. — The  readiness  with  which  the  diagnosis  of  ab- 
scess of  the  liver  may  be  made  will  depend  upon  its  size  and  situation ; 
small  abscesses  can  only  be  suspected.  Abscess  of  the  liver  may  be  mis- 
taken for  hydatids  of  the  liver,  cancer,  localized  pleurisy,  intercostal  neu- 
ralgia, abscess  of  the  abdominal  ivalls,  enlarged  gall-bladder,  perihepatitis, 
suppurative  pylephlebitis,  a.r\d  active  hyper cemia  ot  the  liver. 

Hydatids  occur  most  frequently  in  those  living  in  northern  climates, 
and  abscesses  most  in  those  who  live,  or  have  lived,  in  hot  climates.  Hyda- 
tid tumors  run  a  chronic  course,  and  are  slow  in  growth  ;  while  abscess 
is  usually  a  rapid  and  acute  disease.  Accompanying  hydatids  there  is  no 
pain,  rigors,  hectic,  or  sweats  ;  but  these  are  important  symptoms  in  abscess. 
Gastric  disturbances  and  a  rapidly  developing  cachexia  are  prominent  in 
abscess,  and  absent  in  hydatids.  In  some  cases  of  hydatid  tumor  the  hyda- 
tid "thrill"  or  fremitus  can  be  detected  ;  it  is  never  present  in  abscess. 
With  the  exploring  trochar  the  liquid  in  the  one  will  be  found  to  be  pus,  in 
the  other  a  clear  saline  fluid  containing  booklets  of  the  echinococci. 

Cancer  of  the  liver  is  generally  associated  with  cancer  of  the  stomach, 
breast,  or  some  other  organ,  primary  cancer  of  the  liver  being  very  rare. 
23 


354  DISEASES    OF   THE   DIGESTIVE   SYSTEM. 

In  cancer,  the  hepatic  enlargement  is  slower  than  in  abscess,  and  there  is 
usually  a  more  or  less  marked  cancerous  cachexia.  Suppurative  fever,  chills, 
hectic,  and  sweating  are  present  in  abscess,  and  absent  in  cancer.  The  temper- 
ature in  cancer  is  normal  or  sub-normal,  and  jaundice,  if  present,  is  persist- 
ent. Ascites  is  common  in  cancer,  and  rarely  present  in  abscess.  In  can- 
cer, palpation  discovers  scattered  nodular  masses,  which  rarely  fluctuate ; 
while  in  abscess  a  large  fluctuating  tumor  can  usually  be  made  out.  The 
exploring  needle  withdraws  pus  from  an  abscess,  while  blood  follows  the 
puncture  of  a  cancer  nodule. 

Pleurisy  on  the  rigid  side  can  usually  be  readily  distinguished  from  ab- 
scess of  the  liver  by  the  physical  signs  alone.  The  grazing  friction  sound 
accompanies  loss  of  vocal  fremitus  ;  the  dulness  on  percussion,  the  feeble 
respiratory  murmur,  and  the  crepitant  friction  sound  decide  the  question. 

Intercostal  neuralgia  occurs  most  frequently  in  women  with  a  neuralgic 
history.  The  pain  is  located  in  the  region  of  the  sixth,  seventh,  and  eighth 
intercostal  spaces,  and  the  three  points  of  tenderness  are  almost  diagnostic. 
When  the  pain  of  abscess  becomes  as  excruciating  as  that  of  neuralgia,  in- 
spection, palpation,  and  percussion  will  all  reveal  well-marked  enlargement 
of  the  liver.  Gastric  disturbances,  chills  and  profuse  sweats  are  prominent 
signs  of  abscess,  and  are  absent  in  intercostal  neuralgia. 

In  abscess  of  the  abdominal  walls,  there  is  no  history  of  pyaemia,  dysentery, 
or  internal  ulceration,  which  so  often  precede  an  hepatic  abscess.  In  he- 
patic abscess  the  line  of  dulness  is  well  marked,  and  corresponds  in  outline  to 
the  hepatic  area  ;  while  in  abscess  of  the  abdominal  walls  the  line  of  dulness  is 
ill  defined,  and  does  not  follow  the  hepatic  outline.  A  tense,  shining,  oedem- 
atous  skin,  and  superficial  tenderness  and  hardness  appear  early  in  abscess 
of  the  abdominal  walls.  The  signs  of  pus  formation  are  early  in  abscess  or 
the  abdominal  wall,  and  very  late  in  abscess  of  the  liver,  if  they  appear  at 
all.  The  respiratory  movements  cause  an  upward  and  downward  motion 
in  the  tumor  of  an  hepatic  abscess  ;  while  an  abscess  of  the  abdominal  wall 
will  remain  stationary  during  the  respiratory  acts. 

'  An  enlarged  gall-bladder  will  usually  be  accompanied  by  a  history  of  bil- 
iary colic.  The  presence  of  a  pear-shaped,  movable,  fluctuating  tumor,  oc- 
cupying the  normal  position  of  the  gall-bladder,  a  history  of  Jaundice,  and 
the  absence  of  constitutional  symptoms  indicate  enlarged  gall-bladder ; 
while  the  tumor  in  abscess  of  the  liver  is  broader,  less  movable,  less  globu- 
lar in  shape,  and  is  attended  by  chills  and  sweats. 

Prognosis. — The  majority  of  abscesses  of  the  liver  terminate  fatally.  Py- 
aemic  abscesses  are  generally  mviltiple ;  their  average  duration  is  three 
months  ;  I  have  known  death  to  occur  within  three  weeks  after  the  com- 
mencement, and  I  have  known  them  to  be  prolonged  over  a  period  of  two 
years.  In  abscess  from  other  causes  than  pysemia,  the  prognosis  is  favora- 
ble whenever  there  are  no  indications  of  an  opening  into  the  pericardium, 
peritoneum,  or  pleural  cavity.  When  an  hepatic  abscess  complicates  a  severe 
attack  of  dysentery,  the  prognosis  is  unfavorable.  Their  duration  is  shorter, 
and  the  prognosis  is  better  when  they  open  externally ;  their  next  most 
favorable  termination  is  when  they  open  into  a  bronchus,  or  into  the  intes- 


CIRCUMSCRIBED    SUPPURATIVE   HEPATITIS.  355 

tinal  canal.  Pyaemia  and  dysentery  often  cause  death  when  the  accompany- 
ing abscess  is  too  recent  to  have  induced  it.  Exhaustion  from  suppuration 
may  cause  death,  especially  when  accompanied  by  intestinal  catarrh.  Peri- 
tonitis, 23eri carditis,  pneumonia,  and  empyema  sometimes  cause  the  fatal 
result. 

Treatment. — When  multiple  abscesses  occur,  antiseptics  have  been  pro- 
posed, but  there  is  no  evidence  that  they  arrest  the  progress,  or  diminish 
the  severity  of  the  suppurative  process.  When  supjDurative  hepatitis  can 
be  recognized  early,  it  should  be  treated  according  to  the  rules  which  have 
been  given  for  the  management  of  acute  hepatic  liypereemia.  Local  blood- 
letting by  leeches  may  be  employed  when  the  symptoms  are  localized  and 
well  defined  ;  and  mercurial  purges  may  be  given  at  the  onset,  in  combina- 
tion with  large  doses  of  quinine,  but  they  should  be  discontinued  when  sup- 
puration is  established.  We  rarely  have  an  opportunity  to  carry  out  the 
preventive  treatment,  for  the  abscess  is  formed  before  the  patient  seeks 
medical  advice.  When  pus  has  formed,  and  the  locality  of  the  abscess  can 
be  determined,  aspiration  should  be  performed.  If  the  withdrawal  of  the 
pus  is  followed  by  decided  signs  of  improvement,  the  aspiration  may  be 
repeated  at  intervals  indicated  by  the  amount  and  effects  of  the  purulent 
accumulation.  Few  cases,  however,  will  be  permanently  benefited  by  aspira- 
tion. I  question  very  much  if  those  cases  reported  cured  by  one  or  two 
aspirations  were  true  hepatic  abscesses.  The  dysentery  and  the  gastro~in- 
testinal  catarrh,  which  are  so  often  attendants  of  hepatic  abscess,  are  best 
treated  with  large  doses  of  ipecacuanha  ;  a  fuller  description  of  this  method 
of  treatment  will  be  found  under  the  head  of  dysentery. 

The  question  of  operative  interference  is  one  which  it  is  often  difficult 
to  decide.  Strong  opinions  have  been  given  for  and  against  it.  On  the 
one  hand,  it  is  claimed  that  if  a  free  opening  is  not  made,  death  may  result 
from  exhaustion  produced  by  large  purulent  accumulations,  or  the  abscess 
may  open  into  the  peritoneal  cavity,  pericardial  sac,  or  pleura,  and  thus 
cause  death.  The  process  is  a  progressive  one,  and  each  day  more  and  more 
of  hepatic  tissue  will  be  involved,  and  thus  diminish  the  chances  of  recov- 
ery. On  the  other  hand,  those  who  oppose  opening  the  abscess  say  that 
peritonitis  and  the  entrance  of  air  may  result  from  it,  that  the  ribs  are  more 
liable  to  become  eroded,  and  the  surrounding  tissue  to  become  gangrenous, 
when  an  opening  is  made.  Some  regard  it  as  highly  dangerous  to  pass  an 
instrument  into  the  liver,  claiming  that  it  may  excite  a  suppurative  process 
in  healthy  liver-tissue.  All  these  objections  are  removed  if  Lister's 
method  is  employed.  If  no  adhesions  have  formed  between  the  liver  and 
the  abdominal  walls,  they  should  be  established  by  caustics,  and  then  the  sac 
may  be  opened  ;  if  it  is  very  large,  all  of  the  pus  should  not  be  allowed  to 
escape  at  once.  It  is  always  safest  to  open  the  sac  by  means  of  caustics,  using 
the  knife  to  divide  the  superficial  tissues.  The  abscess  should  be  opened  as 
soon  as  possible.  When  hepatic  abscesses  open  into  the  bronchi,  colon  or 
gall-bladder,  absolute  rest  must  be  insisted  upon.  In  all  cases,  during  con- 
valescence, absolute  rest  and  a  careful  regimen  must  be  maintained  for 
months.     The  diet  throughout  the  whole  course  of  the  disease  should  bo 


356 


DISEASES    OF   THE    DIGESTIVE   SYSTEM. 


the  most  nutritious,  and  stimulants  should  be  freely  given.     The  impor- 
tance of  sustaining  the  patient  in  every  possible  way  is  apparent. 

DIFFUSE    PARENCHYMATOUS    HEPATITIS. 


This  disease,  also  called  acute  yellow  atrophy  and  malignant  jaundice, 
has  been  regarded  as  a  '* passive  degeneration,"  the  metamorphosis  being 
more  rapid  than  in  any  other  gland  structure  in  the  body.  Some  think  it 
due  to  bilious  liquefication  ox  polycholia,  and  that  it  is  a  general  disease — 
like  typhoid  fever  or  cerebro-spinal  meningitis — with  a  local  lesion.  The 
more  recent  views  are  that  acute  yellow  atrophy  is  a  diffuse  inflammation  of 
the  whole  hepatic  structure,  where  the  inflammatory  changes  are  so  rapid  as 
to  lead  to  disintegration  and  complete  destruction  of  the  liver  cells  and  sub- 
sequent atrophy.  Whether  it  is  an  exudative  process,  or  one  in  which  there 
first  occurs  albuminoid  infiltration  of  the  hepatic  cells,  and  then  molecular 
change,  is  still  a  disputed  question,  but  the  more  reasonable  view  is  that  it 
comes  from  albuminoid  infiltration,  irregular  cloudy  swelling  of  the  cells, 
and  subsequent  softening  of  the  hepatic  tissue. 

Morbid  Anatomy, — It  is  seldom  that  one  sees  a  liver  that  is  the  seat  of 
diffuse  hepatitis  until  after  the  process  is  completed,  but  the  few  that  have 
been  studied  present  the  evidences  of  having  been  the  seat  of  an  intense 
congestive  and  exudative  process.  The  liver  lobules  have  a  dark  gray 
muddy  ring  at  the  periphery,  due  to  granular  degeneration  or  albuminoid 
swelling  of  the  peripheral  cells,  while  the  liver  structure  immediately  sur- 
rounding the  central  vein  is  normal.  The  latter  is,  however,  soon  involved, 
and  in  place  of  liver  cells  there  are  fat  and  pigment  granules,  with  traces  of 

leucin  and  tyrosin.  All  outline  of  lobular 
structure  disappears,  the  capillaries  are 
intensely  engorged,  and  the  bile-ducts 
become  more  or  less  completely  closed, 
owing  to  the  compression  which  they 
suffer  from  peripheral  exudation.  Thus 
the  bile  formed  between  the  central  vein 
and  the  exterior  of  the  lobule  has  no 
mode  of  escape,  except  through  the  cen- 
tral vein.  The  liver  is  diminished  in  size, 
sometimes  to  two-thirds  of  its  normal  size; 
in  the  early  stage  the  organ  is  supposed 
to  be  very  slightly  enlarged.  The  diminu^ 
tion  is  most  marked  in  the  right  lobe. 
It  is  so  soft  that  it  folds  upon  itself,  and 
takes  any  shape  and  position  from  the 
pressure  of  the  adjacent  organs.  At  the 
post-mortem,  the  body  will  be  emaciated, 
the  skin  A^ery  much  discolored,  and  ecchymotic  spots  will  often  be  found 
scattered  over  the  surface. 

TJie  capsule  is  loose,  freely  movable,  very  much  wrinkled,  and  opaque  or 


Fig.  78. 


Cells,  etc. 


from  an  hepatic  lobule  in  Acute 
Yellow  Atrophy. 

A,  A.  Hepatic  cells  filled  with  granvlar  detritus, 
zvith  obscuration  of  nuclei  and  cell  walls. 

B.  A  group  of  atrophied  cells. 

C.  Cells  with  fatty  infiltration. 

D,  E.  Pigment   granules^  with  blood  and  ty- 
rosin crystals,     x  300. 


DIFFUSE   PARESrCHYMATOUS   HEPATITIS.  357 

yellowish  in  appearance.     The  parenchyma  is  soft,  flabby,  and  brittle,  and 
varies  in  color  from  a  bright  yellow  to  a  yellow-red. 

On  section,  when  the  disease  is  far  advanced,  the  color  of  the  cut  sur- 
face is  of  a  rhubarb  red,  the  outlines  of  the  lobules  are  lost,  and  only  a 
detritus  of  granular  matter  is  left.  The  blood  is  darker  and  thicker  than 
normal  and  coagulates  imperfectly.  It  may  contain  leucin  and  traces 
of  urea.  If  the  organ  be  set  aside  for  a  while  it  becomes  covered  with  crys- 
tals of  leucin  and  tyrosin. 

The  heart  is  jaundiced,  fatty  and  pultaceous. 

The  spleen  is  enlarged  and  softened,  and  leucin  is  found  in  it.  The  gall- 
bladder is  empty,  or  contains  a  small  amount  of  pale  bile  or  mucus. 

The  Tcidneys  are  slightly  enlarged,  and  in  most  cases  are  in  a  state  of 
acute  fatty  degeneration.  Hemorrhages  from  the  surface  of  the  mucous 
membrane  of  the  stomach  and  intestines  are  common.  Occasionally  there 
is  softening  of  the  central  portion  of  the  cerebral  substance,  and  staining 
of  the  meninges.  The  serous  cavities  contain  fluid,  often  bloody,  and  in 
rare  instances  nearly  every  organ  in  the  body  is  blood  stained  and  has 
leucin  and  tyrosin  in  its  tissues. 

Etiology. — Acute  yellow  atrophy  is  a  rare  form  of  disease.  Its  causes  are 
regarded  by  some  as  constitutional,  by  others  as  due  to  a  peculiar  miasm. 
Two-thirds  of  the  cases  occur  in  pregnant  females,  between  the  ages  of 
twenty  and  thirty.  The  supposed  predisposing  causes  are  sex,  pregnancy, 
chronic  alcoholism,  syphilis,  malaria,  sexual  excess,  and  a  prolonged  course 
of  mercurials.  But  with  our  present  knowledge,  it  is  difficult  to  say 
whether  these  are  really  predisposing  causes,  or  that  the  acute  yellow 
atrophy  is  an  intercurrent  accident.  Among  the  exciting  causes  may  be 
named  mental  emotion,  great  grief,  or  fear.  It  is  doubtful  if  obstruction 
of  the  bile-ducts  alone  can  excite  acute  yellow  atrophy  ;  some  are  inclined 
to  regard  malaria  as  an  exciting  cause,  rather  than  a  predisjDOsing  one. 
While  its  etiology  is  still  so  obscure,  the  history  of  its  development  leads  to 
the  conclusion  that  a  malarial  poisoning  is  present  in  a  large  proportion  of 
cases. 

Symptoms. — The  symptoms  of  the  early  stage  of  acute  yellow  atrophy 
usually  pass  unnoticed,  for  they  are  not  in  themselves  distinctive.  When 
the  disease  is  slow  in  its  advent,  loss  of  appetite,  occasional  vomiting,  a 
furred  tongue,  slight  headache,  and  a  sense  of  fulness  in  the  right  hypo- 
chondrium  may  be  the  only  symptoms  for  the  first  week.  Jaundice  may 
precede  it  for  a  week  or  two.  In  cases  where  its  advent  is  sudden,  it  will 
be  ushered  in  by  constant  vomiting  and  great  prostration.  In  either  case 
during  its  early  stage  the  temperature  will  be  raised  only  a  degree  or  two, 
and  the  pulse  but  slightly  accelerated.  A  condition  of  despondency  is  often 
present,  there  are  wandering  pains  simulating  rheumatism,  and  a  sense  of 
great  depression.  Delirium  and  convulsions  may  be  the  only  ushering-in 
symptoms.  After  from  three  to  five  days,  the  characteristic  symptoms  of 
the  disease  are  developed  ;  of  these  jaundice  is  the  earliest  and  most  con- 
stant, it  is  progressive  and  never  very  intense,  first  affecting  the  upper  half 
of  the  body.     The  rise  in    temperature  and  increased  pulse-rate  which 


858  DISEASES    OF   THE    DIGESTIVE    SYSTEM. 

marked  its  premonitory  stage  disappear,  and  now  even  a  retarded  pulse 
and  sub-normal  temperature  may  exist.  In  a  few  instances,  after  the  first 
twenty-four  hours,  the  temperature  ranges  from  100°  to  101°  E.  during  the 
whole  course  of  the  disease.  The  vomited  material  consists  of  mucus 
tinged  with  bile  ;  later  it  assumes  the  nature  of  black  vomit,  similar  to  that 
in  yellow  fever,  the  color  being  due  to  gastric  capillary  hemorrhage.  There 
is  intense  pain  in  the  epigastiic  and  right  hypochondriac  regions,  which  is 
increased  by  firm  pressure  over  the  liver.  In  the  stage  of  coma,  the  liepatic 
tenderness  is  so  great  that  pressing  the  liver  up  against  the  diaphragm  may 
rouse  the  patient.  At  first  the  cerebral  symptoms  are  those  of  mental  de- 
pression and  slight  headache,  which  rapidly  increases  in  severity ;  this, 
later,  gives  place  to  wild  delirium,  jactitation,  and  convulsions.  Twitch- 
ings  of  the  voluntary  muscles  of  the  head  and  neck  (trismus)  mark  the 
convulsive  stage  of  the  disease.  These  spasms  usually  follow  the  vomiting, 
but  in  cases  where  the  disease  runs  a  rapid  course,  typhoid  symptoms 
make  their  appearance,  sordes  collect  on  the  teeth,  while  low  muttering 
delirium,  subsultus,  muscular  tremors,  and  partial  stupor  precede  the 
convulsions.  The  convulsions  are  epileptiform,  and  are  sometimes  ushered 
in  by  a  peculiar  shrill  cry. 

During  the  period  of  nervous  excitement,  the  pulse  undergoes  remark- 
able changes.  It  may  rapidly  rise  to  120,  130,  or  even  140  beats  in  a 
minute,  falling  in  moments  of  calm  to  80  or  90,  the  temperature  remain- 
ing unchanged.  The  breathing  during  the  convulsions  is  interrupted 
or  stertorous,  and  a  peculiar  groaning  noise  is  heard  with  each  inspira- 
tion ;  the  expirations  are  prolonged  and  puffing.  Whether  the  convulsions 
have  been  preceded  by  typhoid  symptoms  or  not,  the  patient  gradually  be- 
comes more  and  more  tranquil,  passes  into  stupor,  and  finally  into  deep 
coma,  from  which  he  cannot  be  aroused.  The  discharges  from  the 
bowels  and  bladder  are  either  passed  involuntarily  or  retained.  The 
pupils  are  normal  or  slightly  dilated,  and  respond  to  light  slowly.  The 
breathing  becomes  sighing,  the  pulse  reaches  140  to  150,  and  grows  shorter 
and  shorter  until  death  occurs.  The  skin  during  the  progress  of  the  disease 
has  become  more  or  less  deeply  jaundiced,  ecchymotic  and  petechial  spots 
sometimes  appear  on  the  surface,  and  there  may  be  hemorrhages  from  the 
stomach,  nose,  intestine,  uterus,  and  kidneys.  In  pregnant  females  abor- 
tion is  likely  to  occur  before  death.  The  fceces  are  firm,  clay-colored,  and 
often  blood-stained.  The  urine  is  acid  and  dark  in  color,  is  not  quite 
up  to  the  normal  amount,  and  often  contains  albumen  and  blood  ;  urea 
and  uric  acid  have  totally  disappeared,  the  sulphates  and  phosphates  are 
diminished  in  quantity,  and  leucin  and  tyrosin  are  found  in  their  place. 
The  duration  of  the  disease  varies  from  one  to  three  weeks. 

Physical  Signs. — Palpation  elicits  extreme  tenderness  over  the  epigas- 
trium and  right  hypochondrium. 

Percussion. — The  area  of  hepatic  dulness  rapidly  diminishes  from  day 
to  day,  and  as  the  liver  decreases  in  size  it  is  displaced  backward,  so  that 
there  is  no  well-defined  area  of  hepatic  dulness  in  front.  As  the  liver 
diminishes  in  size  the  spleen  enlarges. 


DIFFUSE   PARENCHYMATOUS   HEPATITIS.  359 

Differential  Diagnosis. — Diffuse  parenchymatous  hepatitis  may  be  mis- 
taken for  yellow  fever,  pymnia,  typhoid  fever,  and  the  bilious  remittent 
variety  of  pernicious  fever. 

In  acute  yellow  atrophy,  the  liver  is  diminishing  in  size  from  day  to 
day,  while  in  yellotu  fever  it  is  steadily  increasing.  The  spleen  is  increased 
in  size  in  acute  yellow  atrophy,  and  is  unchanged  in  yellow  fever.  T!io 
urine  in  yellow  atrophy  is  acid  throughout,  and  contains  leucin  and  tyro- 
sin  ;  while  as  soon  as  jaundice  appears  in  yellow  fever  the  urine  becomes 
alkaline.  Yellow  fever  is  ushered  in  by  a  distinct  chill,  while  yellow 
atrophy  of  the  liver  rarely  begins  with  a  chill.  The  pulse,  in  severe  forms 
of  yellow  fever,  is  gaseous  in  character  and  is  rarely  over  110,  while  in 
acute  atrophy  the  juilse  may  reach  140  or  150  per  minute.  The  stools  are 
dark  and  fluid  in  yellow  fever,  and  firm  and  clay-colored  in  acute  atrophy. 

Pymmia  is  ushered  in  by  distinct  chills.  The  chills  in  pyaemia  are 
followed  by  irregular  rigors  and  exhausting  sweats,  which  do  not  occur  in 
acute  atrophy.  In  pyasmia  there  is  diarrhoea,  and  in  acute  yellow  atrophy 
the  stools  are  firm  and  clay-colored.  In  pyaemia  there  is  a  peculiar  sweet 
sickish  breath,  which  is  absent  in  acute  atrophy.  Evidences  of  multiple 
abscesses,  especially  in  the  lungs,  soon  follow  the  sweats  of  pyaemia  ;  these 
do  not  occur  in  acute  atrophy.  The  presence  of  leucin  and  tyrosin  and 
the  absence  of  urea,  with  the  other  urinary  symptoms  of  acute  atrophy, 
are  in  marked  contrast  with  the  normal  urine  of  pyaemia.  Physical 
(hepatic)  signs  are  negative  in  pyaemia,  while  a  daily  diminishing  area  of 
hepatic  dulness  is  usually  present  in  acute  yellow  atrophy. 

Typhoid  fever  has  nearly  the  same  premonitory  symptoms  as  acute 
yellow  atrophy,  but  the  steady  rise  in  temperature  with  the  typical  morn- 
ing and  evening  exacerbations  and  remissions  during  the  first  week,  are  in 
marked  contrast  with  the  continual  low  temperature  of  acute  atrophy. 
The  delirium  is  wandering  in  typhoid,  and  wild  in  acute  yellow  atrophy. 
The  characteristic  *'  rose  rash  "  ajDpears  about  the  seventh  day  of  typhoid 
fever.  Diarrhoea  is  the  rule  in  typhoid  fever,  while  constipation  and  clay- 
colored  faeces  are  the  rule  in  acute  atrophy.  In  typhoid,  the  urine  is 
simply  diminished  in  amount,  and  the  urea  is  increased,  while  in  acute 
yellow  atrophy  the  urea  is  greatly  diminished  in  quantity,  and  often  com- 
pletely absent,  and  the  other  (mentioned)  urinary  changes  are  present.  In 
typhoid  fever  the  liver  is  slightly  enlarged,  while  in  acute  yellow  atrophy  it 
is  markedly  diminished  in  size. 

The  "  iilious  remittent "  form  of  pernicious  fever  very  closely  re- 
sembles in  its  symptoms  acute  atrophy  of  the  liver.  The  severe  sudden 
chill,  rapid  rise  in  temperature  to  105°  or  107°,  the  sweating,  and  the  re- 
mission in  pernicious'fever  are  all,  however,  absent  in  acute  atrophy.  Eree 
pigment  exists  in  the  blood  in  bilious  fever,  and  is  absent  in  atrophy. 
Jaundice  is  a  late  symptom  of  pernicious  fever,  but  occurs  early  in  acute 
atrophy.  The  liver  is  markedly  enlarged  in  pernicious  fever,  and  as 
markedly  diminished  in  size  in  acute  yellow  atrophy.  Poisoning  from 
phosphorus  can  only  be  diagnosticated  from  acute  yellow  atrophy  when  we 
know  the  drug  has  been  taken. 


360  DISEASES    OF   THE   DIGESTIVE   SYSTEM. 

Prognosis. — This  is  exceedingly  unfavorable,  and  those  cases  where  a  cure 
has  been  reported  are  in  the  doubtful  list.  The  average  duration  is  one 
week,  the  extreme  limits  being  twelve  hours  and  four  weeks.  Cholsemia 
and  urgemia,  by  inducing  the  cerebral  symptoms  which  have  been  referred 
to,  may  be  the  direct  cause  of  death.  Peritonitis  and  hemorrhages  from 
the  stomach  and  bowels  are  also  frequent  causes  of  death. 

Treatment. — All  plans  of  treatment  have  thus  far  failed  either  to  arrest 
the  progress,  or  to  diminish  the  fatal  tendency  of  this  disease.  It  has 
been  preferred,  in  the  early  stages,  to  administer  drastic  purges,  and  apply 
leeches  over  the  region  of  the  liver  and  about  the  anus,  and  in  the  robust 
and  plethoric  to  practice  venesection  ;  there  is,  however,  no  evidence  that 
these  measures  have  any  controlling  influence  over  the  disease.  Pregnant 
females  should  be  placed  in  pleasant  apartments,  with  cheerful  surround- 
ings. When  the  pain  over  the  liver  is  intense,  leeches  and  hot  fomenta- 
tions over  the  hepatic  region,  with  morphine  hypodermically,  will  afford 
relief.  When  the  cerebral  symptoms  develop,  chloric  ether, in  drachm 
doses  every  hour  will  often  quiet  the  wildest  delirium.  Hemorrhages  from 
the  mucous  surfaces  can  usually  be  checked  by  astringents  and  cold.  Bis- 
muth or  strychnia  will  sometimes  relieve  the  vomiting.  Bi-carbonate  of 
soda  in  ten  grain  doses  every  hour  has  been  given  with  apparent  benefit. 

PEEIHEPATITIS. 

Perihepatitis  is  an  inflammation  of  the  capsule  of  the  liver.  It  is  im- 
portant to  remember  that  the  liver  has  two  envelopes,  the  outer,  the  serous 
covering  which  is  part  of  the  peritoneum,  and  an  inner,  its  true  fibrous 
covering,  the  capsule  of  Glisson. 

Morbid  Anatomy. — A  liver  which  has  been  the  seat  of  perihepatitis  is 
diminished  in  size,  except  when  it  is  complicated  by  those  diseases  of  the 
organ  which  give  rise  to  enlargement.  The  capsule  is  thickened,  the  thick- 
ening varying  from  a  few  lines  to  half  an  inch ;  it  is  more  or  less  firmly 
adherent  to  the  colon,  stomach,  diaphragm,  and  abdominal  walls.  In 
syphilitic  perihepatitis,  Glisson's  capsule  is  hard  and  leathery  and  has  a 
granular  appearance.  Sometimes  the  capsule  is  so  thickened  and  con- 
tracted in  the  transverse  fissure  of  the  liver  as  to  obstruct  the  portal  vein 
and  hepatic  duct.  The  liver  substance  usually  remains  normal,  being  only 
slightly  compressed  on  the  surface  of  the  organ,  corresponding  to  the  fur- 
rows between  the  larger  lobules.  In  "  perihepatitis  syphilitica  "  prolonga- 
tions of  new  connective-tissue  will  penetrate  the  parenchyma,  and  the  out- 
lines of  the  lobules  will  be  indistinct.  This  condition  is  called  induration. 
Slight  atrophy  of  the  parenchyma  may  occur  at  points  corresponding  to 
the  circumscribed  capsular  thickening.  The  coats  of  the  hepatic  veins 
may  be  thickened  and  the  bile-ducts  dilated.  The  gall-bladder  is  some- 
times displaced  by  the  contraction  of  the  new  tissue,  and  the  ductus 
communis  may  be  partially  occluded  by  fibrous  bands.  Perihepatitis  is 
usually  accompanied  by  pleurisy  in  the  lower  part  of  the  right  pleural 
cavity. 


PERIHEPATITIS,  361 

Etiology. — Exposure  to  cold,  when  the  liver  is  in  a  state  of  active  hy- 
persemia,  is  the  most  frequent  cause  of  perihepatitis.  Blows  over  the 
hepatic  region  often  excite  it,  and  it  may  come  from  an  extension  of  in- 
flammation from  the  peritoneum  or  from  the  right  pleura.  In  all  in- 
flammatory forms  of  hepatic  disease  and  during  the  development  of  new 
growths,  perihepatitis  is  of  frequent  occurrence.  Syphilis  is  a  very  com- 
mon cause. 

Symptoms.— It  is  often  ushered  in  by  a  chill,  followed  by  a  slight  rise 
in  temperature  and  a  corresponding  increase  in  the  pulse  rate.  The  pulse  is 
tense  and  wiry  in  character  ;  pain  in  the  hepatic  region  is  its  most  constant 
symptom,  and  is  increased  by  pressure,  by  a  full  inspiration,  by  coughing, 
and  by  lying  on  the  right  side.  Jaundice  is  rare,  but  when  the  new  tissue 
compresses  the  common  duct  it  may  be  developed.  A  dry,  hacking  cough 
is  rarely  absent.  New  tissue  developments  in  the  transverse  flssure  may 
cause  suflBcient  obstruction  to  the  portal  vein  to  produce  ascites.  From 
obstructions  of  the  common  duct,  under  similar  circumstances,  gall-stones 
may  form  and  be  found  in  the  faeces. 

Physical  Signs. — On  palpation  the  liver  will  be  found  intensely  tender, 
slight  pressure  causing  severe  pain.  It  may  be  diminished  in  size,  its 
edges  lobulated,  rounded,  smooth  and  harsh. 

Percussion. — The  area  of  hepatic  dulness  is  somewhat  smaller  than 
normal. 

Auscultation. — In  the  early  stage  there  is  sometimes  heard  over  the  liver 
a  rubbing  sound,  like  the  friction  sound  in  pleurisy. 

Differential  Diagnosis. — Perihepatitis  may  be  confounded  with  intercos- 
tal neuralgia  of  the  right  side,  with  pleurisy,  and  with  abscess  of  the 
liver. 

In  intercostal  neuralgia  there  is  usually  a  neuralgic  history  and  three 
diagnostic  points  of  tenderness  : — -first,  at  the  exit  of  the  nerve  from  the 
spinal  canal ;  second,  midway  between  the  sternum  and  the  spine ;  third, 
just  at  the  edge  of  the  sternum.  The  pain  is  usually  confined  to  the  sixth, 
seventh  and  eighth  intercostal  spaces.  In  perihepatitis  there  is  generally 
e§'w«?  tenderness  over  the  whole  hepatic  region,  and  pressure  up  under  the 
ribs  increases  the  pain.  Elevation  of  temperature,  increase  in  the  pulse- 
rate,  and  the  history  of  a  chill  are  all  absent  in  intercostal  neuralgia. 

In  pleurisy,  the  pain  is  located  under  the  right  nipple.  The  pain  is 
lower  down  in  perihepatitis,  and  pressure  up  under  the  ribs  will  cause  a 
marked  increase  in  its  severity.  The  dyspncea  is  more  urgent  in  pleurisy 
and  the  cough  has  a  teasing,  hacking  character.  With  the  advent  of  plas- 
tic exudation  in  pleurisy,  there  is  diminished  vocal  fremitus,  dulness  on 
percussion,  feeble  respiratory  murmur,  and  a  *' sticky  "crepitating  friction- 
sound. 

Perihepatitis  often  accompanies  abscess  of  the  liver,  and  then  the  dif- 
ferential diagnosis  is  difficult.  In  abscess  there  are  hectic,  rigors,  and  re- 
curring sweats  ;  while  in  perihepatitis  there  is  but  one  chill,  and  that  at  the 
commencement.  The  temperature  in  abscess  is  103°  and  105°,  while  it  is 
lower,   rarely  above  101°  F.,  in  perihepatitis.     Urgent  gastric  symptoms. 


362  DISEASES   OF   THE    DIGESTIVE    SYSTEM. 

profuse  and  persistent  bilious  vomiting,  are  marked  in  abscess  of  the 
liver,  and  absent  i  n  perihepatitis.  In  abscess  there  is  a  rapidly  developing 
cachexi.1,  which  does  not  exist  in  perihepatitis.  In  abscess,  distinct  fluctua- 
tion on  palpation  is  often  present,  while  it  never  occurs  in  perihepatitis. 
Percussion  in  abscess  shows  an  area  of  hepatic  dulness  either  uniformly 
increased,  or  increased  in  one  direction,  while  the  area  of  hepatic  dulness 
is  never  increased  in  perihepatitis. 

Prognosis. — The  prognosis  in  perihepatitis  is  good  ;  it  is  influenced,  how- 
ever, by  the  disease  which  it  accompanies.  The  chief  danger  is  that 
repeated  attacks  will  lead  to  ''induration"  or  compression  of  the  portal 
vein,  and  subsequent  atrophy  of  the  liver.  In  the  latter  case,  all  the 
symptoms  of  cirrhosis  will  follow.  When  obstruction  to  the  ductus 
communis  is  sufficient  to  cause  jaundice,  the  prognosis, is  unfavorable. 

Treatment. — Rest  in  the  recumbent  posture  is  essential  to  the  successful 
treatment  of  this  disease.  The  severe  pain  which  usually  attends  it  can 
be  relieved  by  hypodermic  injections  of  morphia  and  the  application  of 
leeches  over  the  hepatic  region.  Warm  anodyne  poultices  should  be  ap- 
plied after  the  leeches.  In  those  cases  where  there  is  active  hepatic  hy- 
persemia,  a  mercurial  or  saline  purge  is  indicated,  unless  general  peritonitis 
exist.  In  all  cases  the  diet  should  be  non-stimulating  and  nutritious,  and 
an  individual  who  has  once  had  perihepatitis  should  abstain  from  all  forms 
of  alcoholic  stimulants. 

PYLEPHLEBITIS. 

PylephleUtis  is  an  inflammation  of  the  portal  vein,  accompanied  by 
coagulation  of  its  contents.  Under  this  term  are  now  included  all  cases 
of  ''portal  thrombosis,-*'  whether  the  thrombosis  is  preceded,  followed,  or 
unattended  by  an  inflammatory  process.  It  is  of  two  varieties,  adhesive 
and  siippiirative.  In  adhesive  pylephlebitis  there  is  more  or  less  extensive 
obliteration  of  the  veins ;  in  suppurative,  the  thrombus  which  forms  in 
the  vein  becomes  a  centre  of  purulent  accumulation.  When  the  unquali- 
fied term  pylephlebitis  is  used,  the  adhesive  variety  is  always  indicated. 
'  Morbid  Anatomy. — In  adhesive  pylephlebitis  the  coats  of  the  portal  veins 
become  thickened  and  their  calibre  is  diminished,  fibrin  collects  upon  the 
constricted  portion,  and  thus  thrombi  are  formed.  Sometimes  the  coagu- 
lum  forms  before  any  recognizable  change  in  the  coats  of  the  vein  has 
occurred.  When  this  happens,  the  process  may  commence  in  a  small  branch 
and  extend  to  the  main  trunk,  or  a  single  spot  in  a  large  branch  may  be 
the  point  where  blood  first  coagulates.  In  either  case,  obliteration  of  the 
vein  is  the  result.  The  wall  of  the  vein  is  the  seat  of  hyperplasia, 
adhesion  of  its  two  surfaces  occurs,  and  as  a  result  the  vein  is  obliterated 
and  a  fibro-cellular  cord  alone  remains.  As  a  rule  the  liver  is  smaller  in 
size  than  normal,  and  may  exhibit  on  its  surface  cicatricial  contraction, 
showing  the  lines  of  the  obliterated  vein. 

On  section,  coagula  may  be  found  in  all  stages  of  formation. 

Tlie  spleen  is  usually  found  much  enlarged.     The  abdominal  cavity  is 


PYLEPHLEBITIS.  363 

often  filled  with  fluid,  and  the  superficial  abdominal  veins  on  the  right 
side  are  enlarged  and  tortuous.  The  gall-hladder  is  usually  found  full  of 
greenish  bile. 

Etiology. — Certain  blood  conditions  predispose  to  adhesive  pylephlebitis, 
and  chief  among  these  are  acute  septic  and  malarial  poisons.  The  most 
common  and  direct  cause  is  narrowing  of  the  trunk  of  the  portal  vein,  from 
contraction  of  cicatricial  tissue  in  the  transverse  fissure  of  the  liver,  or  from 
pressure  of  enlarged  lymphatic  glands,  tumors  of  the  pancreas,  omentum, 
or  stomach  : — hence  cirrhosis  plays  the  most  important  part.  Blows,  in- 
juries to  the  walls  of  the  vein,  and  inflammation  of  the  tissue  immediately 
about  it,  act  as  direct  causes.  The  secondary  causes  are  an  extension  of 
inflammation  from  inflamed  hemorrhoidal  tumors,  from  the  umbilical  phle- 
bitis of  the  new-born,  from  severe  local  inflammation  of  the  intes- 
tine, from  extension  of  inflammation  from  the  mesentery  to  the  mesenteric 
vein,  from  a  peculiar  form  of  phlebitis  called  "gouty,"  and  from  a  chronic 
inflammation  excited  by  pressure  of  gall-stones. 

Symptoms. — When  the  main  trunk  of  the  portal  vein  or  its  larger  branches 
are  not  involved,  the  disease  cannot  be  recognized.  But  when  they  are  exten- 
sively involved,  fluid  rapidly  accumulates  in  the  peritoneal  cavity,  and  after 
withdrawal  it  quickly  reaccumulates.  This  is  an  important  point  in  the 
diagnosis.  The  veins  of  the  abdomen,  and  often  those  of  the  thorax,  be- 
come enlarged,  tortuous  and  promirnent ;  at  the  same  time  hemorrhoids, 
which  often  attain  immense  size  and  become  yery  painful,  are  developed. 
The  spleen  enlarges  so  rapidly  in  some  cases  that  the  extent  of  the  enlarge- 
ment can  be  determined  each  day.  Profuse  and  exhausting  vomiting,  with 
hsematemesis,  is  common,  and  diarrhoea,  with  frequent  discharges  of  fluid 
blood  from  the  bowels,  marks  the  advanced  stage.  Gastro-intestinal  hem- 
orrhages and  epistaxis  may  lead  to  fatal  syncope.  In  the  majority  of  cases 
its  course  is  rapid  ; — if  it  is  slow  in  its  development,  it  gives  rise  to  precisely 
the  same  symptoms  as  those  of  the  latter  stage  of  cirrhosis  of  the  liver.  Jaun- 
dice is  never  a  prominent  symptom.  If  it  does  occur,  it  is  usually  due  to 
a  complicating  catarrh  of  the  bile-ducts. 

Physical  Signs. — Inspection  o^ndi palpation  will  give  the  evidences  of  fluid 
in  the  abdominal  cavity,  and  the  superficial  veins  will  be  markedly  enlarged 
and  cord-like. 

Percussion. — The  normal  area  of  the  hepatic  dulness  is  diminished,  un- 
less waxy  degeneration  or  some  other  disease  of  the  liv^r  precedes  its  devel- 
opment.    The  spleen  is  enlarged  in  all  cases. 

Differential  Diagnosis. — C'irrJwsis  is  the  only  disease  which  would  be  liable 
to  be  confounded  with  pylephlebitis.  In  the  advanced  stage,  it  is  impossi- 
ble to  make  a  differential  diagnosis.  The  previous  history  of  the  patient  is 
important : — in  cirrhosis  it  is  one  of  chronic  alcoholismus,  gout,  rheuma- 
tism, or  syphilis,  none  of  which  can  be  regarded  as  causes  of  pylephlebitis. 
Cirrhosis  is  much  slower  in  its  development  than  pylephlebitis.  The  ab- 
dominal dropsy  accumulates  rapidly  in  pylephlebitis,  while  in  cirrhosis  it 
accumulates  slowly,  and  does  not  return  quickly  after  paracentesis.  The 
stools  in  cirrhosis  are  firm  and  clay-colored.     The  urine  contains  abundant 


364  DISEASES    OF   THE   DIGESTIVE    SYSTEM. 

urates  in  cirrhosis  ;  these  are  absent  in  pylephlebitis.     Persistent  tympani- 
tis precedes  the  ascites  of  cirrhosis,  and  is  absent  in  pylephlebitis. 

Prognosis. — The  prognosis  is  unfavorable.  Death  may  result  from  as- 
phyxia, from  gastric  and   intestinal   hemorrhage,   and  from   exhausting 

diarrhoea. 

Treatment. — Medication  avails  little  in  this  disease  ;  the  treatment  is  al- 
together palliative.  The  diarrhoea  and  hemorrhage  should  be  checked  with 
vegetable  astringents.  If  dyspnoea  becomes  urgent,  on  account  of  the  large 
accumulation  of  the  fluid  in  the  abdominal  cavity,  paracentesis  should  be 
performed.  The  food  should  be  highly  nutritious,  and  taken  in  small  quan- 
tities, at  short  intervals. 

SIJPPUEATIVE    PYLEPHLEBITIS. 

Suppurative  inflammation  of  the  portal  vein  is  always  a  secondary  disease, 
and  leads  to  the  formation  of  small  hepatic  abscesses. 

Morbid  Anatomy.— The  wall  of  the  vein  is  the  seat  of  the  inflammatory 
process;  it  becomes  thickened,  and  its  cavity  is  filled  with  a  puriform 
fluid,  coagulated  blood,  or  a  stratified  thrombus.  The  primary  seat  of  the 
process  may  be  the  trunk  of  the  vein  before  it  enters  the  liver.  It  may 
extend  to  the  smaller  branches,  and  from  them  to  the  liver  substance.  If 
coagula  occupy  the  venous  twigs  as  well  as  the  trunk  of  the  vein,  it  is  com- 
mon for  the  puriform  infiltration  to  take  place  only  in  them,  while  a  firm 
€lot  obstructs  the  main  channel.  When  the  veins  near  the  surface  of  the 
liver  are  the  seat  of  suppurative  pylephlebitis,  extension  of  the  process  from 
the  sheath  of  the  vessels  to  the  adjacent  parenchyma  gives  rise  to  small  ab- 
scesses. The  liver  becomes  enlarged  and  softened,  and  circumscribed  col- 
lections of  pus  are  visible  underneath  its  capsule. 

On  section,  the  calibre  of  the  vena  portse  is  seen  enlarged  and  gaping ; 
the  wall  is  thickened.  Its  contents  vary  :  sometimes  it  only  contains  pus; 
at  others,  fibrinous  matter  and  small  coagula  of  blood  are  mixed  in  the 
purulent  fluid.  Abscesses  are  found  along  the  course  of  the  larger  portal 
veins,  and  the  smaller  branches  often  terminate  in  larger  collections  of  pus. 
If  pieces  of  thrombi  have  been  swept  into  the  blood  current,  infarctions  are 
found  in  all  stages,  from  reddish-brown  clots  to  purulent  masses.  The 
spleen  is  usually  found  enlarged,  and  of  a  dark  purplish  color. 

Etiology. — The  chief  causes  are  ulceration  and  inflammatory  processes  in 
the  abdominal  cavity.  Typhlitis,  perityphlitis  and  ulceration  of  the  vermi- 
form appendix  sometimes  induce  it.  Diseases  of  the  rectum,  as  recto-ure- 
thral  fistulse  and  suppurating  hemorrhoidal  tumors,  chronic  peritonitis,  ab- 
scess of  the  spleen,  suppurating  mesenteric  glands,  diseases  of  the  mesen- 
tery which  have  pus  as  their  product,  and  diseases  of  the  bile  ducts,  such 
as  inflammation,  ulceration  and  perforation,  especially  when  caused  by  im- 
pacted gall-stones,  often  excite  suppuration  in  the  portal  vein.  Severe 
blows  over  the  region  of  the  liver  have  been  followed  by  pylephlebitis. 
^Suppurative  gastritis  may  be  followed  by  it. 

Sjrmptoms. — The  symptoms  of  this  disease  are  usually  well  marked.  Pain 


SUPPURATIVE   PYLEPHLEBITIS.  365 

is  the  first  and  most  constant  symptom.  The  location  of  the  pain  varies  in 
different  cases  ;  it  is  generally  most  intense  about  the  umbilicus  and  right 
hypochondriac  region,  just  to  the  right  of  and  below  the  xiphoid  cartilage. 
Frequently  it  is  felt  below  the  spleen,  and  again  it  seems  to  come  from,  or 
extend  to,  the  region  about  the  caecum.  The  pain  is  burning  in  character, 
and  accompanied  by  slight  tympanitis  and  tenderness.  With  the  pain  the 
temperature  is  elevated,  the  pulse-rate  increased,  and  soon  a  more  or  less 
prolonged  rigor  occurs,  during  which  the  temperature  will  rise  to  101°, 
102°  F.,  or  even  higher.  After  this  comes  a  profuse  and  exhausting  sweat. 
The  rigors  and  sweats  continue  for  two  or  three  days,  and  may  occur  so 
regularly  in  the  morning  or  evening  as  to  suggest  the  presence  of  some  form 
of  malarial  fever  ;  usually,  however,  the  chills  are  irregular.  Slight  jaun- 
dice, gradually  deepening,  but  never  very  intense,  is  soon  present,  and 
sometimes  assumes  a  greenish  tint.  The  pulse  is  gradually  increased  in 
frequency,  reaching  in  some  cases  130  per  minute.  The  spleen  increases 
in  size  daily,  and  is  quite  tender  to  pressure.  The  appearance  of  the  patient 
is  that  of  one  suffering  from  some  grave  form  of  disease.  He  becomes 
greatly  emaciated,  and  there  is  more  or  less  profuse  diarrhoea,  often  contain- 
ing blood.  Hgematemesis  and  bilious  vomiting  are  frequently  present,  and 
as  the  disease  advances  the  fever  assumes  a  hectic  type,  with  signs  of  gen- 
eral peritonitis,  accompanied  by  painful  tympanitis  and  obstinate  vomiting. 
Ascites,  if  present,  is  slight.  Petechiee  appear  upon  the  surface,  and  aph- 
thae develop  in  the  mouth.  Typhoid  symptoms  usually  come  on  toward 
the  close,  with  low,  muttering  delirium,  subsultus,  somnolence,  and  fatal 
coma.  The  mind  may  be  clear  to  the  last,  the  patient  dying  in  an  ex- 
tremely emaciated  condition.  In  this  disease  there  sometimes  occur  dis- 
tinct remissions  at  the  end  of  the  first  week,  but  this  must  not  mislead  one, 
for  exhausting  rigors  and  sweats  will  soon  follow  and  lead  to  a  fatal  result. 
The  iirine  is  scanty,  non-albuminous,  and  usually  contains  bile  pig- 
ment. 

Physical  Signs. — By  palpation  and  percussion  both  liver  and  spleen  are 
found  uniformly  enlarged,  and  very  tender,  but  the  spleen  is  relatively 
much  more  enlarged  than  the  liver. 

Differential  Diagnosis. — Suppurative  inflammation  of  the  portal  vein  may 
be  mistaken  for  adhesive  pylephlebitis,  for  malarial  fever,  abscess  of  the 
liver,  and  catarrh  of  the  bile-ducts. 

In  suppurative  pylephlebitis  severe  pain,  rigors  and  sweats  usher  in 
the  disease,  and  recur  irregularly  throughout  its  course  ;  these  never  mark 
the  advent  of  the  adhesive  variety.  A  large  amount  of  fluid  accumulates 
rapidly  in  the  abdominal  cavity  in  adhesive  pylephlebitis,  and  it  rarely,  if 
ever,  occurs  in  suppurative.  Jaundice  is  the  rule  in  suppurative  pylephle- 
bitis, and  the  exception  in  adhesive.  The  liver  is  smaller  than  normal  in 
adhesive,  and  larger  than  normal,  and  tender,  in  suppurative.  The  spleen 
is  enlarged  in  both  diseases,  but  it  is  excessively  tender  in  the  suppurative 
form. 

In  malarial  fever  the  rigors  and  sweats  follow  a  definite  order,  while 
in  suppurative  pylephlebitis  they  occur  irregularly.     There  is  no  pain  in 


366  DISEASES    OP   THE    DIGESTIVE    SYSTEM. 

malaria,  while  in  suppurative  pylephlebitis  it  is  diffused  over  the  hepatic, 
umbilical  and  splenic  regions. 

Diarrhoea  rarely  occurs  in  abscess  of  the  liver,  and  if  present  it  is  of 
short  duration,  often  alternating  with  constipation,  when  the  stools  are 
firm  and  clay-colored  ;  while  profuse  diarrhoea  exists  from  the  commence- 
ment in  suppurative  pylephlebitis.  Jaundice  is  rare  in  hepatic  abscess, 
and  of  common  occurrence  in  suppurative  pylephlebitis.  Fluctuation  is 
often  present  in  abscess  of  the  liver,  and  never  in  suppurative  pylephle- 
bitis. 

In  catarrh  of  the  hile-ducts  slight  fever  soon  gives  place  to  a  normal 
temperature  and  a  slow  pulse,  while  there  is  a  high  temperature  and  rapid 
pulse  throughout  the  course  of  suppurative  pylephlebitis. 

Prognosis. — Nearly  all  the  cases  of  suppurative  pylephlebitis  are  fatal. 
Its  duration  varies  from  one  or  two  weeks  to  one  or  two  months,  the  aver- 
age being  about  one  month.  Death  may  occur  from  diarrhoea,  from  hem- 
orrhage, from  exhaustion,  and  from  the  intense  gastric  catarrh  which  may 
complicate  the  disease. 

Treatment. — We  are  powerless  to  arrest  this  disease  ;  and  its  treatment  is 
altogether  palliative.  Morphia  hypodermatically  is  the  only  reliable  means 
of  relieving  the  pain  which  is  so  distressing.  Diarrhoea  is  a  part  of  its 
natural  history,  and  all  the  resisting  power  of  the  patient  is  required  to 
withstand  the  exhaustion  and  cachexia  which  it  produces.  Although 
quinine  has  no  controlling  power  over  the  disease,  it  may  be  used  as  an 
antipyretic  and  stimulant,  and  should  be  freely  administered  in  connection 
with  stimulants  and  a  most  nutritious  diet. 


AMYLOID    DEGENEEATION. 

The  most  common  degenerations  of  the  liver  are  the  amyloid  and  the 
fatty. 

Amyloid,  waxy  or  lardaceous  degeneration  of  the  liver,  is  never  a  pri- 
mary disease.     It  is  one  of  the  painless  enlargements  of  the  liver. 

Morbid  Anatomy. — The  degenerative  process  begins  in  the  walls  of  the 
capillaries  and  small  arteries,  very  rarely  in  the  veins.  Various  theories 
have  been  advanced  concerning  the  nature  of  this  degeneration  ;  some 
claim  that  it  depends  upon  blood  changes,  and  refer  to  the  connection 
between  waxy  change  and  syphilis  in  support  of  their  views.  Others  main- 
tain that,  the  alkalinity  of  the  blood  being  diminished,  the  normal  relation- 
ship between  its  other  constituents  is  disturbed,  and  as  a  consequence 
amyloid  material  or  "  dealhalized  fibrin  ■'  is  deposited ;  that  the  process 
is  not  one  of  simple  infiltration.  In  detail  the  changes  are  as  follows  : 
— the  capillaries  are  stretched  and  consequently  have  their  diameter 
increased  ;  their  walls  then  become  thickened  by  infiltration  or  deposit,  so 
that  their  channel  is  narrowed  or  wholly  occluded.  The  material  depos- 
ited is  a  substance  resembling  albumen  in  its  reaction  ;  it  is  nitrogenous, 
homogeneous,  and  translucent,  with  a  dull,  shining  surface.     Its  reaction 


AMYLOID   DEGENEEATION". 


367 


is  characteristic,  a  watery  solution  of  iodine  changing  it  to  a  deep  red- 
brown  color,  which  gradually  passes  off  ;  if  before  it  entirely  disappears  a 
drop  of  concentrated  sulphuric  acid  is  poured  over  it,  a  violet  or  deep  blue- 
black  color  results.  The  change  in  the  capillary  walls  is  rapidly  followed 
by  a  similar  one  in  the  walls  of  the  arterioles  ;  all  the  coats  of  the  smaller 
arteries  are  involved  simultaneously,  the  most  marked  change,  however,  be- 
ing in  their  muscular  coat.  The  amyloid  change  in  the  liver  always  begins 
in  the  radicles,  midway  between  the  centre  and  the  periphery  of  the 
hepatic  lobules.  An  extension  of  the  infiltration  to  the  adjacent  liver- 
cells  causes  thera  to  enlarge,  become  irregular  in  outline,  and  coalesce  in 
masses;  finally  a  whole  lobule  becomes  involved.  This  enlargement,  the 
increased  lateral  pressure,  and  the  diminution  of  the  lumen  of  the  vessels, 
cause  a  decrease  in  the  blood  supply,  and  this  leads  to  atrophy  of  the  liver- 
cells.  The  liver  is  uniformly  enlarged,  sometimes  to  such  an  extent  as  to 
nearly  fill  the  abdominal  cavity.  It  is  stony  hard,  non-elastic,  heavier 
than  normal,  its  specific  gravity  is  increased,  and  its  edges  are  sharp  and 
well  defined.  The  capsule  is  tense,  shining,  and  has  a  gray  "  waxy"  look. 
In  some  rare  cases  enlarged  lymphatics  are  found  in  its  transverse  fissure, 
and  then  jaundice  may  be  present. 

On  section,  the  liver  cuts  with  a  '' creaking"  sound,  like  bacon  (hence 
its  name  lardaceous),  and 
the  cut  surface  has  a 
*' cheese  yellow,"  or  dull 
gray,  glistening  appearance. 
The  whole  or  a  part  of  the 
liver  may  be  involved.  If 
the  whole  liver  has  under- 
gone amyloid  degeneration, 
the  cut  surface  presents  a 
homogeneous  appearance, 
and  either  the  outline  of 
the  lobules  is  lost  or  they 
are  seen  to  be  enlarged  and 
irregular ;  sometimes  a 
"  yellow  rim  "  can  be  traced 
at  their  periphery,  due  to 
fatty  change.  The  micro- 
scope shows  the  lobules  to  be 
increased  in  size  ;  the  liver 
cells  at  the  periphery  of 
the  lobules  are  infiltrated 
with  small  spherules  of  fat ; 
midway  between  the  sur- 
face and  centre  of  the  lobule  there  is  a  zone  of  amyloid  matter,  and  in 
some  instances  there  is  a  pigment  deposit  in  the  zone  just  about  the  vena 
centralis.  We  have,  then  ;  first,  the  fatty  zone  at  the  periphery  of  the 
lobules  ;    secondly,  the  waxy  intermediate    zone ;   and,  thirdly,  the  pig-^ 


Pig.  73. 
Amyloid  Degeneration. 

Section  of  a  Lobule  of  the  Liver  in  amyloid  degeneration. 

A.  Central  vein  of  the  lobule. 

B.  Normal  htpaiic  cells. 

C.  Pigmented  cells. 

D.  Commencement  of  the  amyloid  change, 

E.  Waxy  zone— the  hepatic  cells  completely  changed.     At  F, 

cells  are  shown  containing  fat.     x  350. 


368 


DISEASES   OF   THE    DIGESTIVE   SYSTEM. 


Fig.  74. 
Diagram  showing  the  three  Intralobular  Zones. 
V.  Small  branch  of  Pm'tal  Vein. 
A.  Hepatic  Artery. 
D.  Bile  Duct. 
The  three  vessels  are  s^irrounded  by  fibrous  connective- 
tissue.,  a  prolongation  of  Glisson's  capsule,  and  alto- 
gether constitute  the  elements  of  the  Portal  Caned. 


ment  zone  around   the  central  vein.     The  liver  cells  lose  their  polygonal 

outline,'  and  become  irregular  oval 
or  circular  in  shape.  Their  cell- walls 
cannot  be  traced,  but  merge  into 
the  neighboring  mass  of  amyloid 
material.  The  contents  of  the  cell 
are  atrophied,  nuclei  are  not  visi- 
ble, though  occasionally  a  nucleus 
of  one  cell  stands  out  enlarged  and 
shining.  A  semi-transparent  ho- 
mogeneous mass  fills  the  cell,  caus- 
ing it  to  present  the  appearance  of 
''waxy  scales."  Fatty  degenera- 
tion frequently  coexists  with  amy- 
loid change.  The  liver  will  then 
partake  of  the  characters  of  both 
waxy  and  fatty  change.  Cirrhosis 
or  simple  atrophy  may  precede,  or 
be  associated  with  waxy  degenera- 
tion, and  syphilitic  nodules  and 
cicatrices  from  "  perihepatitis  sy- 
philitica "  may  exist  in  a  liver 
which  has  subsequently  undergone  waxy  degeneration.  The  Mdneys 
undergo  amyloid  degeneration.  The  spleen  is  enlarged,  firm  and  waxy  ; 
the  lymphatics  generally,  and  the  gastro-intestinal  mucous  membrane  may 
also  become  the  seat  of  the  amyloid  change. 

Etiology. — Seventy-five  per  cent,  of  the  cases  of  waxy  liver  occur  in  males 
between  twenty  and  fifty  years  of  age.  Syphilis  is  its  chief  cause.  Pro- 
longed suppuration  and  chronic  diseases  of  bone  are  also  prominent  causes. 
Caries,  necrosis,  especially  when  the  larger  Joints  are  involved,  rickets,  dys- 
entery, chronic  intestinal  ulceration,  and  sometimes  chronic  pyelitis  are 
reckoned  among  the  morbid  conditions  which  predispose  to  it.  A  scrofu- 
lous diathesis,  prolonged  exposure  to  malaria,  and  a  cancerous  cachexia  are 
among  the  rarer  conditions  under  which  amyloid  degeneration  is  devel- 
oped. 

Symptoms. — Its  advent  is  never  well  defined,  occurring  as  it  does  with 
diseases  which  are  prone  to  cause  anaemia  and  wasting  of  the  body  ;  its  sub- 
jective symptoms  are  at  first  very  obscure.  There  is  no  pyrexia  accompany- 
ing it.  The  patient  has  a  sense  of  weight,  fulness,  and  constriction  in  the 
right  hypochondrium,  never  amounting  to  pain,  the  sensation  being  rather 
one  of  discomfort.  Jaundice  and  ascites  are  not  part  of  the  natural  his- 
tory of  amyloid  liver.  When  jaundice  is  present,  it  is  due  either  to  an 
intercurrent  catarrh  of  the  bile-ducts,  or  to  pressure  from  the  enlarged 
lymphatics  in  the  transverse  fissure.  Ascitic  accumulations  result  from 
complicating  peritonitis  or  from  the  pressure  of  enlarged  glands  in  the  trans- 
verse fissure.     Late  in  the  disease,  diarrhoea  and  vomiting  are  induced  by 


1  Quite  recently  Cornil,  in  examining  many  specimens,  found  no  change  in  the  hepatic  cells. 


AMYLOID    DEGENERATIOlSr.  369 

the  slightest  irregularities  in  diet,  on  account  of  the  implication  of  the 
gastro-intestinal  tract  in  the  amyloid  change.  On  an  examination  of  the 
blood  of  one  who  has  suffered  from  waxy  degeneration  of  the  liver,  the 
proportion  of  white  blood  globules  will  be  found  increased.  The  skin  has 
a  pale,  "waxy  "look,  and  oftentimes  exhales  a  peculiar  odor.  Early  in 
the  disease  the  faeces  are  firm,  and  pale  in  color,  because  of  absence  of  bile  ; 
later,  when  the  so-called  ''waxy  diarrhoea"  sets  in,  there  are  pale  mucous 
stools,  sometimes  having  a  dysenteric  odor.  The  urine  is  increased  in. 
amount,  is  of  a  pale  lemon-yellow  color,  low  specific  gravity,  averaging 
about  1.010,  and  contains  albumen.  The  amount  of  the  albumen  increases 
as  the  disease  progresses ;  epithelial  and  large  hyaline  casts  are  present. 
Anasarca  may  occur  in  the  advanced  stage  of  the  disease,  with  general 
dropsy. 

Physical  Signs. — Inspection  in  the  advanced  stage  of  the  disease  shows 
bulging  of  the  hepatic  and  splenic  regions.  The  sharp  edge  of  the  liver 
will  be  found  projecting  belov/  the  free  border  of  the  ribs,  with  a  firm,  hard, 
resistant  feel  and  a  smooth  surface.  The  spleen  is  increased  sometimes  to 
three  times  its  normal  size,  and  is  resistant. 

Percussion. — The  areas  of  hepatic  and  splenic  dulness  are  increased 
equally  in  all  directions. 

Differential  Diagnosis. — "Waxy  liver  may  be  confounded  with  the  first 
stage  of  cirrhosis,  which  has  already  been  referred  to,  and  also  with 
fatty  liver,  the  diagnosis  of  which  is  considered  in  the  history  of  that 
disease. 

Prognosis. — The  prognosis  is  unfavorable  ;  the  disease  is  progressive  and 
fatal,  and  we  can  only  hope  to  arrest  its  progress  when  it  occurs  with  syph- 
ilis. Its  exact  duration  cannot  be  estimated,  since  its  beginning  is  so  ob- 
scure. It  is  usually  slow  in  its  development,  and  extends  over  a  period  of 
many  months  and  sometimes  years.  Among  its  most  frequent  complica- 
tions are  diarrhoea,  purulent  peritonitis,  perihepatitis,  fatty  and  waxy 
kidney,  dysentery,  pulmonary  oedema,  pneumonia,  and  pulmonary  gan- 
grene. Death  may  result  from  exhaustion  due  to  faulty  nutrition  or  diar- 
rhoea, from  general  dropsy,  and  from  urgemia  or  other  complicating 
diseases. 

Treatment. — The  first  indication  for  treatment  is  to  be  found  in  its  causa- 
tion. If  it  is  developed  in  connection  with  disease  of  the  bones,  the  diseased 
bones  should  be  removed,  and  prolonged  suppuration  arrested.  If  syphilis 
exist,  antisyphilitic  measures  are  indicated.  In  phthisis,  empyema,  and 
other  similar  diseases,  attention,  must  be  directed  to  the  primary  disease. 
Alkalies  have  been  administered,  on  the  ground  that  the  amyloid  material 
is  "dealkalized  fibrin,"  and  that  with  the  suppurative  process  a  large  quan- 
tity of  alkalies  pass  rapidly  out  of  the  system.  When  once  the  amyloid 
process  is  well-established,  the  diet  should  consist  largely  of  meat;  sugars 
and  starch  should,  be  avoided.  Alcoholic  stimulants  may  be  taken  in  mod- 
eration. The  climate,  clothing,  and  general  hygienic  surroundings  of  the 
patient  are  important.  Tonics,  and  iron  combined  with  some  preparation, 
of  iodine  are  indicated  in  all  cases.  But  when  a  history  of  syphilis  is  clearly 
24 


370  DISEASES    OF   THE    DIGESTIVE    SYSTEM. 

elicited,  then  iodide  of  potassium  may  be  given  in  large  doses,  with  the 
hope  of  arresting  the  progress  of  the  disease.  Alkalies,  chiefly  potassic  salts, 
are  in  great  repute  among  the  advocates  of  the  ''alkaline  treatment,"  and 
they  can  be  given  without  fear  of  injury  in  nearly  every  case.  It  is  claimed 
by  some  that  ammonium  chloride  produces  the  most  beneficial  effects,  but 
my  own  experience  does  not  sustain  the  strong  statements  that  have  been 
made  regarding  it.  The  mineral  waters  are  too  exhausting  for  this  class  of 
patients,  and,  although  they  may  give  temporary  relief,  should  not  be  used 
in  its  treatment.  External  applications,  such  as  iodine  ointments,  and 
nitro-muriatic  acid  baths,  have  been  used,  but  without  any  markedly  favor- 
able results.  If  ursemic  symptoms  develop,  measures  for  their  relief  should 
be  promptly  instituted.  Drastic  purges,  however,  must  not  be  employed, 
for  the  condition  of  the  gastro-intestinal  tract  contra-indicates  their  use. 


CHEOlSriC   ATROPHY    OF   THE    LIVEE. 

The  term  "atrophy"  includes  all  those  forms  of  hepatic  disease  in  which 
there  is  a  diminution  in  the  size  of  the  liver,  due  to  decrease  in  either  the 
number  or  the  size  of  the  hepatic  cells.  Strictly  speaking  there  are  six 
varieties  of  hepatic  atrophy,  viz.: — acute  yellow  atrophy,  induration 
atrophy,  from  repeated  attacks  of  perihepatitis,  cirrhosis,  atrophy  from 
long  continued  Jiypermmia,  atrophy  from  adhesive  pylephleMtis,  and  chronic 
atrophy.  All  these  varieties  have  already  been  considered  under  their 
proper  head,  except  the  one  termed  chronic  atrophy.  The  liver  in  chronic 
atrophy  may  have  a  brown  or  red  color  ;  hence  the  term  chronic  brown  or  red 
atrophy.  The  pathological  processes  which  lead  to  it  are  similar  to  those 
which  take,  place  in  atrophy  of  any  gland  tissue. 

Morbid  Anatomy. — Chronic  atrophy  may  be  partial  or  general.  The 
liver  is  smaller  than  normal,  and  its  diminution  in  size  is  uniform.  Some- 
times its  weight  is  decreased  to  twenty-four  ounces.  It  is  flabby  and 
tenacious,  its  edges  are  thickened,  its  capsule  is  smooth,  of  normal  thick- 
ness, and  free  from  adhesions.  Sometimes  it  is  shrivelled,  but  never 
~"  hob-nailed  "  or  lobulated.  In  partial  atrophy,  there  are  often  large  de- 
pressions on  the  surface,  the  result  of  the  pressure  of  neighboring  organs, 
or  of  tight  lacing,  or  the  wearing  of  belts  tightly  about  the  waist.  A  large 
quantity  of  thin  blood  flows  from  its  cut  surface,  which  has  a  uniform 
brown-red  or  mottled  appearance.  The  sections  of  the  larger  portal  vessels 
gape.  The  outline  of  the  lobules  is  obliterated.  The  portal  vein  and 
its  branches  are  enlarged,  the  walls  assume  a  yellow-red  color,  the  fibrous 
sheath,  derived  from  Glisson's  capsule,  is  thickened,  and  its  finest  ramifica- 
tions end  in  blind  pouches  or  club-shaped  extremities  near  the  periphery  of 
the  lobule.  The  capillaries  are  usually  filled  with  pigment  granules. 
Sometimes  the  hepatic  vein  is  involved,  but  never  to  the  same  degree  as 
the  portal.  The  bile  ducts  are  either  empty  or  contain  a  small  amount  of 
pale,  turbid  fluid,  having  traces  of  albumen.  By  the  microscope  the  gran- 
ular contents  and  nuclei  of  the  hepatic  cells  will  be  found  to  have  dis- 


AMYLOID    DEGENERATION". 


371 


^^f  .%^'^J 


t-A 


Fig.  75. 


Chronic  Atrophy. 
Section  of  portion  of  a  Lobule. 

A.  Hepatic  cells,  shrivelled  and  pigmented,  with  disap- 

pearance of  nvclei. 

B.  Cells  containing  fat  spherules. 

C.  Pigmented  capillaries,     x  300. 


appeared.  The  cell  walls  will  be  indented  and  shrivelled^  and  often 
pigment  granules,  traces  of  bile 
coloring  matter,  or  little  fatty- 
spherules  will  be  seen  occupy- 
ing their  place.  When  the 
atrophy  is  partial,  these  morbid 
changes  will  be  found  to  exist 
underneath  the  depressions  on 
the  surface,  where  pressure  has 
been  long  continued.  The 
spleen  is  usually  enlarged,  but 
only  slightly.  The  gastro-in- 
testinal  mucous  membrane  is 
the  seat  of  catarrh,  and  some- 
times there  are  punctate  hem- 
orrhages beneath  its  mucous 
surface. 

Etiology. — The  causes  of  par- 
tial chronic  red  atrophy  are  tight  lacing  and  pressure  from  peritoneal 
effusions  and  from  abdominal  tumors.  It  may  also  be  caused  by  extensive 
adhesions  to  adjacent  organs.  General  atrophy  may  be  due  to  the  con- 
traction of  the  new  connective-tissue  developed  in  the  substance  and  on  the 
surface  of  the  organ,  and  to  chronic  malarial  infection. 

Symptoms. — The  symptoms  closely  resemble  those  of  cirrhosis  of  the 
liver.  There  is  loss  of  appetite,  furred  tongue,  a  sense  of  weight  in  the 
right  hypochondrium,  accompanied  by  the  train  of  symptoms  which  attend 
chronic  gastritis.  There  is  profuse  and  exhausting  diarrhoea  alternating 
with  constipation,  hemorrhoidal  tumors,  hsematemesis,  intestinal  hemor- 
rhages, tympanitis,  ascites  and  emaciation, — all  which  may  be  present  in 
interstitial  hej)atitis. 

Physical  Signs. — Palpation.  If  the  surface  of  the  liver  can  be  reached, 
it  will  be  found  smooth  and  I'esistant. 

Percussio7i. — The  area  of  hepatic  dulness  will  be  diminished  in  every 
direction. 

Differential  Diagnosis. — The  differential  diagnosis  between  chronic  red 
atrophy  and  cirrhosis  of  the  liver  is  always  difficult.  In  cirrhosis  there 
will  be  the  history  of  spirit  drinking,  of  gout  or  rheumatism ;  none  of 
which  will  form  a  part  of  the  history  of  chronic  atrophy.  In  cirrhosis, 
slight  jaundice  is  common,  to  ward  the  end  of  the  disease  ;  it  never  exists 
in  uncomplicated  red  atrophy.  Venous  stigmata,  which  are  so  often 
met  with  on  the  cheeks  in  cirrhosis  of  the  liver,  are  absent  in  chronic 
atrophy.  Diarrhcea  is  not  so  common  or  persistent  in  cirrhosis  as  in 
atrophy.  The  urine  in  cirrhosis  is  high  colored  and  contains  albumen,  bile 
pigment,  and  lithates ;  while  in  atrophy  it  is  pale,  and  bile  pigment  is 
rarely  present.  In  cirrhosis  the  liver  is  hob-nailed  and  rough  on  palpa- 
tion, while  in  atrophy  it  is  smooth  on  its  surface. 
Prognosis. — Recovery  from  chronic  red  atrophy  never  occurs.     Death 


372 


DISEASES   OF   THE   DIGESTIVE   SYSTEM. 


may  result  from  exhaustion  due  to  the  diarrhoea,  from  haematemesis  or  in- 
testinal hemorrhages,  and  from  general  dropsy. 

Treatment.^Little  can  be  accomplished  in  the  treatment  of  this  disease 
except  to  alleyiate  suffering  and  prolong  life  ;  it  is  incurable.  When  the 
ascites  causes  dyspnoea  it  must  be  removed  by  mechanical  means. 


FATTY    LIVER. 

Fatty  degeneration  of  the  liver  occurs  either  as  a  fatty  infiltratmi  or 
as  a  metamorphosis  of  the  albuminous  elements  of  liver-tissue  into  fat.  It 
is  one  of  the  painless  enlargements  of  the  liver. 

Temporary  fatty  infiltration  of  the  liver  is  a  physiological  state  which 
occurs  after  the  ingestion  of  food  rich  in  hydrocarbons. 

Morbid  Anatomy. — In  fatty  infiltration,  the  liver  is  increased  in  size  and 
has  a  peculiar  flattened  appearance.  Its  surface  is  smooth  and  presents  a 
pale  brown  or  light  yellow  color,  according  to  the  degree  of  infiltration  ; 
its  borders  are  smooth  and  rounded,  and  it  has  a  doughy,  flabby  feel,  and 
pits  on  pressure.  Its  capsule  is  tense,  shining,  and  transparent ;  enlarged 
tortuous  vessels  are  frequently  seen  traversing  it. 

On  section  the  organ  cuts  readily,  and  the  warmed  knife  blade  is  coated 
with  oil  globules ;  little  blood  flows  from  the  cut  surface.  In  the  early 
stage  it  presents  a  reticulated,  mottled  appearance,  of  a  dull  yellow  color. 
This  appearance  is  due  to  the  rim  of  fat  globules  around  the  periphery  of 
the  acini,  while  the  parts  immediately  about  the  central  vein  are  intensely 

congested  and  pigmented.  In 
the  latter  stage,  the  whole 
surface  presents  a  homogene- 
ous bright  "■  butter  yellow  '^ 
color,  and  fat  cells  are  found 
occupying  the  centre  of  the 
lobule.  Amyloid  degeneration 
and  fatty  infiltration  may  be 
found  in  the  same  organ. 
With  the  microscope  the  lobules 
will  be  found  enlarged,  and 
the  cells  at  their  periphery  are 
rounded,  larger  than  normal, 
and  filled  with  fat  globules. 
These  fat  globules  vary  in  size, 
sometimes  a  single  oil  drop 
occupies  the  entire  cell  space, 
the  clouded  nucleus  and  gland- 
ular contents  being  pressed  up 
At  first 


Fig.  76. 
Fatty  Infiltration . 
Section  of  a  Portal  Canal  and  portion  of  three  Lobules. 
A,  A,  A.  Connective-tissve  of  Portal  Canal. 

B.  Branch  of  Portal  Vein. 

C.  Eeiyatic  Artery. 
B,  Hepatic  Buct. 

E.  Periphery  of  a  Lobule,  in  ^ohich  small  fat  globules  oaainst  the  cell  Wall 
are  seen  in  the  liver-cells.  to 

F.  Same  as  LJ,  tvith  increased  amoimt  qfinflltration.    _    -fchc  Capillaries  near  the  Central 

G.  Periphery  of  a  third  Lobule,  in  ivhich  the  lesion  is       _        ^ 

still  further  advanced.    x28o.  vcm   are   distended,    and   the 

cells  about  the  vein  are  infiltrated  with  fat  to  a  slight  extent ;  later  on 


FATTY    LIVEE. 


373 


the  capillaries  are  compressed  and  the  cell  filled  with  pigment  granules. 
Pigment  deposit  and  fatty  infiltration  are  not  often  found  in  the  same 
cell.  When  the  cell-wall  remains  intact,  and  the  accumulation  of  fat  is  very- 
great,  the  outline  of  the  cell  is  uneven.  The  proportion  of  fat  has  ranged 
as  high  as  seventy-eight  per  cent,  when  the  liver  was  freed  of  water,  and 
consisted  of  olein  and  margarin,  with  slight  traces  of  cholesterin  and 
sugar. 

Etiology. — Fatty  Infiltration. — As  has  been  stated,  an  exaggeration  of  the 
normal  physiological  processes  will  lead  to  a  pathological  accumulation  of  fat 
in  the  liver.  Thus  we  find  it  in  those  eating  largely  and  exercising  little, 
especially  if  the  food  taken  is  rich  in  hydrocarbons,  and  if  alcoholic  stimu- 
lants are  freely  used  at  the  same  time.  The  obese  and  the  gourmand  are 
always  subject  to  this  disease.  Females  are  more  liable  than  males  to  fatty 
infiltration  of  the  liver.  Fatty  infiltration  occurs  most  frequently  at  the 
middle  period  of  life,  when  the  time  of  active  physical  exertion  is  past.  A 
warm  and  moist  climate  predisposes  to  it,  especially  when  one  or  more  of 
the  above-named  causes  are  in  operation.  Pulmonary  phthisis  is  often  ac- 
companied by  fatty  infiltration  of  the  liver,  the  deficient  respiratory  power 
causing  imperfect  oxidation.  Extensive  crippling  of  the  lung  from  any 
cause  may  lead  to  it.  In  the  new-born  the  liver  sometimes  contains  an 
abnormal  quantity  of  fat,  and  there  is  undoubtedly  an  hereditary  predispo- 
ition  to  it  in  some  families. 

Fatty  Metamorphosis,  or  true  fatty  degeneration,  may  occur  at  circum- 
scribed spots  in  the  liver,  about  cancer-nodules,  pathological  new  forma- 
tions, and  in  advanced  stages  of  cirrhosis,  chronic  atrophy,  and  amyloid 
degeneration.     It  may  be  uniform  throughout 
the  whole  liver,  as  a  result  of  poisoning  from 
phosphorus,    antimony,    arsenic,    ether,    and 
chloroform,  or  from  blood-changes  in  typhoid, 
yellow,  and  puerperal   fevers,  in   small  pox, 
scarlatina,  pyaemia,  and  any  disease  where  an 
extremely  high  temperature  is  sustained  for  a 
considerable  period.     There  is  a  similar  form 
of  degeneration,   due  to  the  altered  state  of 
the  blood,  in  old  age. 

Symptoms. — The  symptoms  of  fatty  liver, 
with  few  exceptions,  are  decidedly  negative. 
The  fatty  accumulation,  though  not  enough 
to  cause  sufficient  obstruction  to  the  portal 
circulation,  to  lead  to  ascites  or  splenic  en- 
largement, is  sufficient  to  give  rise  to  gastric 
symptoms,  such  as  dyspepsia,  flatulence,  and 
loss  of  appetite.  There  being  no  inter- 
ference with  the  formation  and  outflow  of 
the  bile,  neither  jaundice  nor  changes  in  the 
color  of  the  faeces  occur.  As  the  disease  progresses  the  enlargement  of  the 
liver  may  cause  a  sense  of  fulness  in   the   right  hypochondrium,  never. 


Fig.  77. 

Fatty  degeneration. 

Section  showing  part  of  a  Lobule  in  a 
case  of  poisoning  by  phosphorous. 

A.  Hepatic  cells  showing  the  granvlar 

chavqe  of  true  fatty  degeneration. 
X  3.50. 

B.  Capillaries. 


■374  DISEASES   OF  THE   DIGESTIVE   SYSTEM. 

however,  attended  with  pain.  The  slightest  indiscretion  causes  an  attack 
of  gastric  catarrh  and  diarrhoea,  whicli  persists  long  after  the  removal  of 
the  cause.  The  patient  is  anaemic  and  moody,  and  there  is  a  general  loss 
of  muscular  power,  with  a  disposition  to  sleep.  The  blood  is  hydrsemic. 
The  skin  is  sometimes  shining,  always  ''velvety"  to  the  feel,  and  often 
pasty  and  smooth,  like  that  of  a  wax  figure.  The  integument  all  over  the 
body  feels  smooth,  velvety,  and  flabby.  Dyspnoea  results  as  much  from  the 
weakness  and  anaemia,  as  from  pressure  of  the  enlarged  liver.  When  symp- 
toms of  acholia,  due  to  the  altered  state  of  the  blood,  are  attended  by  absence 
of  bile  in  the  intestinal  tract,  rapid  anaemia,  exhaustion,  delirium  and  col- 
lapse occur,  and  extensive  fatty  metamorphosis  is  then  usually  associated 
with  some  other  hepatic  degeneration.  The  faeces  are  usually  normal  in  color 
and  the  bowels  are  irregular  and  constipated  ;  in  the  highest  grades  of  fatty 
metamorphosis  they  are  pale  and  clay-colored,  and  attacks  of  diarrhoea  are 
frequent.    The  urine  is  pale,  non-albuminous,  and  of  a  low  specific  gravity. 

Physical  Signs. — Palpation.  The  rounded  smooth  edges  of  a  uniformly 
enlarged  liver  are  readily  felt  below  the  border  of  the  ribs ;  the  organ  has 
a  doughy,  soft  feel.  When  fatty  degeneration  occurs  with  waxy  or  colloid 
disease,  the  liver  is  diminished  or  is  of  normal  size  and  smooth. 

Percussion. — The  area  of  hepatic  dulness  is  increased  in  all  directions, 
the  increase  being  mainly  downward  and  forward. 

Differential  Diagnosis. — Fatty  and  waxy  degeneration  are  frequently 
mistaken  for  each  other.  In  ivaxy  liver  a  history  of  syphilis,  prolonged 
suppuration,  or  disease  of  bones  will  be  elicited  ;  in  fatty  liver  there  is  a 
history  of  alcoholism,  prolonged  wasting  disease,  or  one  of  high  living  and 
sedentary  habits.  In  waxy  liver,  the  skin  is  pale,  dry,  and  has  a  peculiar 
odor  resembling  that  of  indigo  ;  in  fatty  liver  the  skin  shines  with  fat, 
and  has  a  velvety  feel.  The  blood  is  hydraemic  in  fatty  liver,  and  is  leu- 
kaemic  in  waxy  liver.  The  urinary  symptoms  in  both  are  distinct  :  in 
waxy  liver  the  urine  is  often  increased  in  amount,  is  albuminous,  and  con- 
tains casts  ;  in  fatty  liver  it  is  normal.  In  waxy  liver  the  faeces  are  early 
deficient  in  bile  and  pale  in  color  ;  in  fatty  liver  they  are  normal  until 
an  advanced  stage  of  the  disease  is  reached.  A  waxy  liver  is  hard  ;  a  fatty 
liver  is  soft  and  flabby.  A  waxy  liver  may  become  much  larger  than  a 
fatty  liver,  and  its  edges  are  sharply  defined  ;  w^hile  in  fatty  liver  they  are 
smooth  and  rounded.  With  a  waxy  liver  the  spleen  is  enlarged,  but  with 
fatty  liver  it  is  normal  in  size. 

Prognosis. — Fatty  infiltration  of  the  liver  is  not  a  grave  form  of  disease. 
There  is  danger  only  when  fatty  degeneration  of  liver-tissue  occurs. 
Death  may  result  from  fatty  heart,  pulmonary  cedema,  acholia,  apo- 
plexy, the  exhausting  diarrhoea,  and  from  the  complications  already  re- 
ferred to. 

Treatment. — When  the  diet,  mode  of  life,  or  climate  is  the  main  element 
in  its  causation,  the  indications  for  treatment  are  simple.  A  restricted 
diet,  with  no  fat  or  sugar,  and  with  regular  daily  exercise  in  the  open  air 
will,  in  most  cases,  increase  the  patient's  strength  and  lessen  the  size  of 
the  liver.    Care  must  be  taken  not  to  stop  alcoholic  stimulants  too  suddenly. 


PIGMENT   DEGENERATION. 


S7L 


for  fatty  heart  may  co-exist.  They  must  be  decreased  gradually.  In  all 
cases,  a  residence  in  an  elevated  temperate  region,  free  from  marshes,  is  im- 
portant. The  vegetable  bitters  combined  with  alkalies  will  aid  in  restor- 
ing the  appetite  when  it  is  lost.  Iron  should  be  administered  in  the  form 
of  the  carbonates  and  lactates.  Ehubarb  and  aloes  will  best  relieve  the 
constipation,  and  vegetable  astringents  control  the  diarrhcea.  In  syphilis, 
iodide  of  potassium  is  of  service.  In  the  fatty  liver  of  phthisis,  nothing  can 
be  expected  from  treatment  so  long  as  the  phthisis  is  progressive. 


PIGMENT   DEGENEEATION. 


The  pigment  or  melanotic  liver  is  that  form  of  hepatic  degeneration  in 
which  there  is  an  abnormal  deposit  in  the  liver  of  pigment  derived  from 
the  coloring  matter  of  the  blood.  In  pigmentation  there  must  be  prima- 
rily a  fault  in  the  circulation  or  in  the  blood-vessels  ;  usually  it  is  the  re- 
sult of  slowing  of  the  blood  curi'ent.  The  red  corpuscles  either  pass 
through  the  walls  entire,  or  liberate  the  haemoglobin,  which  then  transudes 
the  capillary  vessels.  The  blood  from 
the  spleen,  loaded  with  pigment, 
passes  into  the  portal  vein,  is  carried 
through  the  interlobular  veins,  then 
into  the  veins  just  within  the  periph- 
ery of  the  lobule.  Haamoglobin  re- 
maining in  the  portal  capillaries  soon 
breaks  up  into  haematoidin  and,  ac- 
cording to  some,  into  melanin,  though 
we  are  inclined  to-day  to  regard  me- 
lanin as  altered  haematoidin.  This 
haematoidin  is  first  yellowish,  later  it 
consists  either  of  brownish-black 
granules  or  crystals  of  an  intensely 
black  color.  Both  haematoidin  and 
melanin  remain  unaltered  when  once 
formed.  Pigmentation  of  the  liver 
is  confined  to  the  vascular  system. 
Extensive  capillary  stagnation  with 
a  large  amount  of  pigment  matter  oc- 
cluding the  vessels  gives  rise  to  atrophy  of  the  cellular  structure. 

Morbid  Anatomy. — The  liver  is  at  first  enlarged  from  congestion  and 
the  capsule  is  smooth  and  tense  ;  afterward  the  organ  becomes  smaller 
than  normal  and  atrophies,  its  color  being  much  deeper  than  in  the  ear- 
lier stage  and  its  edges  sharply  defined. 

On  section,  in  the  first  stage,  dark  blood  flows  from  the  congested  paren- 
chyma. If  the  cut  surface  presents  a  mottled  appearance  there  is  a  steel- 
gray  or  black  ring  around,  and  slightly  encroaching  on,  each  lobule,  shad- 
ing off  toward  the  central  vein.     In  congestion  of  the  liver  pigmentation 


Fig.  78. 
Pigmentary  Degeneration. 
Section  of  an  Hepatic   Lobule  frcnn  a  case  of  per- 
nicious fever. 

A.  Central  veifi  of  the  lobule. 

B.  Longitudinal  section  of  a  small  hepatic  duct. 

C.  Vessels  containing  small  pigment  grannies  in 
great  numbers.  The  pigmentation  in  this  case 
was  pretty  general  throughout  the  intralobular- 
capillaries.      x  250. 


376 


DISEASES   OF   THE   DIGESTIVE   SYSTEM. 


commences  about  the  central  yein,  and  gradually  diminishes  toward  the 
periphery  of  the  lobule.  If  the  surface  is  uniform  it  presents  a  color  which 
resembles  ''graphite,"  a  blackened  gray  color  having  a  slight  lustre,  and 
the  pigment  deposit  is  seen  to  have  reached  the  central  vein.  Occasionally 
spots  of  extravasation  are  found  scattered  throughout  the  organ.  On  sec- 
tion of  an  atrophied  "  pigment  livefr  "  the  whole  cut  surface  is  black,  and  all 
trace  of  the  lobules  is  frequently  lost.  A  micro scojncal  examination  shows 
the  capillaries,  not  only  portal  but  hepatic,  filled  with  granules  or  crystals, 
either  throughout  their  entire  extent  or  in  isolated  patches.     The  hepatic 

cells  contain  no  pigment,  but  are  filled 
with  oily  or  amyloid  material,  or  some- 
times with  dark-colored  bile.  Leucin 
has  often  been  found  in  the  parenchy- 
ma of  a  pigmented  liver.  In  an 
"atrophied"  liver,  the  lobules  and 
cells  are  shrunken,  and  the  capillary 
system  is  a  mass  of  pigment.  The 
spleen  is  softened  and  usually  enlarged, 
never  smaller  than  normal,  and  is 
more  extensively  pigmented  than  the 
liver.  In  some  cases  of  pigment  liver, 
there  are  evidences  of  hemorrhages 
into  the  various  serous  cavities.  In 
connection  with  pigment  degeneration 
of  the  liver,  pigmentation  may  occur 
in  all  the  organs  of  the  body. 

Etiology. — Malarial  infection  is  the 
only  known  cause  of  melanotic  liver, 
but  whether  a  large  amount  or  peculiar 
Tcind  of  malarial  poison  is  necessary  for  its  development  has  not  as  yet 
been  determined. 

Symptoms. — Frequently  those  who  have  had  extensive  pigment  deposits 
va.  all  the  organs  of  the  body,  have  given  during  life  no  symptoms  to  indi- 
cate their  presence.  The  first  efPectof  extensive  pigmentation  of  the  liver  is 
an  abnormal  secretion  of  bile.  The  liver  is  enlarged  and  tender  to  press- 
ure. The  skin  in  the  milder  forms  is  ash-colored,  and  in  severer  forms  it 
is  of  a  dark-bronze  hue.  There  may  be  slight  jaundice.  There  is  gastro- 
intestinal catarrh  with  nausea,  loss  of  appetite,  flatulence,  painful  tympa- 
nitis, vomiting,  and  diarrhoea  which  may  pass  into  dysentery.  In  severe 
cases,  hemorrhage  from  the  gastro-intestinal  mucous  membrane  and  from 
the  kidney  occurs,  attended  by  exacerbations  and  remissions  correspond- 
ing to  febrile  exacerbations  and  remissions.  There  is  I'apid  emaciation 
and  extreme  exhaustion  with  giddiness,  headache,  and  ringing  in  the  ears. 
Occasionally  the  vertigo  comes  on  so  suddenly  that  the  patient  falls  to  the 
ground  without  the  least  warning.  Active  delirium  is  often  followed  by 
profound  coma.  The  urine  and  fseces  are  passed  involuntarily  during  the 
period  of  stupor.     Coma  is  the  most  frequent  termination  of  the  cerebral 


c- 

Fig.  79. 

Pigment  Degeneration. 

Section  of  the  same  tissue  as  preceding  cut,  show- 
ing the  centime  of  a  lobule  more  highly  magnified. 
A.  Central  vein  of  the  lobule. 

B,  B.  Strongly  pigmented  capillaries. 

C,  C.  Hepatic  cells  infiltrated  with  fat.     x  450. 


CANCEE   OF   THE    LIVEE.  377 

variety  of  pigment  liver.  In  severe  cases  which  terminate  in  recovery  there 
is  often  temporary  loss  of  memory. 

Physical  Signs. — Inspection  shows  the  ashy-gray,  jaundiced,  or  brown 
colored  skin. 

Palpation. — The  surface  of  the  liver  is  smooth,  and  in  the  first  stage  the 
organ  is  larger,  softer,  and  more  tender  than  normal.  In  the  second  stage 
it  is  small  and  hard. 

Percussimi. — In  the  early  stage  the  area  of  hepatic  dulness  is  increased; 
in  the  later  stage  it  is  uniformly  diminished. 

Differential  Diagnosis. — The  liability  of  confounding  pigment  degenera- 
tion with  other  diseases  of  the  liver  is  not  so  great  as  is  the  difficulty  of 
recognizing  its  existence.  If,  in  intense  malarial  infection,  cerebral  or 
urinary  symptoms  come  on  suddenly  with  hemorrhages  from  the  mucous 
surfaces,  a  bronzed  hue  of  the  skin,  and  the  physical  changes  in  the  size  of 
the  liver  already  referred  to,  pigmentation  of  the  liver  may  be  suspected  ; 
and  if,  in  addition  to  these,  pigment  matter  is  found  in  the  blood,  the 
diagnosis  will  be  established. 

Prognosis. — The  prognosis  is  favorable  if  the  patient  can  be  removed 
from  the  source  of  malarial  infection.  The  elements  which  render  the 
prognosis  unfavorable  are  severe  cerebral  and  renal  symptoms  combined 
with  signs  of  extensive  portal  obstruction.  Death  may  occur  from  exhaus- 
tion due  to  the  diarrhoea,  dysentery,  or  intestinal  hemorrhage. 

Treatment. — The  preventive  treatment  corresponds  to  the  preventive 
treatment  of  malarial  fever.  When  the  disease  is  once  established,  the 
chief  indication  is  to  administer  large  doses  of  quinine.  The  symptoms  in 
all  varieties  of  the  disease  remit  as  soon  as  the  individual  is  brought  fully 
under  the  influence  of  this  drug.  Purges  act  unfavorably.  If  the  cere- 
bral symptoms  are  urgent,  ammonia  may  be  combined  with  quinine. 
Preparations  of  iron  and  a  change  of  residence  to  a  non-malarial  district 
are  essential  to  its  successful  management.  The  diet  should  be  of  the  most 
nutritious  character  and  non-stimulating. 

CAlSrCER  OF   THE   LIVEE. 

Cancer  of  the  liver  may  be  either  primary  or  secondary.  It  is  secondary 
to  cancer  of  the  stomach  in  one-half  of  the  cases.  It  has  been  estimated 
that  one  out  of  every  one  hundred  persons  has  cancer  of  the  liver.  The 
varieties  of  cancer  met  with  in  the  liver  are  scirrhus,  medullary,  melanotic, 
and  colloid  cancer.  Infiltrated  cancer  without  any  change  whatever  in  the 
form  of  the  organ  has  been  found. 

Scirrhus  is  usually  primary,  while  medullary  is  almost  always  second- 
ary. Scirrhus  makes  its  appearance  first  as  rounded  masses.  These  masses 
increase  rapidly  and  soon  attain  their  full  size,  which  varies  from  that  of  a  pea 
to  that  of  an  orange  ;  they  then  remain  stationary  for  a  time  until  the  fibrous 
tissue  contracts.  The  number  of  these  nodules  varies  inversely  with  their 
size.  Scirrhus  developments  usually  commence  in  the  interlobular  spaces 
and  gradually  extend  toward  the  centre  of  the  lobule.     As  the  liver-cells 


378  DISEASES   OF   THE   DIGESTIVE   SYSTEM. 

are  being  crowded  upon,  the  portal  capillaries  disappear,  while  the  hepatic 
vessels  enlarge  and  ramify  in  the  cancerous  mass  as  a  new  and  peculiar 
vascular  net-work.  The  neighboring  lymphatic  glands  may  also  become 
infiltrated  with  cancer,  and  often  exert  sufficient  pressure  upon  the  bile- 
ducts  to  obstruct  the  outflow  of  the  bile.  The  cancerous  growth  sometimes 
involves  the  walls  of  the  portal  vein,  and,  extending  in  the  direction  of  the 
capillary  terminations,  fills  up  their  channel.  The  bile-ducts  also  may  be 
obstructed,  distended,  or  ruptured.  With  these  changes,  the  centre  of  the 
cancer-nodule  becomes  harder  and  harder  ;  or  by  shutting  off  its  own 
nutrition,  the  interior  of  the  nodule  becomes  fatty,  while  the  periphery  is 
soft  and  vascular.  The  obliteration  of  the  capillaries  at  the  exterior  of  the 
mass  shuts  off  the  nutrition  of  the  adjacent  liver-cells,  and  this  induces 
fatty  degeneration.  The  theory  of  the  development  of  medullary  cancer 
(the  implantation  theory,  as  it  is  called)  is  that  cancer-cells  pass  through 
the  lymphatics,  or  blood-vessels,  and  reaching  the  interlobular  spaces 
become  the  starting  points  of  the  cancer  development.  This  theory  has 
received  much  attention,  and  experiments  seem  to  warrant  our  adopting  it 
as  one  method,  at  least,  in  which  cancer  may  develop. 

Medtdlary  cancer  is  simply  a  modification  of  scirrhus.  Rapidity  of  de- 
velopment is  the  distinguishing  pathological  difference, — the  line  between 
the  two  forms  often  being  arbitrarily  drawn,  for  scirrhus  may  pass  into 
medullary,  and  vice  versa. 

Melanotic  cancer  of  the  liver  is  also  of  rapid  growth.  The  nodules, 
though  very  numerous,  are  small  in  size.  The  cancer-cells  have  a  deposit 
at  their  centre  of  yellow,  brown  or  blackish  pigment,  the  "  granite  "  look- 
ing spot  shading  off  toward  the  periphery.  Its  course  is  the  same  as  in 
other  varieties  of  hepatic  cancer. 

Colloid  cancer  is  of  rare  occurrence  in  the  liver,  appearing  only  as  a 
degenerated  form  of  scirrhus  or  medullary  cancer.  If  either  of  these  forms 
undergoes  mucoid  or  colloid  degeneration,  a  gelatinous,  gray,  tenacious 
fluid  takes  the  place  of  the  cancer-juice,  while  the  fibrous  framework  be- 
comes more  distinctly  alveolar.  Melanotic  sarcoma  has  been  found ;  it 
often  pursues  as  malignant  a  course  as  true  carcinoma. 

Morbid  Anatomy. — In  scirrhus  cancer  the  liver  is  increased  in  si^e, 
the  right  lobe  being  usually  most  affected.  Sometimes  it  is  so  much  en- 
larged as  to  fill  the  abdominal  cavity.  In  color  it  is  darker  than  normal, 
and  it  is  increased  in  weight,  sometimes  reaching  twenty  pounds.  Upon 
its  surface  are  nodules,  hard,  elastic,  rarely  fluctuating,  and  umbilicated  at 
their  centres.  Occasionally,  there  are  no  nodules  on  the  surface,  the  can- 
cerous developments  being  confined  to  the  interior  of  the  organ.  The  cap- 
sule of  the  liver  is  thickened  and  sometimes  the  seat  of  cancerous  develop- 
ment. Adhesions  connecting  it  to  the  adjacent  parts  are  the  result  of 
intercurrent  local  peritonitis. 

On  section,  if  the  degeneration  is  advanced,  the  liver  cuts  hard,  and 
creaks  like  cartilage  under  the  knife.  The  cut  surface  is  seen  studded  with 
nodules,  the  diameters  of  which  vary  from  one-eighth  of  an  inch  to  four 
inches.     Between  the  nodules  the  liver- tissue  is  sometimes  congested,  and 


CAKCER   OF   THE   LIVEE. 


379 


of  a  dark  red  color,  or  it  is  atrophied.  The  nodules  increase  in  density  from 
their  centre  outward,  or  have  a  central  cavity  filled  with  fatty  granules. 
On  pressing  them,  more  or  less  cancer-juice  exudes  according  to  the  density 
of  the  tumor.  The  color  of  the  tumor  varies  from  a  glistening  dirty  white 
to  a  deep  red,  according  as  the  vascular  net-work  is  meagre  or  abundant. 
If  there  has  been  obstruction  to  the  bile  ducts  the  parenchyma  will  be  of  a 
bright  yellow  color.  Evidences  of  extravasation  from  distended  vessels  may 
be  found  throughout  the  liver-tissue  and  often  in  the  interior  of  the  can- 
cerous growth. 

Under  the  microscope,  a  cancer  nodule  will  be  found  to  consist  of  a  fibrous 
framework  or  '*  stroma  "  in  which  are  cancer-cells  and  cancer-juice.     In 


Pig.  80. 

Cancer  of  the  Liver. 

Section  showing  part  of  a  canceroiis  nodule  with  the  contiguous  hepatic  tissue. 

A .  Connective-tissue  of  a  portal  canal  in  which  the  nodule  was  developed. 

B.  Hepatic  duct  in  lakgitudinal  section. 

C.  Hepatic  artery. 

D.  Stroma  of  cancer. 

E.  Alveoli  of  the  same  filled  with  "  cancer. cells.  " 

F.  Empty  alveoli. 

G.  Periphery  of  an  hepatic  lobule  hordenng  on  the  career,  infiltrated  at  HH. 
I.   Infltratian  of  connective-tissue  with  same,     x  300. 

scirrhus  the  fibrous  stroma  is  greatly  in  excess  of  the  other  elements.  The 
cancer-juice  contains  a  large  amount  of  fine  granular  matter,  nucleated 
cells  and  distinct  free  nuclei.  The  cells  are  of  large  size  and  irregular, 
and  the  nuclei  and  nucleoli  are  often  multiple  and  very  distinct.  The 
walls  of  the  capillary  vessels  in  the  tumor  are  thin,  and  their  calibre  large. 
A  ring  of  liver  cells  at  the  margin  of  the  cancer-nodule  exhibits  well- 
marked  degeneration. 


380  DISEASES   OE   THE    DIGESTIVE    SYSTEM. 

Medullary  Cancer. — The  gross  appearances  of  the  liver  are  the  same 
as  in  soirrhus,  except  that  the  nodules  are  fewer  and  larger.  They  are 
very  soft  and  fluctuating,  and  frequently  the  more  advanced  tumors 
have  ruptured  through  the  peritoneal  envelope  of  the  liver.  In  this 
variety  the  cancer  nodules  are  often  lobulated.  Those  which  occupy  the 
surface  of  tlie  liver  project  as  large  irregular  tumors. 

On  section  large  nodular  masses  of  curdy-white  homogeneous  matter  re- 
sembling foetal  brain-substance  are  found  scattered  throughout  the  liver- 
tissue.  Between  the  cancer  nodules  the  liver  substance  is  more  or  less  in- 
tensely congested.  Dark  red  hemorrhagic  spots  are  seen  scattered  over  its 
cut  surface. 

On  a  microscopic  examination  a  small  amount  of  fibrous  stroma  is  found 
containing  a  very  large  number  of  cells.  The  cells  are  much  larger  than 
in  scirrhus,  though  the  same  in  kind,  and  they  are  the  seat  of  more  fatty 
degeneration. 

Melanotic  Cancer. — In  common  with  the  morbid  appearance  of  all  can- 
cerous developments,  we  find,  besides,  that  the  liver  is  nodular  and  very 
dark. 

On  section  the  surface  presents  a  peculiar  mottled  appearance  resembling 
granite,  and  there  are  numerous  small  nodules  studding  the  whole  gland. 
On  pressure  a  dark  fluid  flows  from  the  cancerous  mass,  varying  in  color 
from  a  gray-brown  to  a  deep  black. 

A  microscopical  examination  shows  a  stroma  varying  in  amount  and 
color.  Sometimes  it  is  colorless,  sometimes  very  dark.  The  degree  of 
vascularity  has  wide  ranges ;  the  cells  at  certain  spots  in  the  liver  often  dis- 
appear and  only  a  peculiar  pigment  color  remains. 

Colloid  Degeneration. — The  surface  of  the  liver  in  this  form  of  cancer 
differs  from  the  other  varieties  in  that  it  is  smooth  with  large  lobulations. 

Under  the  microscope  the  cancerous  mass  is  made  up  of  large  and  spherical 
alveoli  with  thin  walls.  The  alveoli  contain  mucoid  or  colloid  matter, 
with  fatty  material  and  a  few  epithelial  cells. 

Etiology. — The  causation  of  primary  hepatic  cancer  is  unknown  ;  in 
most  instances  there  exists  an  hereditary  predisposition.  It  is  a  disease  of 
middle  life,  occurring  oftenest  between  the  ages  of  forty  and  sixty-five. 
Medullary  cancer  of  the  liver,  especially  when  secondary,  is  sometimes  met 
■with  in  early  life,  even  as  early  as  the  fourth  year.  It  occurs  equally  among 
males  and  females.  Some  have  dated  its  development  from  some  great 
mental  emotion  or  strain,  others  from  the  receipt  of  a  blow  upon  the  right 
hypochondrium.  Cancer  of  the  liver  is  often  secondary  to  cancer  of  the 
stomach,  mamma,  ovary,  uterus,  pancreas,  brain,  or  portal  vein.  Clinical 
exp3rience  indicates  that  extirpation  of  external  cancerous  masses  is  very 
apt  to  be  followed  by  cancer  of  the  liver. 

Symptoms, — The  early  symptoms  of  hepatic  cancer  are  obscure.  The 
more  superficial  its  development,  the  more  marked  are  the  symptoms  and 
the  easier  the  diagnosis.  It  will  be  noticed  that  the  individual  is  gradually 
losing  flesh  and  strength,  he  complains  of  a  sense  of  weight  and  fullness  in 
the  right  hypochondrium,  he  is  anaemic,  and  the  surface  assumes  a  doughy 


CANCER   OF   THE   LIVER. 


381 


hue ;  with  these  there  may  be  pain  localized  over  the  hepatic  region,  or 
shooting  up  toward  the  right  shoulder,  and  sometimes  to  the  back.  The 
pain  soon  becomes  lancinating  in  character,  and  is  localized  at  some  point 
over  the  liver  which  is  tender  to  pressure.  There  is  loss  of  appetite,  flatu- 
lence, nausea,  vomiting,  and  constipation  alternating  with  diarrhoea.  Tlie 
vomiting  is  often  profuse  and  persistent.  There  is  progressive  emaciation, 
and  the  skin  assumes  an  earthy  pallor.  Jaundice  is  present  in  one-half  of 
the  cases,  and  is  due  either  to  compression  of  the  bile  ducts  or  to  intercur- 
rent catarrh  of  the  ducts,  and  when  once  developed  it  is  permanent.  Asci- 
tes occurs  more  frequently  than  jaundice  ;  the  accumulation  at  first  is  in- 
considerable in  amount  and  increases  slowly.  It  is  due  to  compression  of 
the  portal  vein  by  the  cancerous  tumor  or  by  enlarged  glands  in  the  trans- 
verse fissure,  or  to  chronic  peritonitis.  (Edema  of  the  feet  comes  on  late. 
The  temperature  is  normal  or  sub-normaL  Dyspnoea  may  become  an 
urgent  symptom  in  the  advanced  stage  of  hepatic  cancer.  The  cervical 
and  inguinal  glands  may  be  enlarged.  Hemorrhages  from  the  stomach, 
intestines,  mouth,  and  vagina,  with  petechial  and  ecchymotic  spots,  are 
sometimes  accompaniments  of  hepatic  cancer.  It  is  to  be  remembered  that 
hepatic  cancer  may  run  its  entire  course  without  pain,  without  jaundice 
and  without  ascites.  In  medullary  cancer,  loss  of  flesh  and  the  peculiar 
cancer  countenance  may  not  appear  until  the  end  of  the  case.  The  fseces 
are  normal  at  first,  later  they  are  firm  and  clay-colored.  The  fluid  stools 
of  cancer  diarrhoea  contain  no  bile.  The  urine  is  scanty  and  high-colored. 
Deposits  of  lithates  and  of  bile  pigment  are  rarely  absent. 

Physical  Signs. — Inspection.     There  may  be  a  perceptible  bulging  in  the 
right  hypochondrium  and  the  outlines 
of  large  nodules  may  be  visible. 

Palpation  discloses  an  enlarged  and 
irregularly  shaped  liver,  tender  to 
pressure.  Hard,  smooth  nodules  are 
felt  over  its  surface,  which  rarely 
fluctuate.  If  the  nodules  are  um- 
bilicated  it  establishes  the  diagnosis 
of  cancer.  In  colloid  cancer  of  the 
liver,  and  when  the  cancerous  devel- 
opment is  central,  no  nodules  will  be 
felt. 

Percussion. — The  area  of  hepatic 
dulness  is  irregularly  increased  and 
marked  by  an  irregular  line  of  flatness 
below  the  free  border  of  the  ribs. 

Auscultation. — A  friction  sound, 
caused  by  the  rubbing  of  the  rough- 
ened peritoneal  surfaces,  is  sometimes 
heard. 

Differential  Diagnosis.  —  Cancer  of 
the  liver  may  be  mistaken  for  hydatids 


Fig.  81. 

Diagram  sh(nvi?7ff  enlargements  of  the  Liver  as 
determined  by  percussion. 

A,  A.  Line  of  diaphrag7n. 

B,  B.  Lower  border  of  costal  cartilages. 

C.  Dotted  tine  enlargpnent  upivard. 

D.  Shaded  area  indicating  successive  and  in- 

creasing enlargements. 
IS.  Lower  edge  of  Liver  in   Cancer,  Leukamia 
and  Adenoma. 


382  DISEASES    OF   THE    DIGESTIVE    SYSTEM. 

of  the  liver,  abscess  of  the  liver,  luaxy  degeneration  with  gummata,  cancer 
of  the  stomach,  and  an  enlarged  gall-hladder. 

In  hydatids  there  are  no  gastric  or  severe  constitutional  symptoms. 
Cancer  of  the  liver  is  rapid  in  its  development,  rarely  exceeding  one  year 
in  duration,  while  hydatids  are  of  slow  growth,  lasting  from  four  to  eight 
years.  Gastro-intestinal  hemorrhages  are  common  in  cancer,  and  do  not 
occur  in  hydatids.  Pain  is  a  prominent  symptom  in  cancer ;  hydatid 
tumors  are  painless.  In  cancer  the  nodules  are  hard,  tender,  and  firm  ; 
hydatid  tumors  are  large,  soft,  smooth  and  elastic,  and  can  be  freely  manip- 
ulated without  pain.  The  peculiar  hydatid  fremitus  is  sometimes  obtained 
by  percussing  a  hydatid  tumor.  In  hydatids  (with  an  exploring  trochar)  a 
saline  fluid  containing  the  booklets  of  the  echinococci  may  be  withdrawn, 
which  will  decide  the  diagnosis. 

In  waxy  degeneration  of  the  liver,  there  is  a  history  of  syphilis,  pro- 
longed suppuration,  or  disease  of  bone  ;  and  in  cancer  an  hereditary  cancerous 
history,  or  the  evidences  of  carcinoma  elsewhere.  The  progress  of  waxy  liver 
is  slow;  that  of  cancer  is  rapid.  A  waxy  liver  is  painless,  while  pain  in 
cancer  is  constant.  In  waxy  liver  the  spleen  is  markedly  enlarged ;  in  cancer 
it  is  normal  in  size,  unless  it  is  the  seat  of  cancer  infiltration.  Jaundice  and 
ascites  are  rare  in  waxy  degeneration,  and  frequent  in  cancer. 

In  cancer  of  the  stomach  gastric  symptoms  are  urgent  and  appear 
much  earlier  than  in  cancer  of  the  liver.  In  cancer  of  the  stomach  there 
is  usually  coSee-ground  vomiting  and  cancer-cells  in  the  ejected  matter. 
In  cancer  of  the  stomach  the  pain  and  gastric  symptoms  are  aggravated 
after  ingestion  of  food,  while  in  hepatic  cancer  the  pain  and  gastric  symp- 
toms are  constant.  In  cancer  of  the  liver  in  thin  subjects,  immovable 
nodulated  tumors  may  be  felt  by  pressing  up  under  the  ribs ;  while  in 
gastric  cancer  a  single  tumor  which  is  movable,  and  changes  its  posi- 
tion as  the  stomach  is  full  or  empty,  is  usually  felt.  In  hepatic  cancer 
there  is  absolute  dulness  over  the  tumor ;  while  in  cancer  of  the  stomach 
the  percussion  note  has  a  peculiar  tympanitic  quality. 

Cancer  of  the  right  hidney,  impaction  of  fceces,  and  various  alterations 
in  the  size  of  the  healthy  liver  will  not  long  confuse  one  if  the  symptoms 
and  physical  signs  are  carefully  analyzed. 

Prognosis. — Cancer  of  the  liver  is  a  fatal  disease.  The  average  duration 
is  about  one  year.  Medullary  cancer  runs  its  course  in  from  two  weeks  to 
four  months.  The  duration  of  all  varieties  will  be  influenced  by  the  pres- 
ence or  absence  of  complications.  Death  may  result  from  exhaustion, 
from  the  cancerous  cachexia,  dropsy,  diarrhoea,  dysentery  and  hemorrhages, 
or  from  peritonitis,  pneumonia  or  pulmonary  cedema. 

Treatment. — All  varieties  of  cancer  of  the  liver  are  incurable,  hence  the 
absurdity  of  all  the  so  called  curative  measures.  The  diet  should  be  nu- 
tritious, and  care  should  be  exercised  not  to  overfeed  this  class  of  patients. 
Easily  assimilated  preparations  of  iron  are  often  of  service.  Diarrhoea,  if 
present,  may  be  checked  by  such  remedies  as  gallic  acid,  lead,  and  opium. 
The  operation  of  paracentesis  should  be  delayed  as  long  as  possible.  In 
the  advanced  stage  of  the  disease  alcoholic  stimulants  are  often  necessary 


GWJMMY   TUMOE   OF   THE    LIVER.  3b3 

and  beneficial.  In  the  great  majority  of  cases  tlie  principal  ofiice  of  the 
physician  is  to  relieve  pain,  and  morphia  is  our  most  reliable  remedy  for 
this  purpose  ;  it  should  be  given  in  sufficient  quantities  to  keep  the  patient 
comfortable . 

GUMMY    TUMOR    OF   THE    LIVER. 

This  form  of  new  growth  is  perhaps  the  most  characteristic  lesion  of  con- 
stitutional syphilis.  Some  writers  group  these  tumors  under  the  head  of 
syphilitic  disease  of  the  liver.  Those  forms  of  perihepatitis,  cirrhosis,  and 
amyloid  degeneration  which  are  of  evident  syphilitic  origin,  I  have  preferred 
to  describe  in  connection  with  the  other  corresponding  forms,  giving  at  the 
same  time  the  few  differences  due  to  the  syphilitic  causation. 

Morbid  Anatomy. — The  syphilitic  nodules,  gummy  tumors,  or  " gum- 
mata  "  appear  first  as  small  masses  of  reddish-gray,  pulpy,  vascular  tissue, 
scattered  throughout  the  liver.  Their  point  of  origin  I  believe  to  be  the 
wall  of  the  capillaries, — the  cells  and  nuclei  of  the  "  syphiloma"  being  due 
to  the  growth  of  the  nuclei  of  the  capillaries.  The  mass  is  composed  of 
highly  organized  granulation-tissue,  and  is  usually  spherical  in  shape.  The 
liver  may  be  enlarged,  or  may  retain  its  normal  size,  according  to  the  ex- 
tent of  the  waxy  change  which  usually  accompanies  the  development  of 
the  gummata.  Diminution  of  its  size  is  due  to  perihepatitis  causing  re- 
traction. Under  these  circumstances  the  organ  is  lobulated,  and  deep, 
whitish  furrows  indent  it,  the  result  of  cicatricial  contractions.  Fibroid 
nodules  occasionally  lie  in  these  cicatrices.  The  bulgings  are  soft  and  smooth 
to  the  touch.  The  capsule  is  firm  and  opaque,  and  the  seat  of  fibroid  thick- 
ening, and  is  frequently  bound  to  surrounding  parts  by  adhesions. 

On  section  there  will  be  found  scattered  through  the  liver  rounded 
masses  varying  in  size  from  a  pea  to  an  orange,  yellowish-white  in  color, 
either  surrounded  by  congested  parenchyma,  or  as  isolated  spots  in  the 
midst  of  an  infiltrated  homogeneous  grayish-red  mass.  They  may  be  en- 
capsulated, a  layer  of  translucent  fibrous-tissue  surrounding  them  and 
shading  off  imperceptibly  into  the  surrounding  liver-tissue.  Brown  spots 
in  the  tumors  correspond  to  obstructed  bile-ducts.  The  liver  parenchyma, 
between  the  nodules,  undergoes  various  changes  :  at  one  time  it  is  con- 
gested and  hypertrophied,  at  another  it  is  atrophied  and  undergoes  fatty 
degeneration.  In  well-marked  cases  there  are  two  zones,  an  outer,  red  and 
fleshy,  and  an  inner,  dry,  grayish  and  firm.  Again,  nothing  may  remain 
of  a  previous  gumma  but  a  shrivelled  cicatrix. 

A  microscopical  examination  of  a  fully  developed  gummy  tumor  reveals 
three  jorocesses  -.—first,  at  the  periphery,  there  is  a  vascular  mass  of  gran- 
ulation-tissue, embedded  in  which  are  cells  bearing  a  striking  resem- 
blance to  white  blood  globules,  and  some  larger  nucleated  ones.  Sec- 
ondly, just  beneath  this  zone  is  found  a  fibro-nucleated  mass,  the  fibril- 
lations being  very  dense  and  cicatricial.  Thirdly,  in  the  centre  of  the  mass 
are  found  fat-granules  and  broken-down  cells,  with  occasional  traces  of 
cholesterin,  and  sometimes  faint  evidences  of  fibrillar  tissue.  Cheesy  and 
calcareous  masses  are  also  sometimes  found  in  the  centre  of  the  gumma. 


384  DISEASES    OF   THE    DIGESTIVE   SYSTEM. 

Etiology. — As  has  been  stated,  gummata  are  the  most  characteristic  of 
the  lesions  of  internal  syphilis.  They  are  met  with  under  no  other  condi- 
tions. 

Symptoms. — The  subjective  symptoms  of  hepatic  gummata  are  few  and 
inconstant.  At  a  post-mortem,  a  liver  may  be  found  studded  with  gummy 
tumors,  when  no  symptoms  referable  to  the  liver  were  present  during  life. 
There  is  generally  a  history  of  increasing  debility,  and  a  feeling  of  press- 
ure, tightness,  and  dull  pain  in  the  region  of  the  liver.  Sometimes  the  pain 
is  severe  and  localized,  at  other  times  it  is  dull  and  diffused  over  the  whole 
hepatic  region.  The  pain  in  one  case  is  constant,  in  another  intermittent. 
If  jaundice  exists,  it  is  due  to  the  pressure  either  of  the  gummata  or  of  an 
enlarged  lymphatic.  The  temperature  is  normal,  and  the  pulse-rate  is  but 
slightly  increased.  Ascites  may  result  from  pressure  on  the  portal  vein,  or 
from  chronic  peritonitis,  which  oftea  complicates  its  development.  Both 
jaundice  and  ascites  are  not  present  until  the  liver  has  become  very  much 
enlarged.  The  symptoms  which  are  present  in  the  advanced  stage  of  this 
disease,  such  as  diarrhoea,  loss  of  appetite,  vomiting,  hemorrhoids,  gastric 
and  intestinal  hemorrhage,  are  due  rather  to  the  accompanying  hepatic  de- 
generation than  to  the  gummata. 

Physical  Signs. — Palpation  may  show  the  liver  to  be  enlarged  or  normal 
in  size  ;  a  moderate  increase  in  size  is  the  rule.  The  organ  has  smooth 
lobules  upon  its  surface  between  which  run  deep  fissures.  The  lobulations 
are  soft  and  elastic,  never  fluctuating. 

Percussion. — The  area  of  dulness  is  increased  and  its  outline  is  irregular 
below  the  free  border  of  the  ribs.  The  area  of  spleen-dulness  in  the  ma- 
jority of  cases  is  slightly  increased. 

Differential  Diagnosis. — Gummata  of  the  liver  may  be  mistaken  for  can- 
cer, and  if  the  liver  is  diminished  in  size,  for  syphilitic  cirrhosis.  The 
differential  diagnosis  of  both  has  been  considered. 

Prognosis. — Gummata  of  the  liver  rarely  directly  destroy  life.  The  prog- 
nosis is  unfavorable  when  ascites,  gastro-intestinal  hemorrhage,  persist- 
ent diarrhoea,  or  a  marked  cachexia  exists.  Complicating  diseases  also  influ- 
ence the  prognosis  ;  amyloid  degeneration  of  the  spleen  and  kidneys  is  a  bad 
complication.  The  most  frequent  intercurrent  lung  diseases  are  pleurisy, 
pneumonia,  pulmonary  oedema,  and  chronic  bronchitis.  Death  occurs  from 
exhaustion  due  to  the  syphilitic  marasmus,  from  diarrhoea,  dysentery,  and 
dropsy.  Pneumonia  and  pulmonary  oedema  often  cause  it,  and  sometimes 
cholsemia,  with  its  peculiar  symptoms,  ends  in  coma  and  death. 

Treatment. — The  treatment  of  this  afl'ection  resolves  itself  into  the  treat- 
ment of  syphilis.  As  it  is  a  tertiary  symptom,  our  main  reliance  is  on  large 
doses  of  the  iodide  of  potassium  combined  with  mercurial  inunctions.  With 
these  iron  and  cod-liver  oil  should  be  constantly  taken,  and  the  patient 
should  be  placed  under  the  best  hygiene.  The  diet  should  be  nutritious 
and  non-stimulating.  Opium  combined  with  nitric  acid  will  always  con- 
trol the  diarrhoea  if  it  becomes  exhausting. 


HYDATIDS   OF   THE    LIVEB.  385 


HYDATIDS    OF   THE    LIVER. 


Hydatid  tumors  are  cysts  due  to  the  development  in  the  liver  of  the  em- 
bryos of  the  tcenia  ecMnococcus  ;  these  embryos  are  called  "echinococci," 
their  development  ''  hydatids"  ;  they  are  usually  single,  and  for  more  than 
two  or  three  to  be  present  in  the  same  liver  is  a  phenomenal  event. 

Morbid  Anatomy. — An  ovum  of  taenia  echinococcus,  either  during  masti- 
cation or  from  the  action  of  the  digestive  juices,  has  the  envelope  containing 
the  echinococcus  removed,  and  then  by  its  booklets  it  bores  its  way  from 
the  stomach  or  intestine  into  the  liver.  It  there  becomes  encysted:  the 
cyst  consists  of  an  external  laminated  cuticular  layer  and  an  internal  par- 
enchymatous lining.  From  the  internal  layer  numerous  little  heads  bud 
forth  in  the  form  of  vesicles,  and  these,  the  '^  daughter  vesicles,"  in  turn 
bear  a  second  crop,  the  "  grand-daugh- 
ter cells,"  the  mother-sac  meanwhile 
enlarging,  partly  from  the  increase  in  the 
number  of  the  vesicles,  and  partly  from 
its  own  secretion,  which  is  clear  and  wa- 
tery. As  these  successive  generations  of 
vesicles  appear,  broods  of  immature  tae- 
nia C'scolices  ")  in  the  form  of  a  gray- 
ish granular  layer,  are  developed  first 
upon  the  internal  surface  of  the  mother 
sac  and  then  upon  that  of  the  other 
cysts,  in  the  order  of  age.  While  the 
younger  vesicles  cling  to  the  parent- 
walls,  the  larger  and  older  ones  become 

,  ,  ,  Ti^ir    82 

detached,   and  float  m  the  mterior  of  '    " 

, ,  I  •  11  1         •  ;  Sketch  from  an  Hydatid  Tumor  showing  the  tntd- 

the    continually  enlargmg    parent-sac.  ding  vesicles. 

Proliferation  of  connective-tissue  upon  the  exterior  of  the  sac  resulting 
from  the  inflammatory  process  excited  by  the  pressure  of  a  foreign  body, 
develops  a  fibrous  capsule  closely  connected  with  the  adjacent  liver  par- 
enchyma ;  this  is  supplied  with  blood  by  the  hepatic  and  portal  capilla- 
ries. 

During  its  enlargement  the  hydatid  tumor  loses  its  spherical  shape  and 
becomes  indented.  As  it  increases  in  size,  the  fibrous  capsule  becomes 
thickened,  rough  and  cartilaginous  ;  sometimes  it  undergoes  ossification. 
The  echinococci  may  be  destroyed  by  the  bile  which  enters  the  cysts  when 
the  bile-ducts  are  opened,  or  by  the  inflammation  which  is  established  be- 
tween the  connective  tissue  capsule  and  the  wall  of  the  true  sac,  causing 
a  grayish  oily  material  of  variable  consistence  to  be  developed.  The  clear 
fluid  in  the  cavity  of  the  hydatid  becomes  cloudy,  then  opaque,  while  all 
traces  of  the  vesicles  disappear,  and  at  last  only  a  few  booklets  of  the  echi- 
nococci remain.  This  is  a  process  of  fatty  degeneration.  Sometimes 
the  formation  of  vesicles  is  so  rapid  that  their  number  is  beyond  all  pro- 
portion to  the  fluid,  and  then  they  die  and  collapse,  undergoing  no  degen- 
35 


386  DISEASES   OF   THE   DIGESTIVE   SYSTEM. 

erative  process  ;  again,  when  neither  of  these  terminations  is  reached,  tha 
hydatid  tumor  may  continue  to  increase  in  size  until  finally  it  bursts  into 
the  adjacent  cavities. 

The  most  frequent  rupture  is  into  the  right  pleural  cavity.  The  hyda- 
tid tumor,  by  its  pressure  upon  the  diaphragm,  causes  it  to  become  thin, 
and  to  rise  upward,  sometimes  as  high  as  the  second  rib.  Finally  the 
diaphragm  ruptures  and  the  sac  is  discharged  into  the  pleural  cavity,  or 
when  the  pleural  surfaces  become  adherent  the  tumor  ruptures  into  the 
lung-tissue  or  bronchi.  These  tumors  sometimes  rupture  into  the  perito- 
neal cavity,  and  peritonitis  results,  or  the  stomach  or  intestinal  canal  may 
communicate  by  a  small  aperture  with  the  hydatid  sac.  A  communication 
is  sometimes  established  between  the  bile-ducts  and  the  hydatid  tumor,  and 
the  ducts  become  filled  with  the  contents  of  the  hydatid  mass  ;  the  ductus 
communis  may  become  obstructed  by  a  large  hydatid  vesicle.  Another 
mode  of  termination  is  by  an  intense  inflammatory  action,  causing  sup- 
puration of  the  liver-tissue  in  the  vicinity  of  a  ruptured  hydatid  tumor, 
which  consequently  is  filled  with  coagulated  blood  and  pus  ;  more  rarely 
a  gangrenous  process  may  be  established  in  it. 

The  liver  is  irregularly  enlarged  and  displaced.  The  increase  in  size 
varies  with  that  of  the  projecting  cysts,  which  are  sometimes  large  enough 
to  fill  the  abdominal,  and  a  portion  of  the  thoracic,  cavity.  The  bulging 
is  globular  if  the  cyst  is  simple  and  is  situated  in  the  right  lobe  of  the 
liver.  The  tumor  is  elastic  and  often  fluctuating.  A  uniform  enlarge- 
ment of  the  liver  results  from  a  centrally  located  hydatid.  The  capsule 
covering  the  cyst  is  thickened,  and  adhesions  often  bind  the  liver  to  the 
surrounding  parts. 

071  sectio7i,  the  liver-tissue  in  the  vicinity  of  the  tumor  is  found  com- 
pressed and  atrophied,  or  congested  and  hypertrophied.  The  mother-sac  is 
commonly  the  size  of  a  foetal  head.  The  true  cyst  wall  is  a  gelatinous,  whitish, 
semi-transparent  membrane,  containing  the  hydatid  fluid,  floating  in  which 
are  vesicles  from  the  size  of  a  millet-seed  to  that  of  an  egg,  and  varying 
in  number  from  hundreds  to  thousands.  On  the  inner  walls  of  the  larger 
ones,  and  on  that  of  the  parent-sac,  are  younger  vesicles  about  the  size  of  a 
pin's  head.  On  the  inner  side  of  the  sac  are  also  found  patches  of  white 
granular  matter.  The  cysts  may  be  found  filled  with  atrophied  and  shriv- 
elled vesicles  embedded  in  a  debris  consisting  of  fat-granules,  cholesterin, 
haemaglobin,  and  bile.  Its  consistency  varies  :  sometimes  it  is  liquid  and 
watery,  then  semi-fluid,  gelatinous,  or  like  a  thick  paste ;  at  other  times 
only  a  few  booklets  remain  in  this  gray,  putty-like  mass.  The  cyst  may 
contain  blood  or  pus. 

A  microscopical  examination  shows  the  sac  of  the  hydatid  to  be  a  gela- 
tinous mass  made  up  of  concentric  hyaline  lamellas.  The  scolices  are  from 
1-75  to  1-225  of  an  inch  in  length  ;  the  head  is  furnished  with  four  suckers 
and  a  proboscis,  about  which  are  sicMe-sliapecl  liooklets  in  number  from 
twenty-five  to  fifty.  The  body  is  striped  longitudinally  and  transversely, 
and  has  a  groove  between  it  and  the  head,  which  latter,  being  usually  re- 
tracted into    the  body,  causes  the  animal  to  look  somewhat  like  an  in- 


HYDATIDS   OF   THE    LIVES. 


387 


dented   rubber  ball,   the    hooks  fringing  the   depression. 

clear  or  slightly  opalescent,  it  has  a 

specific  gi'avity  of  1010  to  1015,  is 

usually  neutral   in  reaction,  and  is 

non-albuminous.     It  is  chiefly  water 

containing  chloride  of  sodium. 

Etiology. — The  essential  cause  of 
the  development  of  hydatids  is  the 
entrance  into  the  stomach,  or  intes- 
tines, of  tlie  taenia  echinococcus.  If 
they  remain  in  the  intestine  they  be- 
come tape-worms  ;  when  they  pass 
into  the  liver  they  develop  hydatids. 
Hydatids  are    chiefly  met  with  be- 


The  fluid   is 


i?iG.  83. 

Hj'datids  of  the  Liver. 

A.  Head  of  echinococcus  from  an  hydatid  tumor. — B. 

tween  the  ages  of  thirty  and  fifty.  E.  Fmc/ment' of  capsule  of '  hydatid  tunwr,  showing 
,,^^  ■  T  -1  n         T  Tin  itsiamell(B.—F.  Gei-ms.         x  200. 

Ihey  are  rare  m   childhood  and  old 

age.  They  are  most  common  among  the  poor  and  filthy,  and  in  cold 
climates.  It  is  estimated  that  one  out  of  every  six  of  the  inhabitants  of 
Iceland  has  hydatids  of  the  liver.  Dogs,  sheep,  pigs,  cats,  and  rats  are 
subject  to  tapeworms,  and  as  the  ova  of  these  parasites  are  discharged  in 
the  excrements  of  these  animals,  they  can  only  gain  entrance  into  the 
human  stomach  through  polluted  drinking-water,  or  the  most  filthy  prac- 
tices. 

Symptoms. — If  an  hydatid  tumor  is  deeply  seated  and  of  small  size,  it  gives 
rise  to  no  symptoms  and  cannot  be  recognized.  A  large  hydatid  tumor 
will  cause  sufficient  functional  disturbance  by  its  pressure  to  be  easily 
recognized.  The  patient  may  first  see  or  feel  a  tumor  in  the  region  of  the 
liver,  and  have  a  sense  of  weight  and  dragging  in  the  right  hypochon- 
driiim.  Symptoms  of  pressure  of  the  tumor  on  adjacent  organs  are  the 
first,  and  often  the  only  ones  which  attract  attention.  Dyspnosa,  a  dry 
hacking  cough,  and  bronchial  catarrh  may  result  from  the  upward  press- 
ure of  the  tumor.  When  the  heart  is  displaced  by  the  tumor,  there  is 
palpitation  ;  and  when  the  stomach  is  encroached  upon  there  is  vomiting, 
dyspeptic  symptoms  and  emaciation.  When  the  portal  vein  or  vena  cava 
is  pressed  upon  by  the  hydatid  tumor,  ascites,  jaundice  and  hemorrhoids 
may  result.  When  the  hydatid  compresses  the  bile  duct,  or  when  there  is 
intercurrent  catarrh  of  the  ducts,  or  when  they  have  become  obstructed  by 
the  hydatid  vesicles,  jaundice  sets  in  and  absence  of  bile  in  the  freces  is 
noted.  A  large  vesicle  may,  in  passing  the  duct,  give  every  symptom 
of  gall-stone  colic,  and  thus  be  confounded  with  it. 

When  the  pleura  is  perforated,  the  symptoms  of  acute  pleurisy  are  devel- 
oped, and  in  most  cases  the  cavity  is  rapidly  filled  with  pus  containing 
hydatid  vesicles.  Peritonitis  may  result  from  spontaneous  or  traumatic 
rupture  of  an  hydatid  cyst.  The  opening  into  the  stomach  or  intestines 
being  usually  very  small,  it  is  rarely  attended  either  by  peritonitis  or  sec- 
ondary abscess  ;  when  a  cyst  is  evacuated  in  this  way  the  case  usually  ter- 
minates in  recovery.     When  shreds  of  hydatid  vesicles  and  echinococci  are 


388  DISEASES   OF   THE   DIGESTIVE   SYSTEM. 

found  in  the  urine,  it  indicates  that  the  rupture  has  taken  place  into  the 
urinary  passages.  When  the  hydatid  tumor  is  to  discharge  itself  through 
the  abdominal  parietes,  redness  of  the  skin,  tenderness,  pain,  and  fluctua- 
tion will  precede  its  discharge.  If,  in  a  patient  who  is  known  to  have 
hydatids  of  the  liver,  there  is  pain,  elevation  of  pulse  and  temperature, 
extreme  sensitiveness  over  the  hepatic  region  with  a  peculiar  friction  sound 
on  auscultation,  it  may  be  suspected  that  inflammation  in  and  around  the 
sac  has  occurred.  In  such  case  abscess  may  be  excluded  by  the  absence  of 
rigors  and  sweats. 

Finally,  the  growth  of  an  hydatid  of  the  liver  is  in  rare  cases  attended 
with  pain  caused  by  its  pressure.  The  feeces  are  normal  unless  jaundice 
exists,  in  which  case  they  are  firm  and  clay-colored.  The  urine  is  generally 
normal,  but  if  pus  or  albumen  is  found  in  it,  pyelitis  exists  as  a  result  of 
the  pressure  of  the  tumor  on  the  renal  vein. 

Physical  Signs. — Inspection  may  show  a  distinct  bulging  in  the  right 
hypochondrium,  which  has  the  appearance  of  a  globular  elevation  over  the 
right  or  left  lobe  of  the  liver.  The  ribs  often  project,  and  respiratory 
movements  on  the  right  side  are  interfered  with. 

Palpation  discovers  an  enlarged  liver,  elastic  to  the  touch  when  the 
tumor  is  deeply  seated  ;  when  it  is  superficial,  fluctuation  may  be  detected. 
The  tumor  is  smooth,  but  if  two,  three  or  more  cysts  exist,  the  liver  will 
have  a  lobulated  outline  below  the  free  border  of  the  ribs. 

Percussion. — The  normal  area  of  hepatic  dulness  is  increased  in  some 
one  direction.  When  the  tumor  is  superficial,  the  hydatid  thrill  or  "fre- 
mitus "  is  elicited  by  firm  percussion.  This  sign,  peculiar  to  hydatids  of 
the  liver,  is  elicited  in  the  following  manner  :  place  three  fingers,  slightly 
separated,  firmly  over  the  most  prominent  part  of  the  tumor  ;  give  a  sharp 
blow  upon  the  middle  one,  and  a  vibration  or  fremitus  will  be  communicated 
to  the  other  two. 

Differential  Diagnosis. — Hydatids  of  the  liver  may  be  mistaken  for  cancer ^ 
abscess,  abdominal  aneurism,  enlarged  gall-Madder,  pleurisy,  rarely  multi- 
locular  hydatids,  and  a  cyst  of  the  right  Tcidney.  In  aMominal  aneurism 
there  will  be  severe  and  constant  pain  in  the  back ;  the  tumor  is  soft, 
doughy,  and  compressible,  has  an  '^^ expansive"  pulsation  and  is  immov- 
able, while  an  hydatid  tumor  moves  up  and  down  with  the  respiratory 
movements  and  fluctuates.  A  "bruit"  synchronous  with  the  heart  and 
often  double  will  be  heard  over  an  aneurism,  while  neither  of  these  is 
ever  present  in  hydatids.  The  femoral  pulse  will  be  altered  in  an  abdom- 
inal aneurism,  but  normal  in  hydatids  of  the  liver. 

When  di,  pendulous  hydatid  cyst  is  attached  to  the  liver  by  a  pedicle,  we 
may  readily  mistake  it  for  an  enlarged  gall-bladder.  An  enlarged  gall- 
bladder is  usually  preceded  by  jaundice,  biliary  colic,  or  symptoms  ol 
catarrh  of  the  ducts,  while  an  hydatid  has  no  such  previous  history.  On. 
palpation  it  will  be  found  that  an  hydatid  does  not  correspond  exactly  to 
the  position  of  the  gall-bladder.  The  gall-bladder  is  pear-shaped  and  evades 
manipulation  or  pressure,  while  an  hydatid  tumor  is  globular  and  readily 
manipulated. 


HYJOATIDS    OF   THE    LIVER.  389 

When  hydatids  extend  into  the  pleural  cavity  so  as  to  be  mistaken  for 
pleurisy,  the  heart  will  be  displaced  much  more  than  ever  occurs  in  pleu- 
risy. Percussion  in  pleurisy  marks  out  a  line  of  dulness  which  is  trans- 
.  verse  when  the  patient  is  erect,  and  which  changes  with  his  position,  while 
in  hydatids  the  upper  limit  of  dulness  is  irregular  and  stationary,  being 
lower  near  the  median  line  of  the  body  than  toward  the  axilla.  This  is 
an  important  point.  In  hydatids  the  lower  edge  of  the  liver  is  below 
the  free  border  of  the  ribs  and  rises  and  falls  with  the  respiration  ;  in 
pleurisy  the  liver  occupies  nearly  its  normal  position  and  is  station- 
ary. 

In  a  cyst  of  the  rigid  kidney,  there  is  the  history  of  a  growth  from  below 
upward,  while  in  hydatids  the  tumor  grows  from  above  downward.  In 
cystic  kidney  the  colon  lies  in  front  of  the  tumor,  while  in  hydatids  of  the 
liver  the  colon  is  behind  the  tumor.  An  hydatid  of  the  liver  rises  and  falls 
with  respiration,  while  a  cyst  of  the  kidney  is  motionless.  In  hydatids  of 
the  liver,  an  exploring  needle  will  withdraw  a  non-albuminous,  salty  fluid, 
containing  booklets  of  the  ecbinococci,  while  from  a  cyst  of  the  kidney  it 
will  withdraw  an  albuminous  fluid  with  chlorides  and  perhaps  pus. 

Prognosis. — Hydatids  are  dangerous  in  proportion  to  their  size  and  the 
direction  of  their  growth  ;  if  they  cease  to  enlarge,  they  may  be  regarded  as 
harmless.  Their  average  duration  is  about  four  years.  They  have  been 
known  to  exist  twenty-five  years.  If  they  rupture  into  the  pleura,  lung, 
peritoneum,  pericardium,  or  through  the  abdominal  walls,  the  prognosis  is 
unfavorable.  When  the  discharge  takes  place  into  the  intestines,  stomach, 
or  bronchi,  the  prognosis  is  favorable.  Death  occurs  from  exhaustion  caused 
by  the  pressure  of  a  very  large  hydatid,  rarely  from  that  caused  by  ascites 
through  pressure  on  the  vena  cava.  Suppuration  of  the  cyst,  or  an  abscess 
developed  secondarily  to  phlebitis  may  induce  fatal  exhaustion.  Any  one 
of  the  pulmonary  complications  referred  to  may  cause  death.  A  fatal  result 
has,  in  some  few  cases,  followed  hemorrhage  from  the  sac  through  an  ex- 
ternal opening.  Peritonitis,  pericarditis,  and  uraemia  are  infrequent  causes 
of  death,  and  when  the  pulmonary  artery  is  plugged,  when  the  vena  cava 
is  opened,  or  when  a  large  vesicle  is  lodged  in  a  bronchus,  asphyxia  is  the 
immediate  cause  of  death. 

Treatment. — Prophylactic  measures  consist  in  preventing  the  drinking- 
warter  from  being  contaminated  by  the  evacuations  of  animals,  and  in  not  al- 
lowing dogs  to  feed  upon  the  offal  of  sheep.  Chloride  of  sodium  and  iodide 
of  potassium  have  been  proposed  as  internal  remedies  to  destroy  the  echino- 
cocci.  The  chief  solid  ingredient  of  hydatid  fluid  is  chloride  of  sodium, 
but  no  trace  of  iodide  of  potassium  has  ever  been  found  in  the  fluid  after 
the  administration  has  been  continued  for  months. 

If  the  tumor  is  of  large  size,  and  is  still  increasing  in  size,  operative  inter- 
ference is  necessary.  Select  the  point  where  the  hydatid  tumor  is  most 
prominent,  and  puncture  with  a  fine  aspirating  needle.  The  dangers  which 
have  been  feared  in  this  procedure  are  peritonitis,  and  the  entrance  of  air 
into  the  peritoneal  cavity.  Peritonitis  maybe  avoided  by  pressing  the  parts 
about  the  puncture  firmly  against  the  tumor  as  the  aspirating  needle  is 


390  DISEASES    OF   THE    DIGESTIVE   SYSTEM. 

withdrawn,  so  that  no  fluid  can  escape  into  the  peritoneal  cavity.  All  dan- 
ger of  the  entrance  of  air  is  obviated  if  a  small  aspirating  needle  is  used  ;  all 
of  the  fluid  should  not  be  withdrawn  from  the  cyst  at  the  first  aspiration. 
It  is  important  to  enjoin  absolute  rest  after  the  operation  for  two  or  three 
days  ;  febrile  symptoms  and  pain  will  follow  the  withdrawal  of  the  fluid, 
and  the  tumor  will  decrease  in  size  ;  usually  a  second  puncture  will  be  re- 
quired. It  is  not  essential  to  wait  for  adhesions  to  form  between  the  tumor 
and  abdominal  wall,  though  it  is  much  safer  if  they  exist. 

Where  simple  puncture  is  not  sufficient  to  destroy  the  echinococci,  iodine 
or  bile  may  be  injected  into  the  cavity  of  the  sac.  When  the  fluid  with- 
drawn is  pus,  or  when  the  symptoms  are  indicative  of  a  suppurating  cavity, 
it  is  best  to  establish  adhesions  by  caustics.  Vienna  paste  is  to  be  preferred 
for  this  purpose,  and  the  same  precautions  are  to  be  exercised  as  in  the 
opening  of  an  hepatic  abscess.  Puncture  of  the  cyst  by  insulated  needles, — 
electrolysis,— has  been  claimed  to  be  very  successful  in  those  cases  where  it 
has  been  resorted  to,  but  it  seems  to  me  that  it  is  the  puncture,  rather  than 
the  electric  influence,  which  produced  the  favorable  result  claimed  for  it. 
Never  hesitate  to  aspirate  an  hydatid  tumor  when  it  is  well  developed  and 
elevated  above  the  level  of  the  abdominal  walls  ;  the  nearer  the  cyst  is  to 
the  surface,  the  better  the  result  of  the  aspiration. 

MULTILOCULAR    HYDATIDS. 

Multilocular  hydatids  in  their  pathology  are  similar  to  the  ordinary  hyd- 
atid, except  that  in  the  one  case  a  cyst  is  formed,  and  in  the  other  it  is 
wanting. 

Morbid  Anatomy. — The  liver  is  enlarged,  the  right  lobe  being  out  of  all 
proportion  to  the  rest  of  the  organ  ;  it  is  hard,  and  sometimes  has  a  carti- 
laginous feel.  There  are  large  nodules  on  its  surface,  the  tumors  often 
being  as  large  as  a  child's  head.  The  capsule  is  thickened  and  opaque  over 
the  tumor,  and  adhesions  may  be  formed  with  surrounding  parts. 

On  sectio7i  a  tumor  is  usually  found  embedded  in  the  right  lobe,  varying 
in  size  from  that  of  an  orange  to  a  cocoanut,  with  a  reticulated  surface. 
The  stroma  is  connective-tissue,  dull-yellow  in  color,  and  the  spaces  are 
rounded,  oval,  or  caudate,  from  the  size  of  a  ]3in's  head  to  that  of  a  pea, 
usually  communicating  with  one  another  by  small  apertures,  and  contain- 
ing a  clear  or  semi-transparent  gelatinous  substance.  The  stroma  gener- 
ally contains  some  hepatic  parenchyma,  which,  at  the  periphery  of  the 
mass,  is  dark-colored  from  pigment  deposit,  and  nearer  the  centre  is  in  a 
state  of  partial  or  complete  fatty  degeneration.  In  the  centre  of  the  mass 
is  usually  found  a  large  spot  of  suppuration,  varying  in  size,  or  a  cavity 
filled  with  a  light-brown  fluid  or  a  greenish  fetid  pus.  This  cavity  is  well 
defined,  having  a  wall  whose  lining  membrane  is  sacculated  at  points,  with 
openings  into  neighboring  cavities.  This  membrane  frequently  has  clus- 
ters of  hydatid  vesicles  upon  it.  The  surface  cavities  are  much  smaller 
than  the  central  one,  and  are  strung  along  like  "strings  of  pearls,"  com- 
pressing and  occluding  the  branches  of  all  the  vessels  of  the  liver  at  the 


MULTILOCULAR   HYDATIDS.  391 

point  whence  the  growth  develops.     The  rest  of  the  liver  is  congested  or 
hjpertrophied. 

Microscopically,  the  gelatinous  contents  in  one  of  the  alveoli  ai-e  found  to 
be  made  up  of  the  laminated  structure  of  the  vesicle  and  containing  echi- 
nococci  with  their  circlets  of  booklets  ;  it  is  rare,  however,  to  find  perfect 
"scolices."  The  cyst-wall  may  exhibit  calcareous,  fatty,  or  pigmentary 
degeneration.  Between  the  cysts  small  globules,  consisting  of  calcare- 
ous matter,  are  sometimes  found,  and  also  granular  and  crystalline  haema- 
toidin.     The  spleen  is  usually  enlarged. 

Etiology. — The  etiology  of  multilocular  hydatids  is  the  same  as  that  of 
a  single  hydatid  tumor.  When  the  ova  of  the  taenia  reach  the  liver,  the  ques- 
tion arises:  what  is  it  that  causes  the  peculiar  alveolar  or  colloid  arrange- 
ment of  the  vesicles  ?  This  has  been  variously  explained  :  some  claim  that 
when  the  embryo  enters  either  the  lymphatics,  blood-vessels,  or  bile-ducts, 
the  growth  extends  along  the  channels  of  either  system,  since  it  cannot  ex- 
tend concentrically  because  of  the  exterior  pressure.  I  am  inclined  to 
agree  with  those  who  think  that  when  a  cyst-wall  is  developed  around  the 
embryo  and  no  connective-tissue  encapsulates  the  cyst,  it  can  grow  in  all 
directions.     Their  development  is  yet  obscure. 

Symptoms. — The  insidious  apjDroacli  and  slow  progression  which  mark 
the  course  of  single  hydatid  tumors  are  present  here.  The  effects  of  pressure 
may  be  shown  by  vomiting  and  dyspepsia  when  the  stomach  is  encroached 
upon  ;  constipation  and  difficulty  in  defecating  when  the  intestines  are 
pressed  upon ;  and  ascites,  cedema,  hemorrhoids,  and  enlarged  spleen, 
when  the  portal  trunk  or  vena  cava  is  compressed.  There  are  no  subjective 
signs.  When  suppuration  occurs  there  will  be  a  slight  rise  in  temperature, 
increased  frequency  in  the  pulse,  and  other  symptoms  which  attend  the 
formation  of  pus  in  the  liver.  G-astro-intestinal  hemorrhages,  and  hemor- 
rhages from  mucous  surfaces  rarely  occur.  When  the  bile-ducts  are  in- 
volved, jaundice  is  the  first,  or  an  early  symptom  ;  the  jaundice  gradually 
deepens  and  is  persistent.     The  faeces  are  clay-colored. 

Physical  Signs. — Palpation  shows  the  liver  early  enlarged,  having  slight 
elevations^  with  a  smooth  feel.  Later  it  is  hard,  resistant,  nodular,  and 
uneven.  The  tumors  are  confined  to  the  right  lobe,  or,  at  least,  are  best 
marked  there. 

Percussion. — The  area  of  hepatic  dulness,  in  the  region  of  the  right  lobe 
especially,  is  increased,  and  the  spleen  is  enlarged  with  multilocular  hyda- 
tids.    There  is  neither  fluctuation  nor  the  "  hydatid  thrill." 

Differential  Diagnosis. — When  the  bile-ducts  are  involved  a  diagnosis  may 
be  made  by  exclusion  ;  in  other  cases,  the  affection  is  liable  to  be  con- 
founded with  cancer,  cirrhosis,  and  nodular  (syphilitic)  loaxy  liver. 

In  cancer  of  the  liver  there  is  a  history  of  a  gradually  developing  ca- 
chexia and  lancinating,  almost  constant,  pain,  with  evidences  of  cancer  else- 
where, or  an  hereditary  tendency  ;  while  in  multilocular  hydatids  there  are 
no  constitutional  symptoms  and  no  pain,  the  hepatic  region  merely  being 
tender.  The  duration  of  cancer  is  rarely  more  than  a  year,  while  the  de- 
velopment of  multilocular  hydatids  is  protracted  to  two  or  three  years.     A 


392  DISEASES    OF   THE    DIGESTIVE   SYSTEM. 

cancer  nodule,  on  palpation,  is  usually  umbilicated  and  soft  at  the  centre  ; 
while  a  multilocular  hydatid  is  smooth  and  elastic.  An  exploring  trochar 
will  remove  all  doubt. 

In  cirrhosis  of  the  liver  there  is  a  history  either  of  alcohol  drinking, 
rheumatism,  gout,  or  syphilis  ;  in  multilocular  hydatids  no  such  history 
necessarily  exists.  In  cirrhosis  the  liver  is  smaller  than  normal  and  hob- 
nailed ;  in  multilocular  hydatids  it  is  enlarged  and  the  nodules  are  of  a 
larger  size.     Ascites  is  common  in  cirrhosis  ;  while  it  is  rare  in  hydatids. 

In  a  nodular  waxy  liver  there  is  a  well-marked  history  of  syphilis  ;  there 
is  a  complicating  diarrhoea,  albuminuria,  and  the  characteristic  waxy 
cachexia,  which  are  absent  in  multilocular  hydatids. 

An  hydatid  tumor  can  only  be  diagnosticated  from  multilocular  hydatids 
by  the  exploring  trochar.  The  fluid  in  multilocular  hydatids  contains  pus 
in  varying  quantities,  a  few  booklets  of  the  echinococci,  and  numerous 
small  vesicles  ;  while  that  from  an  ordinary  hydatid  is  nearly  pure  water, 
containing  the  booklets  and  2ifeiv  vesicles.  In  many  instances  the  hydatid 
thrill  is  present  in  a  single  hydatid  tumor,  but  never  present  in  multilocu- 
lar hydatids. 

Prognosis. — In  those  cases  in  which  the  jaundice  is  intense,  the  disease 
may  run  its  course  in  six  months  ;  in  other  cases,  the  course  is  as  pro- 
longed as  in  single  hydatids.  Peritonitis  is  a  frequent  complication,  and 
amyloid  degeneration  of  the  liver  may  also  occur  with  it.  Death  results 
from  the  exhaustion  due  to  the  suppuration  or  from  the  complicating  peri- 
tonitis. 

Treatment. — There  is  no  medicinal  treatment  which  can  in  any  way  affect 
the  course  of  this  disease  ;  and  operative  interference  has  thus  far  proved 
unsuccessful.  This  class  of  patients  must  be  sustained  during  the  exhaus- 
tion of  the  supervening  suppuration.  The  pain,  if  severe,  may  be  relieved 
by  hypodermatics  of  morphia. 

TUBEECULOSIS    OF   THE    LIVER. 

Tubercle  of  the  liver  is  always  secondary  to  tubercle  elsewhere.  Though 
rare,  it  is  probably  more  common  than  is  usually  supposed,  from  the  fact 
that  hepatic  tubercle  is  always  microscopic. 

Morbid  Anatomy.— The  liver  is  slightly  but  uniformly  enlarged  in  size. 
On  close  inspection  the  surface  is  seen  to  be  irregularly  elevated  and  de- 
pressed, and  looks  and  feels,  in  this  respect,  like  the  surface  of  an  orange. 

On  section  the  liver  cuts  hard,  the  parenchyma  being  tense  and  tough. 
The  tissue  is  pale  and  yellow,  resembling  a  fatty  liver.  The  bile-ducts  at 
points  are  expanded,  the  walls  being  thinned.  They  contain  a  turbid  fluid 
mainly  composed  of  mucus  and  bile.  There  are  also  small  cavities  filled 
with  pus  and  bile.  When  the  tubercle  has  undergone  retrograde  metamor- 
phosis, small  gray  masses  the  size  of  a  pin's  head  are  seen,  and,  also,  "  yellow 
tubercle  "  or  larger  yellow  masses  the  size  of  a  pea;  these  changes  are  usually 
best  marked  just  beneath  the  capsule. 

A  microscopic  examination  shows  miliary  tubercles  scattered  between  the 


JAUNDICE.  393 

lobules.  When,  as  a  result  of  obliteration  of  blood-vessels,  tubercles  under- 
go fatty  degeneration,  the  so-called  "yellow  tubercle"  is  the  product. 

Etiology.— Hepatic  tubercle  occurs  as  part  of  acute  miliary  tuberculosis, 
and  is  secondary  to  tubercle  in  the  lungs,  peritoneum,  spleen,  and  lym- 
phatics. 

Symptoms.— There  are  no  symptoms  indicative  of  hepatic  tuberculosis, 
independent  of  those  of  genera]  tuberculosis. ' 

JAUNDICE. 

Jaundice  is  a  yellow  discoloration  of  the  skin,  due  to  the  presence  of  bile 
or  blood  pigment.  There  are  two  varieties,  hepatogenous  or  obstructive 
jaundice,  and  hematogenous  or  non-obstructive. 

Hepatogenous  Jaundice  is  the  more  common  variety,  and  is  caused  by 
the  absorption  of  bile,  its  passage  into  the  ductus  communis  or  intestine 
being  prevented  by  some  mechanical  obstruction. 

Hematogenous  Jaundice  results,  probably,  from  a  change  in  the  blood, 
whereby  its  coloring  matter  is  set  free  in  excess. 

Morbid  Anatomy  of  hepatogenous  Jaundice.  In  a  normal  state,  the  liver- 
cells  are  constantly  manufacturing  bile,  which  flows  along  the  bile-ducts 
into  the  ductus  communis.  The  cause  of  its  outward  flow  is  the  vis  a  tergo, — 
the  secretion  of  the  bile  in  the  hepatic  cells, — for  there  are  no  muscular 
fibres  except  in  the  larger  bile-ducts  ;  the  respiratory  movements  also  assist 
slightly  in  its  outward  flow.  When  from  any  causes  the  bile  cannot  enter 
the  common  duct  or  the  duodenum,  the  small  ducts  and  then  the  hepatic 
cells  become  overfull  and  distended.  In  consequence  of  this  increased 
pressure,  bile  passes  through  the  wall  of  the  smaller  ducts  into  the  blood- 
vessels and  lymph  channels.  If  the  normal  tension  of  the  capillary  system 
in  the  liver  is  diminished,  then  the  passage  of  bile  through  the  walls  of  the 
vessels  is  favored  and  Jaundice  results.  Bile  pigment  with  serum  exudes 
and  stains  the  tissues,  even  the  bones,  the  teeth  and  pathological  new  forma- 
tions. In  both  hepatogenous  and  hematogenous  Jaundice,  the  staining  occurs 
in  the  same  way. 

Hematogenous  Jaundice. — In  health  the  bile  pigment  is  formed  within 
the  liver,  by  transformation  of  the  coloring  matter  of  the  blood,  and  after 
it  has  been  poured  into  the  intestine,  it  is  partly  absorbed  by  the  blood  and 
appears,  after  another  change,  as  one  of  the  coloring  matters  of  the  urine. 
Under  abnormal  conditions,  and  as  the  result  of  processes  that  are  not  fully 
understood,  coloring  matter  is  either  set  free  in  excess  or  is  not  excreted 
with  the  bile,  and  is  then  deposited  in  the  tissues  producing  Jaundice.  As 
this  variety  of  Jaundice  is  thought  to  have  its  origin  in  morbid  conditions 
of  the  blood,  it  is  called  hematogenous. 

The  anatomical  lesions  which  are  associated  with  hematogenous  Jaundice 
have  already  been  considered  in  connection  with  the  history  of  the  different 
hepatic  affections  in  which  it  occurs. 

'  Lymphatic  formations,  simple  cysts,  dermoid  cysts,  erectile  cavernous  tumors,  and  benign  fibrous 
growths  occur  in  the  liver,  but  are  only  of  pathological  Interest. 


394  DISEASES    OF   THE   DIGESTIVE   SYSTEM. 

Etiology. — The  causes  of  hepatogenous  jaundice  may  be  included  under 
three  heads  : 

I.  Thoso  which  obstruct  the  larger  hepatic  ducts. 
II.  Those  which  obstruct  the  hepatic  radicles. 

III.  Those  which  diminish  capillary  tension. 

Those  obstructions  of  the  larger  hepatic  duct  which  have  their  seat  within 
the  duct  are  : 

(1)  Inflammations  of,  or  inflammatory  exudations  from,  the  lining  mem- 
brane of  the  duct,  that  which  accompanies  duodenal  catarrh  being  the  most 
frequent,  (2)  Biliary  calculi.  (3)  Inspissated  bile  and  mucus.  (4)  Hydatid 
vesicles.  (5)  Distomata.  (6)  Foreign  bodies  from  the  intestinal  canal,  such 
as  stones  of  fruits  and  round  worms.  (7)  Congenital  occlusion,  or  plugging 
of  the  duct.  (8)  Cicatrices  from  ulcers  on  the  mucous  membrane  of  the 
duct.    (9)  Carcinomatous  growths  from  the  lining  membrane  of  the  ducts. 

The  causes  which  obstruct  the  duct  by  external  pressure,  are  • 

(1)  Contraction  from  perihepatitis,  or  from  inflammation  of  thehepatico- 
duodenal  ligament.  (2)  Tumors  of  the  pyloric  extremity  of  the  stomach, 
of  the  head  of  the  pancreas,  and  of  the  kidney.  (3)  Pressure  from  a  preg- 
nant uterus,  from  ovarian  and  fibroid  tumors,  from  omental  tumors,  and 
from  large  impaction  of  faeces.  (4)  Enlarged  lymphatic  glands  in  the  trans- 
verse fissure  from  waxy,  cancerous,  or  tubercular  change,  abdominal  aneu- 
rism, and  the  new  tissue  in  hypertrophic  cirrhosis  of  the  liver.. 

Slight  hepatogenous  jaundice  may  be  caused  by  compression  or  oblitera- 
tion of  the  hepatic  radicles,  such  as  occurs  in  cirrhosis  and  the  other  atro- 
phies of  the  liver,  in  active  and  passive  hypersemia,  in  hydatid  tumors  and 
multilocular  hydatids,  in  cancerous  and  syphilitic  tumors,  in  abscess  of  the 
liver,  in  adhesive  pylephlebitis,  and  perhaps  in  acute  yellow  atro]3hy. 

Finally, the  bile  may  be  prevented  from  entering  the  intestine  in  its  normal 
amount  when  capillary  tension  is  diminished.  This  may  occur  in  severe 
right  diaphragmatic  pleurisy,  in  perihepatitis,  in  thrombosis  of  the  trunk 
or  of  the  larger  branches  of  the  vena  portae,  and  in  exhausting  hemorrhage 
from  the  radicles  of  the  portal  vein. 

The  causes  of  hematogenous  jaundice  are  fevers,  especially  yellow,  typhus, 
typhoid,  and  the  malarial  fevers.  It  is  often  an  attendant  of  pyaemia,  puer- 
peral fever,  septicaemia,  and  suppurative  pylephlebitis.  The  poison  of 
snake-bites,  phosphorus,  mercury,  copper,  antimony,  and  the  excessive 
use  of  ether  and  chloroform  may  cause  it.  Pneumonia,  probably  by  its 
action  on  resiDiration,  and  ulcerative  endocarditis  induce  it ;  it  may  follow 
a  fright,  a  fit  of  anger,  great  anxiety,  or  cerebral  concussion.  A  long  con- 
tinued hepatogenous  jaundice  may  lead  to  a  hematogenous  jaundice  ;  and 
it  is  yet  undecided  whether  the  icterus  in  yellow  atrophy  belongs  to  the 
first  or  second  named  group. 

DiflFerential  Diagnosis. — Hematogenous  jaundice  accompanies  acute  in- 
fectious fevers  and  other  conditions  of  blood  poison,  while  hepatogenous 
jaundice  can  be  traced  to  some  mechanical  interference  with  the  outflow 
of  the  bile.  The  yellow  staining  is  slight  in  hematogenous  jaundice  ; 
while  the  discolorization  in  hepatogenous  jaundice  is  more  intense  and  may 


CATAREH   OF   THE   BILE-DUCTS.  395 

appear  suddenly  without  constitutional  disturbances.  A  feeble  and  irreg- 
ular heart-action>  a  small  pulse,  and  a  tendency  to  hemorrhages  attend 
hematogenous  jaundice;  while  an  unimpaired  heart-action,  a  slow  pulse,  and 
a  low  temperature  mark  the  development  of  hepatogenous  jaundice.  There 
is  great  itching  of  the  surface  in  hepatogenous  jaundice  which  is  absent  in 
the  hematogenous  variety.  The  faeces  are  dark  in  hematogenous  jaundice, 
and  white  or  clay-colored  in  hepatogenous.  The  urine  is  albuminous,  con- 
tains a  small  amount  of  bile  pigment,  and  deposits  a  sediment  of  uric  acid 
in  the  hematogenous  variety,  while  it  is  rarely  albuminous  in  hepatogenous 
jaundice  and  contains  bile-pigment  in  considerable  amouAt,  the  quantity 
varying  with  the  intensity  of  the  jaundice. 

DISEASES  OF  THE  GALL-BLADDER  AND  GALL-DUCTS 

will  be  considered  under  the  following  heads  : 

I.   Catarrhal  Inflammation  of  tJie  III.    Cancer  of  the  Gall-Bladder. 

Biliary  Passages.  IV.   Enlargement  of  the  Gall-Blad- 
II.  Exudative  Inflammation  of  the  der. 

Biliary  Passages  {croupous  V.   Gall  Stories. 
or  diphtheritic). 

CATAERH    OF   THE    BILE-DUCTS. 

Morbid  Anatomy. — Catarrhal  inflammation  of  the  mucous  membrane  of 
the  larger  bile-ducts,  the  ductus  communis,  and  the  gall-bladder  is  similar 
to  that  of  other  mucous  surfaces.  There  is  hyper^emia  followed  by  an  ab- 
normal secretion  of  mucus  and  muco-pus  which  more  or  less  obstructs  the 
outflow  of  bile.  The  catarrhal  process  usually  begins  in  the  duodenum 
and  extends  inward,  and  in  severe  cases  may  be  so  rapid  that  pus  will  be 
the  product  of  the  inflammation,  in  which  case  the  deeper  tissues  are  in- 
volved and  numerous  little  ulcers  may  form,  and  Avhen  the  duct  is  perfo- 
rated by  them,  cavities  of  varying  sizes,  resembling  small  abscesses,  result. 
When  the  catarrh  becomes  chronic  the  deeper  tissues  are  infiltrated,  caus- 
ing thickening  and  induration  of  the  ducts  from  the  consequent  obstruction 
to  the  exit  of  the  bile.  Dilatations  occur  at  points  along  the  bile  ducts  ; 
these  dilatations  often  become  very  large  and  occasionally  form  cysts  ;  at 
other  times  the  alternate  dilatations  and  constrictions  give  the  appearance 
of  a  string  of  beads.  The  lymphatics  often  become  involved,  and  their  en- 
largement gives  a  nodular  appearance  to  the  mucous  membrane.  Ulcera- 
tive processes  are  more  frequent  in  chronic  catarrh  of  the  bile  passages 
than  in  acute.  The  liver  is  uniformly  enlarged  and  its  margins  are  firm 
and  sharp. 

On  section,  its  substance  presents  a  mottled  appearance,  resembling  a 
nutmeg,  and  varies  in  color  from  a  deep  yellow  to  an  olive  green.  The 
color  is  deeper  at  the  centre  of  a  lobule  and  shades  oif  toward  its  periphery. 
The  gall-ducts  commonly  have  their  mucous  membrane  pale  and  covered 
with  a.  thick,  purulent  mucus  ;  and  plugs  of  mucus  and  epithelial  debris 


396  DISEASES   OP  THE   DIGESTIVE   SYSTEM. 

are  found  in  them,  most  frequently  near  or  at  the  opening  of  the  duct  into 
the  duodenum.  The  gall-bladder  is  enlarged,  and  the  cystic  and  common 
ducts  often  attain  immense  size  ;  in  one  case  this  diameter  reached  an  inch 
and  a  half. 

In  chronic  catarrh  the  liver  is  normal  or  diminished  in  size,  and  is  soft, 
flabby  and  shrivelled. 

On  section  it  is  greenish-black  in  color,  the  hepatic  ducts  are  dilated, 
forming  cysts,  and  little  points  of  ulceration  are  formed  on  the  mucous 
surface  of  the  duct,  often  extending  into  the  adjacent  parenchyma  which 
is  atrophied.  The  ramifications  of  the  vena  portse  are  compressed  by  the 
ducts,  and  thickened  bile  may  cause  these  ducts  to  present  the  appearance 
of  a  dark  brown  tube.  The  gall-bladder  is  enlarged  in  size,  and  sometimes 
there  are  spots  of  ulceration  upon  its  walls  which  may  also  undergo  cal- 
careous changes. 

Etiology. — The  most  frequent  cause  of  biliary  catarrh  is  extension  of  a 
gastro-duodenal  catarrh.  Most  of  the  structural  diseases  of  the  liver  may 
lead  to  or  be  attended  by  catarrhal  inflammation  of  the  bile  ducts.  Thoracic 
disease  where  the  venous  return  is  impeded  (as  in  cardiac  valvular  lesions 
and  emphysema)  may  cause  catarrh  of  the  biliary  passages.  General  blood 
diseases,  syphilis  and  pyaemia  prominently,  and  mineral  poisons,  phos- 
phorus, and  perhaps  arsenic,  cause  it.  A  gouty  diathesis  causes  or  pre- 
disposes to  a  catarrh  of  the  biliary  passages,  just  as  it  does  to  catarrhal 
inflammations  of  the  mucous  membranes  elsewhere  in  the  body — bronchitis, 
for  instance.  Foreign  bodies,  as  calculi  and  parasites,  in  the  bile  passages 
may  cause  biliary  catarrh.  Exposure  to  cold  and  an  altered  condition  of 
the  bile  may  induce  it. 

Symptoms. — The  subjective  symptoms  of  biliary  catarrh  are  at  first  obscure. 
It  is  usually  preceded  by  the  symptoms  of  gastro-duodenal  catarrh,  and 
hence  for  a  few  days  there  will  be  loss  of  appetite,  furred  tongue,  flatulence, 
nausea  and  vomiting.  There  is  also  some  pain  and  tenderness  in  the  epi- 
gastrium, and  in  most  cases  the  temperature  will  be  slightly  raised,  and  the 
pulse  accelerated.  The  bowels  are  constipated,  unless  it  is  accompanied 
by  extensive  intestinal  catarrh,  when  diarrhoea  will  be  present.  The  fsecal 
discharges  are  of  a  light  clay  color  and  contain  no  bile.  The  urine  is  of  a 
dark  green  color,  and  contains  bile  pigment.  The  liver  is  enlarged  and 
tender,  especially  over  the  region  of  the  gall-bladder.  The  absence  of 
bile  from  the  intestine  favors  gaseous  distention  of  the  bowel.  The 
sclerotic  becomes  yellow,  and  gradually  the  entire  surface  assumes  a  yellow 
hue.  The  temperature  falls  to  normal  and  the  pulse  is  slowed.  As  the 
jaundice  deepens,  there  is  a  noticeable  loss  of  strength,  the  patient  becomes 
apathetic  and  disposed  to  sleep  during  the  day.  There  is  headache,  vertigo, 
and  great  depression  of  spirits  ;  itching  of  the  surface  becomes  exceedingly 
troublesome. 

All  these  symptoms  remit,  the  appetite  returns,  and  the  fseces  and  urine 
return  to  their  normal  color  ;  or  the  catarrh  becomes  chronic  and  continues 
for  months,  the  jaundice  deepening,  exhaustion  and  emaciation  becoming 
extreme.     Then  gastric  and  intestinal  hemorrhages  frequently  occur,  and 


CATAEBH   OF   THE   BILE    DUCTS.  397 

ascites  may  be  followed  by  general  anasarca  ;  coma  closes  the  scene.  The 
last  stage  of  chronic  catarrh  is  accompanied  by  evidences  of  atrophy  of  the 
liver. 

Physical  Signs. — Inspection  reveals  a  jaundiced  condition  of  the  skin 
and  conjunctivae,  and  perhaps  a  bulging  in  the  right  hypochondrium. 

Falpation  discovers  an  enlarged,  smooth  and  tender  liver.  The  gall- 
bladder is  enlarged,  and  sometimes  there  is  a  pear-shaped  fluctuating  tumor 
at  its  anterior  margin.  The  gall-bladder  is  tender  on  firm  pressure.  Late 
in  chronic  catarrh  the  liver  is  diminished  in  size. 

Percussion  shows  a  uniform  increase  in  the  area  of  hepatic  dulness, 
which,  however,  in  chronic  disease  may  be  normal  or  diminished. 

Differential  Diagnosis.— This  condition  may  be  mistaken  for  suppurative 
pylephlebitis  and  exudative  inflammations  of  the  ducts.  The  former  has 
already  been  considered,  the  latter  will  be  considered  under  exudative  in- 
flammations. 

Prognosis. — This  is  good ;  catarrh  of  the  bile  ducts  is  not  a  dangerous 
disease.  The  jaundice  usually  continues  from  three  to  five  weeks,  but 
sometimes  it  continues  for  months.  The  prognosis  is  rendered  unfavorable 
when  oft-repeated  biliary  catarrhs  lead  to  permanent  closure  of  the  ducts 
and  atrophy  of  the  liver.  Catarrh  of  the  bile-ducts  may  be  complicated 
by  peritonitis,  pleurisy,  pneumonia,  dysentery,  suppurative  hepatitis,  or 
acholia.  Death  then  results  from  exhaustion,  from  faulty  nutrition,  or 
dropsy,  from  intercurrent  diseases,  rupture  of  the  ducts,  or  with  brain 
symptoms — "  acholia." 

Treatment. — It  should  be  remembered  that  the  jaundice  is  only  a  symp- 
tom, and  requires  no  treatment.  The  treatment  of  this  catarrh  is  mostly 
symptomatic  ;  it  is  usually  self-limiting  and  will  subside  without  remedial 
measures.  If  the  hepatic  pain  is  severe,  leeches  followed  by  an  anodyne 
poultice  over  the  points  of  greatest  tenderness  will  usually  relieve  it.  When 
the  bowels  are  constipated,  "  blue-pill,"  or  a  saline  purgative  is  first  de- 
manded, after  which  old  cider  or  tamarinds  will  regulate  the  bowels  for  the 
remainder  of  the  attack  ;  nitro-muriatic  acid  acts  favorably  in  most  cases. 
If  there  is  diarrhoea,  ipecacuanha  or  Dover's  powder  will  readily  control  it. 
When  the  urinary  secretion  is  much  diminished  the  salts  of  potash  in  com- 
bination with  diaphoretics  may  be  administered.  The  diet  throughout 
should  contain  no  carbo-hydrates  ;  the  food  should  consist  principally  of 
lean  or  prepared  meats,  vegetables,  and  skimmed  milk. 

When  there  is  a  gouty  diathesis,  colchicum  and  iodide  of  potassium  are 
often  of  service.  In  a  syphilitic  diathesis,  chloride  of  ammonium  and  the 
bi-chloride  of  mercury  are  indicated.  Emetics  rather  aggravate  the  gastric 
intestinal  catarrh  than  cause  the  expulsion  of  a  hypothetical  plug  in  the 
common  duct,  and  should  not  be  administered.  Finally,  if  the  hepatic 
parenchyma  become  involved,  a  tonic  and  diuretic  plan,  similar  to  that 
adopted  in  cirrhosis,  may  be  adopted.  The  use  of  mineral  waters  must  be 
determined  by  the  influence  which  they  exert  on  each  patient ;  in  some 
cases  increased  appetite  results,  while  in  others  they  seem  to  hasten  the 
wasting  process. 


398  DISEASES    OF   THE    DIGESTIVE    SYSTEM. 


EXUDATIVE    INFLAMMATIOlsr    OF    BILIAEY   PASSAGES. 

Under  the  head  of  exudative  inflammation  of  the  biliary  passages  I  in- 
clude both  a  croupous  and  Si  diphtheritic  process.  Both  are  rare  and  seldom 
recognizable  during  life. 

Morbid  Anatomy.— The  commencement  of  croupous  inflammation  is  the 
same  as  catarrh  ;  but  the  inflammatory  product  is  fibrinous. 

In  diphtheritic  inflammation,  the  deeper  tissues  of  the  walls  of  the  gall- 
bladder and  bile-ducts  are  involved,  and  large  gray  sloughs,  more  firmly 
adherent  than  in  croupous  inflammation,  are  formed  upon  their  walls.  The 
liver  is  usually  enlarged. 

On  section  the  ducts  within  the  liver  are  seen  clogged  with  inspissated 
bile,  and  occasionally  there  are  abscesses.  When  constriction  and  occlu- 
sion of  the  ducts  exist,  they  become  dilated  behind  the  narrowed  portion, 
and  resemble  cysts,  containing  a  pale  yellow  fluid  with  loose  coagula  floating 
in  it.  The  gall-bladder  is  sometimes  filled  with  a  gray- white  liquid,  neutral, 
albuminous,  and  sometimes  containing  leucin  ;  at  other  times  the  liquid  is 
purulent,  or  thick  and  dark  like  tar.  On  the  mucous  membrane  of  the 
gall-bladder  and  common  duct  is  a  yellowish- white  fibrinous  layer,  varying 
in  thickness  and  tenacity,  having  all  the  anatomical  characteristics  of  a 
diphtheritic  exudation.  The  walls  of  the  gall-bladder  and  larger  ducts  are 
thickened  and  sometimes  ulcerated.  The  ulceration  may  lead  to  perfora- 
tion and  fistulous  openings.  Adhesions  sometimes  bind  the  gall-bladder 
to  the  surrounding  parts.  If  the  diphtheritic  process  extends  to  the  venous 
coats  pylephlebitis  may  result ;  sometimes  the  bile-ducts  open  into  branches 
of  the  ,vena  portse. 

Etiology. — These  inflammations  occur  with  typhus  and  typhoid  fevers, 
cholera,  diphtheria,  pyaemia,  septicaemia,  bilious  fever,  and  from  the 
irritation  produced  by  biliary  calculi. 

Symptoms. — The  first  symptom  of  exudative  inflammation  of  the  biliary 
passages  is  a  sense  of  constriction  in  the  right  hypochohdrium.  This  is  soon 
followed  by  pain,  increased  by  pressure  in  the  region  of  the  gall-bladder, 
and  vomiting.  There  are  active  febrile  symptoms,  but  these  are  usually 
not  marked.  If  ulceration  of  the  ducts  or  implication  of  the  branches 
of  the  portal  vein  occurs,  then  chills,  sweats,  and  the  other  symptoms  of 
pygemic  abscesses  of  the  liver  result,  or  the  symptoms  of  pylephlebitis  are 
developed.  When  an  opening  into  the  peritoneal  cavity  occurs,  rapidly 
fatal  peritonitis  is  the  result.  If  there  is  no  obstruction  to  the  outflow  of 
bile,  neither  jaundice  nor  alteration  in  the  color  of  the  stools  will  be 
present. 

Physical  Signs. — Inspection  may  show  a  slight  elevation  of  the  free  border 
of  the  ribs. 

Palpation  discovers  a  pear-shaped,  tender,  movable  tumor  at  the  nor- 
mal site  of  the  gall-bladder.     Slight  pressure  over  it  gives  pain. 

Percussion. — The  area  of  liver  dulness  is  normal  or  slightly  increased  ; 
over  the  enlarged  gall-bladder  the  percussion  note  is  dull  and  somewhat 
tympanitic  in  character. 


CANCER   OF  THE   GALL-BLADDER.  399 

DiiFerential  Diagnosis. — Exudative  inflammation  of  the  bile-ducts  may  be 
mistaken  for  simple  Mliary  catarrh.  The  points  which  will  aid  in  a  di- 
agnosis are  the  occurrence  of  intense  pain,  actiye  febrile  symptoms,  and  a 
careful  study  of  the  etiology  of  each  case. 

Prognosis. — This  is  determined  by  the  disease  which  it  accompanies. 
It  usually  terminates  in  death. 

Treatment. — Absolute  rest  is  important.  To  relieve  the  pain  leeches  may 
be  applied  over  the  tumor,  followed  by  poultices  and,  later,  by  counter- 
irritation.  The  diet  and  saline  purgatives  should  be  the  same  as  in  sim- 
ple catarrh,  unless  the  primary  disease  contraindicates  their  use.  If  symp- 
toms of  pus  formation  are  present,  quinine  may  be  given  in  large  doses 
a.nd  tonics  are  indicated.  If  the  tumor  becomes  large,  so  that  there  is 
danger  of  its  rupture,  it  may  be  aspirated,  the  same  rules  being  observed 
as  in  hydatids  and  abscess. 

CANCER  OF   THE  GALL-BLADDEE. 

Cancer  of  the  gall-bladder  is  usually  associated  with  cancer  of  the  liver 
substance,  and  is  often  the  primary  seat  of  the  development  of  scirrhus 
or  medullary  cancer  of  the  liver. 

Morbid  Anatomy. — The  gall-bladder  is  enlarged,  nodular  and  adher- 
ent to  the  surrounding  parts  ;  sometimes  there  are  spots  of  ulceration  on 
its  surface,  and  there  may  be  fistulse  from  the  gall-bladder  to  the  intestine. 
On  section  its  wall  is  found  thickened,  and  the  cavity  sometimes  filled  with 
a  cancerous  mass  in  which  are  embedded  numerous  concretions. 

Etiology. — This  is  the  same  as  that  of  cancer  of  the  liver.  It  is  often 
secondary  to  cancer  of  the  stomach.  Concretions  are  so  often  found  that 
some  have  ascribed  its  development  to  gall-stones. 

Symptoms. — The  subjective  symptoms  are  few  :  none  are  constant  except 
the  gastric  derangement  and  the  paroxysms  of  lancinating  pain  ;  vomiting 
is  common  and  severe,  because  of  the  pressure  of  the  tumor  on  the  py- 
lorus. Jaundice  may  be  present  when  the  common  duct  is  involved. 
While  the  tumors  often  increase  very  rapidly,  the  cancerous  cachexia  and 
emaciation  are  slow  in  their  development.  In  some  cases  the  symptoms 
undergo  marked  exacerbations  and  remissions.  Swelling  of  the  glands  in 
the  inguinal  and  axillary  regions  may  occur. 

Physical  Signs. — Palpation  will  discover  over  the  site  of  the  gall-bladder 
a  hard,  nodular  and  immovable  tumor.  It  is  tender,  and  sometimes  fluctu- 
ates at  the  centre. 

Percussion  shows  an  increase  in  the  area  of  hepatic  dulness  below  the  free 
border  of  the  ribs. 

ENLARGED    GALL-BLADDER. 

Dropsy  of  the  gall-bladder  is  a  term  used  to  include  those  cases  where, 
on  account  of  some  obstruction,  bile  is  prevented  from  entering  the  nat- 
ural reservoir,  and  an  increased  secretion  from  its  mucous  surface  leads  to 
its  distention. 


400  DISEASES    OF   THE    DIGESTIVE    SYSTEM, 

Morbid  Anatomy. — The  gall-bladder  is  found  enlarged,  sometimes  reach- 
ing the  size  of  a  cocoa-nut.  The  walls  are  thickened,  at  some  parts  more 
than  at  others,  and  occasionally  sacculations  render  its  outlines  uneven. 
The  cystic  wall  is  often  tense,  and  now  and  then  plates  of  calcareous  matter 
are  found  upon  it.  On  opening  it  there  may  be  a  discharge  of  gas  from  its 
interior,  but  more  commonly  a  curdy  white  fluid  fills  its  cavity.  This  fluid 
contains  whitish  flakes  of  albuminous  matter  resembling  synovial  fluid  ; 
it  may  contain  bile,  and  then  it  is  dark  and  viscid.  On  close  examination 
the  mucous  surface  resembles  a  serous  membrane,  and  the  muscular  fibres 
of  its  wall  are  attenuated  and  wide  apart.  Later  on,  the  fluid  contents  of 
the  cavity  may  disappear,  and  only  a  mass  of  pultaceous  matter  remains. 
When  the  obstruction  has  been  near  the  opening  into  the  duodenum,  the 
ductus  communis  and  the  cystic  duct  are  dilated  and  their  walls  thick- 
ened. 

Etiology. — Hydrops  cystidis  fellm,  as  it  is  sometimes  called,  may  be  caused 
by  a  catarrhal,  croupous,  or  diphtheritic  inflammation  of  the  cystic  duct, 
which  obstructs  the  passage  of  bile  into  the  intestine.  Plugging  of  the 
common  or  cystic  duct,  or  of  the  neck  of  the  gall-bladder,  by  a  calculus, 
may  cause  dropsy  of  the  gall-bladder.  Multilocular  hydatids  or  hydatid 
cysts  may  plug  the  cystic  duct  and  induce  it.  Pressure  by  tumors  outside 
of  the  duct,  as  enlarged  glands  in  chronic  peritonitis,  aneurisms,  impacted 
faeces,  and  cancerous  growths  of  the  adjacent  parts,  occasionally  leads  to  it. 

Symptoms. — When  the  cystic  duct  alone  is  pressed  upon  or  in  some  way 
plugged,  there  are  few  subjective  symptoms.  The  patient  may  notice  a 
bulging  in  the  hepatic  region,  which  steadily  increases,  and  is  accompanied 
by  pain,  nausea,  vomiting,  loss  of  appetite,  and  constipation.  But  the  color 
of  the  skin,  urine,  and  faeces  exhibits  no  change.  If  a  calculus  is  the  cause 
of  the  obstruction,  there  is  usually  a  history  of  "  bilious  colic,"  and  if 
abdominal  tumors  press  upon  the  cystic  duct  there  will  be  the  physical 
evidences  of  their  existence. 

Physical  Signs. — Inspection  msij  reveal  a  globular  tumor  near  the  rectus 
muscle,  at  the  free  border  of  the  ribs.  Palpation  discovers  at  the  normal 
site  of  the  gall-bladder  a  pear-shaped,  extremely  movable  tumor,  which  is 
elastic  and  rarely  fluctuating.  When  the  ductus  communis  is  obstructed, 
jaundice  is  a  prominent  symptom,  and  the  other  symptoms  which  have  been 
described  under  "  catarrh  of  the  bile-ducts  "  are  present.  Occasionally  the 
tumor  suddenly  disappears,  the  stools  become  dark,  and  the  skin  regains 
its  normal  color.  This  denotes  that  the  obstruction,  which  is, then  com- 
monly a  calculus,  has  been  temporarily  removed.  When  external  openings 
are  formed,  or  rupture  into  the  peritoneal  cavity  occurs,  there  are,  in  the 
latter  case,  evidences  of  a  rapidly  developed  peritonitis,  and,  in  the  former, 
a  remission  of  symptoms  with  a  biliary  fistula  discharging  externally. 

Differential  Diagnosis. — Dropsy  of  the  gall-bladder  may  be  mistaken  for 
abscess,  hydatids,  and  medullary  cancer  of  the  liver.  In  medullary  cancer, 
there  is,  in  nine-tenths  of  the  cases,  an  hereditary  predisposition  or  a  his- 
tory of  cancer  of  the  stomach  or  heart ;  while  in  dropsy  of  the  gall-bladder 
we  get  a  history  of  previous  biliary  catarrh,  or  of  the  passage  of  gall-stones 


GALL-STONES. 


401 


In  cancer,  the  constitutional  symptoms  and  cachexia  are  marked,  while 
persistent  gastric  symptoms,  ascites  and.  hemorrhages  from  mucous  surfaces 
are  absent  in  enlarged  gall-bladder.  Cancer  growths  are  slow,  and  precede 
jaundice  if  it  exists,  while  a  gall-bladder  enlarges  rapidly,  and  follows  jaun- 
dice. Palpation,  in  cancer,  discovers  a  nodular,  uneven,  immovable  mass  be- 
low the  free  border  of  the  ribs.  An  enlarged  gall-bladder  gives  rise  to  a 
smooth,  pear-shaped,  elastic,  or  fluctuating  tumor,  which  is  movable  and 
projects  below  the  free  border  of  the  ribs  in  the  direction  of  the  gall-bladder. 

Prognosis. — This  varies  with  the  cause.  When  inflammatory  products  or 
gall-stones  induce  the  dilatation,  it  is  better  than  when  it  is  due  to  external 
pressure  ;  it  is  always  attended  with  more  or  less  danger. 

Treatment. — The  treatment,  when  it  is  the  result  of  catarrhal  inflamma- 
tion of  the  ducts,  has  already  been  considered.  When  it  is  due  to  the  pres- 
ence of  gall-stones,  the  treatment  appropriate  to  such  conditions  is  indica- 
ted. If  the  enlargement  is  very  great  and  shows  no  indications  of  becoming 
stationary  or  diminishing  in  size,  aspiration  should  be  practised. 

GALL-STOl^ES. 


When  bile  is  retained  in  the  gall-bladder  for  a  long  time  it  decomposes, 
and  the  chelate  of  soda  and  other  bile  salts,  with  cholesterin,  globules  of 
bile-resin,  and  granules  are  precipitated.  These  materials  combine  to  form 
concretions,  which  are  called  Mliary  calculi.  Catarrh  of  the  gall-bladder 
always  accompanies  this  retention  and  decomposition  of  bile. 

Morbid  Anatomy. — The  number  of  gall- 
stones varies  :  single  calculi  are  rare  ;  eight 
thousand  were  found  in  one  case.  Their 
usual  number  is  about  thirty.  Their  size 
varies  from  that  of  a  pin's  head  to  that  of 
a  goose  Qgg.     In  shape  they  are  originally 

spherical,  ovoid,  or  pear-shaped  ;  but  when  ^  Ufe^^^^^^^Jr^W'l!']  A 
there  are  many  and  they  lie  in  contact 
with  one  another  for  a  long  time,  they 
have  numerous  facets  developed  on  their 
surface;  six,  or  even  twelve  are  some- 
times found  on  a  single  calculus.  Warty 
or  '^ mulberry"  calculi  are  occasionally 
met  with  ;  solid  or  hollow  casts  of  the 
larger  bile  ducts,  and  those  which  resemble 
rhomboidal  crystals,  and  the  star-like  cal-  ,,,^,j.  f,, 

culi  with  blunt  points   are   rare   forms  of  Imii'lil'.'!  i^^?^  i> 

gall-stones.     These  calculi  are    commonly 
of  a  light-brown  or  greenish-yellow  color  ;  Fig.  84. 

they  may  be  white,   green,    blue,  red, 
black.     The  specific  gravity  of  fresh  calculi 


Oj.  Sketch  of  a  ftall-Uadder  fitted  With  biliary 
calculi.      This     bladder    contained     260 
gall-stones.     At    B    are    single    calculi 
1        i..r>^  I'l  ^■^^/^  n,       shoiuing  fttcets. 

IS  about  1.02,  and  it  may  reach  1  09,  so  that 
they  will  not  float  in  water. 
26 


In  most  cases  a  fresh  biliary  calculus  can  be 


402 


DISEASES    OF   THE    DIGESTIVE   SYSTEM. 


crushed  between  the  fingers.     Gall-stones  may  form  in  the  smallest  radicle 
of  the  hepatic  duct. 

On  section  a  biliary  calculus  will  rarely  be  found  liomogeneous  through- 
out. Its  substance,  if  it  breaks  down  like  clay,  consists  of  cholesterin  and 
lime.  If  it  has  a  saponaceous  fracture,  it  consists  of  bile-resin  and  choles- 
terin. The  i7igredients  of  biliary  calculi  are  cholesterin,  the  coloring 
matter  of  the  bile,  bile  resin,  lime  salts,  mucus,  epithelium,  biliary  acids, 
margarin  and  traces   of  iron.     A  gall-stone  usually  has   a  nucleus,  an 

external  crust,  and  an  intermediate 
portion.  The  nucleus  may  be 
formed  of  crystals  of  cholesterin, 
cholate  of  lime,  mucus,  a  distoma, 
blood-clot,  round  worm  or  foreign 
body.  Most  nuclei  are  formed  of 
casts  of  the  hepatic  ducts.  Some- 
times small  calculi  form  the  nu- 
clei of  larger  ones,  and  in  very  rare 
instances  multiple  nuclei  are  ob- 
FiG.85.  served.     The  external  crust  varies 

Section  of  a  large  Gall-stone,  showing  successivelayers.  in  thicknCSS  at  difEercnt  points,  and 

^'  fJ^^SoTsfze^''^'™'''^'''^'  Portion.-c.  Nu.  jg  distinguished  from  the  interme- 
diate portion  by  its  color ;  it  is 
commonly  composed  of  cholesterin,  and  its  color  is  due  to  a  mixture  of 
cholesterin  and  biliary  pigment ;  carbonate  of  lime  gives  a  rough,  whitish 
crust.  The  intermediate  structure  usually  consists  of  crystalline  radia- 
tions of  cholesterin,  which  substance  forms  about  eighty  per  cent,  of  all 
gall-stones.  In  this  radiation  can  be  seen  evi- 
dences of  a  lamellar  deposit,  and  sometimes, 
when  there  is  no  radiation,  the  layers  are  concen- 
tric, like  those  of  an  onion.  Again,  light  layers 
of  cholesterin  alternate  with  deeper  ones  of  pig- 
ment ;  gall-stones  are  rarely  found  to  undergo  a 
process  of  erosion  or  disintegration. 

The  gall-bladder  may  be  normal,  or  enlarged 
and  sacculated,  and  is  often  adherent  to  the  in- 
testine, abdominal  wall,  and  adjacent  organs.    Its  -piG.  86. 
walls  are  thickened,  and  there  are  evidences  of  a  crystals  of  dwiestenn  from  gaiu 

s,  showi 


local  or  general  catarrh  ;  late  in  the  disease  there  pS,  'SZi^cmmerZaS- 
may  be  fibroid  contraction  and  calcareous  degen-  ^  ^°°" 
eration  in  the  cystic  walls.  Ulceration  of  the  walls  is  frequently  found  in 
a  bladder  distended  with  calculi.  When  a  gall-stone  becomes  impacted 
near  the  entrance  of  the  ductus  communis  into  the  duodenum,  the  duct 
may  become  enormously  dilated,  and  have  its  walls  thickened,  hyper- 
trophied,  or  calcareously  degenerated. 

When  the  ulcerative  process  extends  through  the  walls  of  the  gall-blad- 
der or  of  the  larger  ducts,  we  may  have  openings  externally  through  the 
abdominal  walls,  usually  about  the  umbilicus,   called   ''biliary  fistulas/' 


GALL-STONES.  403 

These  fistulous  openings  may  lead  from  the  gall-bladder  or  ductus  com- 
munis to  the  duodenum,  stomach,  colon,  right  ureter,  trunk  of  vena  portae, 
pleura,  or  vagina.  When  calculi  are  found  in  the  smaller  ducts,  they  may 
excite  abscess  of  the  liver,  local  fatty  degeneration,  inflammation  of  the 
ducts  or  pylephlebitis.  Either  by  rupture  into  the  cavity,  or  by  extension 
of  inflammation,  peritonitis  may  be  caused  by  the  presence  of  gall-stones. 
'They  may  also  excite  ulceration  and  gangrene  of  the  intestines,  and  there 
are  rare  cases  where  gall-stones,  having  escaped  into  the  intestines,  have 
caused  death  by  intestinal  obstruction. 

Etiology. — Gall-stones  may  be  formed  at  any  period  of  life,  but  are  most 
frequent  after  thirty-five.  A  sedentary,  physically  inactive  life  is  a  great 
factor  in  their  etiology,  and  I  regard  the  greater  prevalence  of  calculi  in 
women  than  in  men  as  due  to  their  less  active  mode  of  life.  Those  who 
have  to  pass  the  greater  part  of  their  lives  in  bed,  and  prisoners  who  are 
confined  in  cells  for  a  long  time,  are  especially  liable  to  the  formation  of 
gall-stones.  A  diet  over-rich  in  fats,  animal  food,  or  alcoholic  beverages, 
predisposes  to  the  formation  of  biliary  calculi.  Cancerous  growths  in  the 
liver  and  gall-bladder,  catarrh  of  the  gall-bladder,  and  in  fact  any  morbid 
condition  interfering  with  the  excretion  of  bile  and  favoring  its  retention 
in  the  gall-bladder,  predispose  to  the  development  of  calculi.  I  have  been 
able  in  a  few  cases  to  make  out  an  hereditary  predisposition  to  the  forma- 
tion of  gall-stones.  The  menstrual  epoch  seems  to  have  some  peculiar 
influence  upon  their  formation. 

Symptoms. — Small  gall-stones,— ''gravel," — in  the  hepatic  ducts  may  cause 
hepatic  congestion,  but  without  enlargement  of  the  liver,  and  give  rise  to 
dull  pain,  a  sense  of  weight  and  constriction  in  the  right  hypochondrium, 
with  nausea  and  the  other  symptoms  of  gastric  disturbance.  Jaundice  in 
these  cases  is  of  rare  occurrence.  When  the  hepatic  and  larger  ducts  are 
occluded,  the  liver  becomes  enlarged,  and  there  is  jaundice,  sharp  pains, 
colic,  and  sometimes  rigors  and  sweats.  If  the  hepatic  duct  is  closed,  the 
gall-bladder  is  normal  in  size.  Fatal  rupture  of  the  ductus  hepaticus 
sometimes,  though  rarely,  is  the  result  of  the  impaction  of  a  calculus  in  it. 

When  small  calculi  are  formed  within  the  gall-bladder,  they  often  cause 
no  inconvenience  ;  when  they  reach  a  large  size  they  excite  inflammation, 
which  may  ultimately  cause  closure  of  the  neck  of  the  gall-bladder.  When 
the  gall-bladder  contains  a  large  number  of  calculi,  violent  physical  exer- 
tion causes  pain,  which  disappears  during  rest.  Sometimes  the  patient  may 
actually  "feel  something  rolling  around  "  in  the  vicinity  of  the  gall-blad- 
der, which  on  a  physical  examination  is  found  enlarged,  more  or  less 
tender,  hard,  and  nodulated,  and  by  a  stethoscopic  examination  gives  to 
the  ear  the  impression  of  a  number  of  pebbles  being  grated  together  in 
water. 

If  biliary  calculi  in  this  situation  cause  perforation  of  the  gall-bladder, 
a  fatal  peritonitis  follows,  or  a  biliary  fistula  may  be  formed  between  the 
gall-bladder  and  the  stomach,  which  will  be  attended  by  sudden  intense 
pain,  with  obstinate  vomiting ;  sometimes  one  or  more  calculi  are  found  in 
•^16  vomited  matter.    The  vomiting  of  a  gall-stone  cannot  be  accounted  for 


404  DISEASES    OF   THE    DIGESTIVE    SYSTEM. 

on  the  ground  of  reversed  peristaltic  action  after  the  stone  has  passed  the 
ductus  communis  into  the  duodenum.  Again,  when  calculi  are  formed  in 
the  gall-bladder,  a  fistulous  opening  into  the  duodenum  may  occur,  followed 
by  vomiting  and  signs  of  a  local  peritonitis,  or  of  intestinal  hemorrhage 
and  haamatemesis.  An  opening  from  the  bladder  into  the  colon  is  exceed- 
ingly rare,  for  the  colon  is  very  movable.  The  symptoms  which  attend 
such  a  perforation  are  obscure.  The  gall-bladder  may  open  into  the  pelvis 
of  the  right  kidney,  and  then  biliary  concretions  will  be  voided  in  the 
urine.  There  is  an  instance  on  record  where,  during  pregnancy,  a  com- 
munication was  made  between  the  gall-bladder  and  the  uterus,  the  discharge 
of  the  calculi  taking  place  at  the  birth  of  the  infant.  If  an  opening  from 
the  gall-bladder  into  the  vena  portse  occurs,  symptoms  of  pytemia  will  de- 
velop very  rapidly.  If  perforation  of  the  left  pleural  cavity  occurs,  fatal 
pleurisy  will  result.  A  single,  rarely  a  double,  fistulous  canal  may  connect 
the  gall-bladder  with  the  external  surface  ;  the  opening  is  usually  near  the 
umbilicus,  and  may  discharge  for  months.  It  may  cicatrize,  and  form  a 
mass  of  fibrous  induration  ;  or  abscesses  may  form  when  a  large  calculus 
plugs  the  fistula  formed  by  previous  perforation.  If  perforation  occurs, 
recovery  is  most  frequent  when  an  external  opening  is  established. 

When  a  gall-stone  has  by  any  means  entered  the  intestinal  canal,  it  may 
be  voided  j^er  anum  or  it  may  lead  to  an  intestinal  obstruction,  ulceration, 
or  gangrene  of  the  intestine.  Obstruction  in  the  common  duct  may  be 
temporary  or  permanent.  If  temporary  there  is  no  Jaundice  ;  if  the 
obstruction  is  complete  and  is  continued  for  twenty-four  hours.  Jaundice  is 
added  to  the  other  symptoms  ;  this  Jaundice  increases  and  is  persistent 
when  the  obstruction  is  permanent. 

Biliary  colic,  or  the  passage  of  gall-stones,  is  the  name  applied  to  the  pe- 
culiar and  severely  painful  symptoms  produced  by  the  passage  of  one  or 
more  calculi  along  some  one  of  the  larger  biliary  ducts.  Usually  after  a 
hearty  meal,  or  after  some  Jolting  exercise,  as  horseback  riding,  the  patient 
is  suddenly  seized  with  a  severe  pain  in  the  epigastrium,  which  is  increased 
by  change  of  position  or  pressure.  Sometimes  slight  rigors,  nausea,  eruc- 
tations, and  attacks  of  yawning  precede  the  colic.  The  pain  is  paroxysmal, 
and  has  its  seat  at  a  point  where  a  line  from  the  right  nipple  to  the  anterior 
superior  spinous  process  of  the  left  ilium  crosses  the  free  margin  of  the 
ribs.  It  radiates  backward  and  upward,  often  as  far  back  as  the  right 
shoulder,  and  may  extend  over  both  hypochondriac  regions.  It  has  been 
described  by  patients  as  boring,  tearing,  piercing,  or  lancinating.  It  is 
often  so  agonizing  that  patients  will  roll  about  the  floor  or  bed,  double 
themselves  up,  and  groan  with  the  pain.  The  face  is  pale  and  covered  with 
cold  sweat,  and  the  pulse  is  very  small.  The  abdominal  muscles  are  rigid, 
and  pressure  greatly  augments  the  pain.  Vomiting,  hiccough,  a  distended 
and  tympanitic  abdomen  are  often  present  during  an  attack,  and  a  weak  or 
feeble  subject  may  faint,  or  pass  into  convulsions,  which  are  epileptiform 
in  character.  Fatal  syncope  has  occurred  during  an  attack  of  gall-stone 
colic.  After  a  few  hours,  sometimes  a  day,  of  exhausting  and  intense  pain, 
the  patient  experiences  sudden  relief,  and  the  pain  entirely  disappears; 


GALL-STONES.  405 

often  the  pain  remits,  but  does  not  cease  until  tlie  calculus  enters  the  du- 
odenum ;  an  exacerbation  occurs  at  the  moment  the  calculus  enters  the  in- 
testinal canal.  Jaundice  is  often  present,  but  not  until  the  attack  has  con- 
tinued for  twenty-four  hours.  During  the  colic,  the  gall-bladder  is  very 
sensitive  to  pressure  ;  during  and  after  the  attack,  the  patient  is  very  much 
exhausted,  and  shows  great  lassitude.  When  jaundice  is  present  the  fseces 
are  clay-colored,  and  the  bowels  are  apt  to  be  constipated.  After  the  at- 
tack, gall-stones  may  be  found  in  the  fseces.  It  is  to  be  remembered  that 
fresh  gall-stones  are  slightly  heavier  than  water.  The  urine,  if  jaundice 
exists,  contains  bile-pigment  and  is  mahogany  in  color;  after  the  colic,  it 
deposits  lithates  and  lithic  acid. 

Diflferential  Diagnosis. — Gall-stone  colic  may  be  mistaken  for  cardialgia, 
intestinal  and  renal  Colic.  Cardialgia  may  be  mistaken  for  biliary  colic 
when  there  is  no  jaundice  present.  In  cardialgia,  pain  comes  on  immedi- 
ately after  eating;  gall-stone  colic  has  no  necessary  connection  with  taking 
food.  In  cardialgia,  the  symptoms  are  referred  to  the  epigastrium  alone, 
while  in  biliary  colic  the  pain  shoots  to  the  right  shoulder  and  back.  In 
cardialgiaj  the  pain  gradually  diminishes ;  in  biliary  colic  it  suddenly 
ceases.  In  gall-stone  colic,  the  presence  of  a  gall-stone  in  the  fseces  is 
pathognomonic. 

in  intestinal  colic,  the  pain  begins  at  the  umbilicus,  and  radiates  over 
the  abdomen ;  in  gall-stone  colic  it  has  its  seat  at  the  free  border  of 
the  ribs,  and  shoots  to  the  back  and  upward  to  the  right  siioulder.  In  in- 
testinal colic,  pressure  relieves  the  pain  ;  in  gall-stone  colic  it  aggravates  it. 
In  intestinal  colic,  the  pain  is  intermittent ;  in  gall-stone  colic  it  is  con- 
stant, though  paroxysmal.  In  intestinal  colic,  jaundice  is  never  present, 
while  it  may  exist  in  biliary  colic.  Intestinal  colic  accompanies  or  is  fol- 
lowed by  diarrhoea  ;  in  gall-stone  colic,  the  fseces  are  firm  and  may  be  clay- 
colored. 

With  renal  colic,  the  pain  shoots  from  the  region  of  the  affected  kidney 
to  the  inner  part  of  the  thigh  and  end  of  the  penis,  and  the  testicle  is 
retracted ;  in  gall-stone  colic,  the  direction  of  the  pain  is  upward  and  back- 
ward. In  renal  colic  there  is  a  constant  desire  to  micturate.  There  is  no 
urinary  disturbance  in  biliary  colic.  In  renal  colic,  after  the  cessation  of 
pain,  pus,  blood  and  epithelium  are  found  in  the  urine ;  after  gall-stone 
colic,  bile-pigment  is  found  in  the  urine.  Jaundice  and  clay-colored  stools 
frequently  containing  gall-stones  may  be  present  in  biliary  colic  ;  they  are 
all  absent  m  renal  colic.  The  gall-bladder  is  very  tender  after  biliary  colic  ; 
while  there  may  be  dull  pains  in  the  region  of  the  loins  after  the  passage  of 
a  renal  calculus. 

Cancer  of  the  head  of  the  pancreas  may  readily  be  mistaken  for  gall-stones 
in  the  common  duct. 

Prognosis. — The  sudden  and  unexpected  terminations  and  varied  conse- 
quences due  to  the  formation  of  a  gall-stone,  render  it  impossible  to 
give  any  rule  for  the  prognosis.  When  a  large  stone,  without  facets, 
has  been  voided,  in  any  manner,  from  the  bile  passages,  the  prognosis  is 
better  than   when   small  facetted   calculi   are  found.      Oft-repeated  at- 


406  DISEASES    OF   THE    DIGESTIVE   SYSTEM. 

tacks  of  biliary  colic  are  bad.  Catarrhal  and  exudative  inflammations  of 
the  bile  passages  are  frequent  accompaniments  of  gall-stones,  and  pulmon- 
ary gangrene,  empyema  and  pneumonia  may  sometimes  complicate.  Though 
it  is  not  necessarily  a  fatal  disease,  death  may  result  from  peritonitis,  ulcer- 
ation, gangrene  or  obstruction  of  the  intestines,  pyaemia,  pylephlebitis,  ab- 
scess of  the  liver,  from  exhaustion  or  from  the  escape  of  bile  through  an 
external  opening.  Death  may  occur  during  an  attack  of  colic,  from  un- 
explained causes. 

Treatment— An  attack  of  biliary  colic  demands  that  attention  be  given, 
first,  to  the  pain  :  this  is  relieved  best  by  opium,  or  morphine,  which  should 
be  given  hypodermically  or  per  rectum,  when  it  is  not  possible  to  give  it 
by  the  mouth.  At  the  same  time  put  the  patient  in  a  tepid  bath,  or 
wrap  warm  cloths  about  the  abdomen.  In  mild  cases,  and  when  opium  is 
contra-indicated,  belladonna  will  be  sufficient,  in  connection  with  anodyne 
fomentations  over  the  region  of  the  gall-bladder.  Inhalations  of  chloro- 
form or  ether  may  be  employed  to  relieve  the  severity  of  the  spasm.  The 
application  of  two  or  three  leeches  over  the  gall-bladder  is  often  followed 
by  relief,  and  diminishes  the  enhances  of  inflammation  of  the  bile-ducts. 
Large  draughts  of  warm  water,  containing  bicarbonate  of  soda,  often  re- 
lieve the  pain  at  the  onset  of  the  attack.  If  the  patient  shows  signs  of 
collapse,  stimulants,  ammonia  and  brandy  should  be  administered. 

A  patient  who  has  passed  gall-stones  must  be  put  on  a  restricted  diet : 
wines  or  fats  should  be  prohibited ;  exercise  in  the  open  air,  and  an 
entire  change  in  the  mode  of  life  are  important.  Mineral  waters,  whether 
by  giving  an  alkaline  bile  or  by  an  increase  in  the  amount  secreted,  cause 
the  number  of  gall-stones  to  diminish,  and  also  allow  them  to  be  passed 
with  less  pain.  A  prolonged  course  of  alkaline  mineral  water  has  been 
found  the  best  remedy  against  the  formation  of  gall-stones.  Ether,  tur- 
pentine, chloroform  and  hydrate  of  chloral  have  been  proposed  as  specifics, 
it  being  thought  that  they  have  the  power  of  dissolving  the  gall-stones. 

FUNCTIONAL    DERANGEMENTS    OF   THE     LIVER. 

The  terms  biliousness  and  torpid  liver '  were  more  frequently  used 
twenty  years  ago  than  now.  Many  indeed  have  denied  that  any  such  con- 
ditions exist,  but  there  is  undoubtedly  a  variety  of  symptoms  (such  as 
constipation,  yellow  and  itching  skin,  dark  urine,  headache,  lassitude, 
furred  tongue,  bitter  taste  in  the  mouth,  etc.,  etc.),  which  can  properly 
be  classed  as  functional  derangement  of  the  liver.  Writers  describe  ten 
varieties,  I  shall  only  briefly  consider  those  which  are  the  most  common. 
In  these  functional  hepatic  derangements  there  are  no  morbid  appearances 
in  the  organ  itself  to  account  for  the  symptoms. 

Etiology. — Functional  derangement  of  the  liver  may  be  due  to  struct- 
ural diseases  (e.  g.,  cirrhosis,  abscess,  and  acute  yellow  atrophy),  to  dyspep- 
sia, both  gastric  and  intestinal,  to  atony  of  the  bowels,  to  obstructive  diseases 
of  the  heart  and  lungs,  to  the  specific  fevers,  malaria  especially,  to  faulty 
diet,  the  food  being  too  rich  in  hydrocarbons,  to  the  daily  use  of  alcoholic 


FUNCTIONAL   DERANGEMENTS   OF   THE    LIVER.  407 

beverages,  especially  ales  and  sweet  wines  and  liquors  (not  from  whiskey, 
brandy  or  gin,  unless  in  the  form  of  a  hot  toddy  or  sweet  punch),  to  badly 
ventilated,  hot,  and  moist  apartments,  sedentary  habits,  a  deficient  supply 
of  oxygen,  a  warm  climate  (India,  for  instance),  and  finally  to  anxiety  and 
prolonged  mental  labor.  In  many  cases  the  tendency  to  "  liver  complaint " 
is  inherited  ;  the  children  of  the  diabetic  or  gouty  are  very  prone  to  func- 
tional derangements  of  the  liver. 

Symptoms. — Few  cases  are  exactly  alike.  The  prominent  symptoms 
which  usually  first  attract  the  patient's  attention  are  anorexia,  a  bitter 
taste  in  the  mouth  (due  to  taurocholic  acid  in  the  blood),  flatulency, 
"acidity"  and  pyrosis.'  The  tongue  is  large,  pale,  and  flabby,  with  inden- 
tations of  the  teeth  along  its  edges.  It  may  be  white,  showing  elongated 
papillae-like  villi.  The  faeces  are  pale,  unless  they  have  remained  long  in 
the  large  bowel,  when  they  are  blackish.  Constipation  and  diarrhoea  may 
alternate.  When  bile  is  in  excess  the  faeces  are  semi-fluid  and  contain  more 
bile  than  normal.  It  is  a  question  whether  melaena  ever  occurs  as  a  sole 
vesult  of  hepatic  derangement,  but  hemorrhoids  are  very  common.  There 
is  often  a  sense  of  weight,  fulness,  tightness,  burning,  or  even  actual  pain 
over  the  liver.  Those  who  suffer  from  functional  derangement  of  the  liver 
may  become  very  fat,  or  they  may  emaciate  rapidly.  Emaciation  results 
either  from  deficient  production  of  bile  or  from  derangement  of  the  glyco- 
genic function  of  the  liver.  Bile  may  saturate  the  texture  of  the  body  for 
months,  and  yet  no  symptoms  of  blood  poisoning  occur  so  long  as  the 
eliminating  function  of  the  kidneys  is  not  impaired. 

A  deficient  elimination  of  cholesterin  may  give  rise  to  "  biliousness," 
and  thus  be  a  part  of  functional  derangement  of  the  liver.  ^  "  Cholester- 
gemia  "  is  said  to  be  associated  with  obstinate  constipation,  and  Dr.  Murchi- 
son  regards  this  as  "torpor  of  the  liver,"  or  at  least  one,  and  a  frequent, 
form  of  it.  Lithates  and  pigments  deposited  in  the  urine  should  al- 
ways be  regarded  as  signs  of  functional  derangement  of  the  liver  arising 
from  causes  sometimes  temporary  and  sometimes  permanent.  Murchison 
says  "  lithuria,  like  glycosuria,  must  be  classed  as  a  functional  derangement 
of  the  liver,"  and  he  calls  the  antecedent  morbid  blood  state  litlimmia.  In 
many,  who  by  heredity  are  predisposed  to  "liver  troubles,"  the  liver  is 
capable  of  performing  its  healthy  functions  only  under  the  most  favorable 
circumstances,  and  functional  derangement  is  at  once  induced  by  articles 
of  diet  which  most  persons  can  easily  digest. 

"  Gouty  dyspepsia,"  "latent  gout,"  suppressed,  anomalous  or  irregular 
gout,  are  terms  which  in  many  instances  should  be  dismissed,  and  "func- 
tional derangement  of  the  liver  "  substituted  for  them,  for  the  symptoms 
which  have  been  ascribed  to  them  occur  in  those  who  neither  inherit  nor 

•  The  functions  of  a  healthy  liverare.  fir»t.  sanguinification  ;  second,  the  re-combination  of  albuminous 
matter  derived  f r  om  the  food  and  tissues  ;  Hard,  the  formation  of  urea  and  lithic  acid,  both  of  which  are 
afterward  eliminated  by  the  kidneys  ;  fourth,  the  secretion  of  bile,  most  of  which  is  reabsorbed  ;  fifth,  the 
glycogenic  function.  Among  the  most  constant  results  of  functional  hepatic  derangement  is  imperfect 
formation  of  urea  evidenced  by  the  deposit  of  lithic  acid  or  lithates  in  the  urine.  When  a  great  part  of  the 
liver  has  been  destroyed  by  disease  the  urea  is  lessened  or  disappears  from  the  urine.  Destructive 
nitrogenous  metamorphosis  is  unquestionalily  an  impoitant  function  of  the  liver. 

a  Virchow'8  Archiv.  Bd.  65,  p.  410.    1875. 


408  DISEASES    OF   THE   DIGESTIVE    SYSTEM. 

ever  have  shown  any  gouty  tendencies/  Biliary  calculi  (cholesterin  and 
bile-pigment)  may  result  from  hepatic  derangement.  Frerichs  regards 
the  coincidence  of  gall-stones  and  urinary  calculi  in  the  same  individ- 
ual as  purely  accidental.  Since  the  kidneys  eliminate  certain  products 
of  the  liver,  renal  derangements  may  be  a  consequence  of  faulty  hepatic 
digestion.  Hence  Murchison  places  lithfemia  among  the  chief  causes  of 
Bright's  disease  of  the  kidneys.^  Many  suppose  that  albuminuria  may  be 
induced  by  functional  derangement  of  the  liver,  independent  of  any  mor- 
bid kidney  change,  and  this  accords  with  the  modern  theories  of  albu- 
minuria. 

After  the  functions  of  a  liver  have  been  interfered  with  for  some  time, 
the  structure  of  the  liver  is  very  liable  to  become  diseased.  Fatty  liver  and 
cirrhosis  are  common  sequelae,  and  their  causes  are  closely  allied  to  func- 
tional derangement  of  the  liver.  ^  Senile  decay  (sometimes  premature), 
fatty,  calcareous  and  atheromatous  arterial  changes  are  very  frequently 
direct  sequelae  of  functional  hepatic  derangement.  It  is  questionable 
whether  the  rheumatic  hyperinosis  is  due  to  non-destruction  of  fibrin  in 
the  liver,  as  Murchison  would  have  us  believe.  But  the  anaemia  of  this 
cachexia  is  undoubtedly  often  due  to  it. 

Symptoms. — Those  who  suffer  from  torpor  of  the  liver  complain  of  lassi- 
tude, drowsiness,  pain  in  the  limbs,  dull  pain  in  the  right  hypochondrmm 
often  shooting  up  the  right  side  to  the  shoulder,  and  not  infrequently  of 
sciatica  and  lumbago.  Circumscribed  patches  of  skin,  usually  on  the  ex- 
tremities, often  become  hot  and  burning.  Headache,  usually  frontal,  is 
very  common,  and  when  induced  by  indiscretions  in  diet  it  is  called  "  bil- 
ious "  or  "  sick  headache,"  and  the  patient  states  that  he  has  had  another 
^'bilious  attack."  Dizziness,  dim  vision,  and  muscae  volitantes  are  fre- 
quent results  of  over-eating  in  those  whose  livers  are  functionally  deranged. 
Convulsions,  paresis  and  cramps  in  the  legs  are  rare,  but  they  may  occur. 
Melancholia,  insomnia,  hypochondriasis,  irritability  of  temper,  and  moodi- 
ness are  consequences  of  deranged  liver-function.  The  term  '^  bilious 
temperament "  has  passed  into  common  use.  In  some  cases  there  are  car- 
diac palpitations,  an  irritable,  irregular  or  even  intermittent  pulse,  cold 
extremities,  and  slight  lividity  or  cyanosis,  and,  according  to  Sir  James 
Paget,  venous  thrombosis  may  result  from  functional  derangement  of  the 
liver.  Paget  and  Murchison  regard  lithaemia,  i.  e.,  functional  derange- 
ment of  the  liver,  as  causing  acute  urethritis  (non-specific)  in  many  in- 
stances.* 

After  prolonged  hepatic  derangement  psoriasis,  lichen,  eczema,  lepra, 
urticaria,  boils,  carbuncles,  pigment-spots  (popularly  called  liver  spots), 
and  pruritus  are  liable  to  appear.  Frequently  the  same  individual  will 
within  a  year  have  three  or  four  of  the  above-named  skin  diseases  as  a 
direct  result  of  functional  derangement  of  the  liver. 

1  Gout  is  one  result  of  lithsemia  ;  and  urinary  calculi  are  frequently  but  an  exhibition  of  functional  de- 
rangement of  the  liver. 

2  Clin.  Lee.  Dis.  Liver,  pp.  572-573. 

*  Trousseau  describes  a  chronic  gouty  hepatitis  that  comes  under  this  head. 
•*  British  Med.  Journal,  1875,  i.  70L 


FUNCTIONAL   DERANGEMENTS   OF   THE   LIVEE.  409 

The  diagnosis  is  made  by  a  consideration  of  the  conditions  and  habits  of 
life  of  the  patient,  the  sequence  of  symptoms,  its  long  duration,  inter- 
rupted by  "acute  bilious  attacks,"  and  by  the  exclusion  of  structural 
hepatic  and  kidney  disease. 

The  prognosis  depends  on  the  cause  :  if  due  to  diet,  a  cure  can  be  easily 
effected  if  the  individual  obeys  instructions  ;  if  hereditary,  a  definite  prog- 
nosis should  never  be  given. 

Treatment, — The  treatment  in  the  main  is  dietetic  and  hygienic ;  all 
starchy  and  saccharine  substances  should  be  avoided  or  taken  in  small 
quantities.  Wines  and  ales  should  be  wholly  discarded.  Fresh  air,  sea- 
air  especially,  and  moderate  exercise,  attention  to  the  cutaneous  functions, 
and  abandonment  of  severe  mental  work  should  be  recommended.  Min- 
eral waters  (Hunyadi  Janos  and  Pullna  especially)  should  be  freely  drunk 
at  all  times.  Kochelle,  Glauber's  and  Epsom  salts  are  beneficial.  The 
bowels  should  always  be  kept  freely  opened.  Alkalies,  especially  the  car- 
bonate of  soda,  are  always  of  service.  Chlorine,  bromine  and  iodine  are 
useful  in  some  cases,  and  the  bromide  of  potash  is  highly  beneficial 
when  combined  with  ammonium  chloride.  The  mineral  acids  are  apt  to 
do  more  harm  than  good,  although  in  works  on  materia  medica  the  nitro- 
muriatic  acid  is  said  to  be  almost  a  specific  for  torpor  of  the  liver.  ^  Acetic 
extract  of  colchicum  is  indicated  in  gouty  and  rheumatic  subjects.  Tar- 
axacum was  formerly  thought  to  have  a  powerful  effect  on  the  liver  ;  its 
only  action  is  that  of  a  cathartic. 

Mercury,  in  the  form  of  bhie  pill,  is  more  efficacious  in  affording  tem- 
porary relief  in  the  so-called  bilious  attacks  than  any  other  drug.  It  is 
denied  by  many  that  mercury  is  a  cholagogue  ;  still  there  are  few  who  do 
not  recommend  "  blue-mass "  in  functional  hepatic  disturbances,  and 
although  experimental  therapeusis  shows  that  mercury  simply  increases  the 
biliary  secretion  by  acting  on  the  upper  portion  of  the  small  intestine,  yet 
there  must  be  some  action  of  mercury  now  unknown,  which  makes  it  the 
most  reliable  drug  in  functional  derangement  of  the  liver.  It  is  suggested 
that  by  promoting  or  in  some  way  influencing  the  disintegration  of  albu- 
men the  liver  is  relieved,  and  thus  the  effects  of  an  overtasked  or  naturally 
feeble  organ  are  overcome.  A  dose  of  calomel  at  night,  followed  in  the 
morning  by  a  saline  purge,  relieves  both  the  hepatic  and  urinary  symptoms. 
Podophyllum  (^  gr.  of  the  resin)  given  with  cannabis  indica  or  henbane  is 
by  many  thought  equal  to  mercury.  Tonics  and  opium  are  to  be  expressly 
forbidden  ;  iron  does  positive  harm. 

'  Prof.  Rutherford  states  that  in  dogs  it  has  no  effect  upon  the  bile  secretion. 


410  DISEASES   OF   THE   DIGESTIVE   SYSTEM. 


DISEASES  OF  THE  PANCREAS. 

Diseases  of  the  pancreas  are  almost  always  secondary  to,  or  associated 
with,  disease  of  neighboring  organs  ;  I  shall  briefly  consider  them  under  the 
following  heads  : 

I.  Acute  and  Chronic  Pancreatitis.    IV.   Cysts  of  the  Pancreas. 

II.  Degenerations,  Fatty  and  Waxy.      V.   Calculi  and  Parasites. 

III.  Morbid  Groiuths  :~Cancer,  Tubercle,  Sarcoma,  and  Gummata. 

ACUTE    PAI^CKEATITIS. 

This  is  a  rare  affection,  and  is  chiefly  of  interest  from  a  pathological 
standpoint. 

Morbid  Anatomy. — The  pancreas  is  enlarged,  hyperaemic  and  firmer  than 
normal.  When  the  hyperemia  is  intense,  small  hemorrhages  occur  in  its 
substance.  In  febrile  diseases  the  whole  organ  is  seen  to  have  undergone 
diffuse  parenchymatous  changes.  In  suppurative  pancreatitis  there  i& 
either  a  diffuse  infiltration  of  pus,  or  numerous  small  abscesses  are 
formed.  In  some  instances  the  surrounding  connective-tissue  and  lym- 
phatic glands  are  involved  and  the  pancreas  is  surrounded  by  pus.  Pus 
may  form  in  the  ducts,  acini,  or  the  cellular  tissue.  Pancreatic  abscesses 
may  open  into  the  stomach,  peritoneal  cavity,  duodenum,  or  externally. 

Etiology. — This  is  obscure  ;  it  may  possibly  be  caused  by  acute  alcoholis- 
mus  and  by  blows  over  the  organ.  It  occurs  more  frequently  in  men  than 
in  women.  Acute  tuberculosis,  typhoid  fever,  pyaemia,  septicaemia,  and 
parotitis  (from  metastasis)  are  sometimes  followed  by  it. 

Symptoms. — These  are  obscure  and  variable,  the  most  constant  is  colicky 
or  deep-seated  dull  pain  over  the  pancreas,  shooting  to  the  back  and  shoul- 
der. Fever,  dyspnoea,  anorexia,  and  vomiting  of  a  thin,  viscid  fluid,  some- 
times containing  bile,  are  nearly  always  present.  There  is  great  thirst  and 
restlessness.  The  pulse  is  rapid,  the  pain  is  greatly  increased  by  firm  press- 
ure over  the  pancreas,  and  symptoms  of  collapse  are  often  present.  There 
is  marked  anxiety  and  depression  from  its  onset.  The  bowels  are  consti- 
pated. In  some  cases  of  metastatic  pancreatitis  the  stools  are  watery  and 
like  saliva.     In  these  cases  diarrhoea  is  generally  present. 

Differential  Diagnosis. — Hepatic  diseases  are  excluded  by  the  absence  of 
jaundice.  But  it  is  frequently  impossible  to  exclude  acute  gastritis  or  duo- 
denitis except  by  the  site  and  distribution  of  the  pain,  and  by  the  presence 
of  fever  and  the  irregular  heart-action. 

Prognosis. — It  usually  terminates  in  death  after  a  very  rapid  course.  It 
may  become  chronic,  terminating  in  abscess  or  induration. 

Treatment. — Rest,  a  mild,  fluid  diet,  and  anodynes  are  the  only  means  to 
be  employed  in  its  treatment.  The  eflficacy  of  ice  or  poultices  over  the 
epigastrium  is  questionable. 


CHRONIC   PANCREATITIS.  411 


CHRONIC     PANCEEATITIS. 


MorMd  Anatomy. — The  changes  are  identical  with  cirrhotic  processes 
elsewhere,  e.  g.,  in  the  liver  and  spleen.  This  process  may  lead  to  complete 
disappearance  of  the  gland  substance  or  to  closure  of  the  duct  and  the  con- 
sequent formation  of  cysts.  The  head  of  the  gland  is  most  involved  in  the 
cirrhotic  process.  Interstitial  hemorrhages  may  occur,  or  little  cysts  may 
stud  the  gland.  Adhesions  generally  bind  the  organ  to  the  adjacent  parts. 
In  chronic  su]3purative  pancreatitis  the  pus  may  infiltrate  the  gland,  or 
there  may  be  one  or  more  small  abscesses.  The  contents  of  the  latter  may 
become  cheesy  or  calcareous. 

Etiology. — The  causes  are  similar  to  those  of  cirrhosis  of  the  liver  ; — cal- 
culi, the  pressure  of  an  adjacent  tumor,  or  extension  of  inflammation  from 
adjacent  parts,  especially  ulcers  of  the  stomach  and  duodenum.  It  may  be 
associated  with  syphilitic  infection. 

Symptoms. — The  only  symptoms  that  could  lead  to  a  diagnosis  are  fatty 
stools,  intercurrent  mellituria,  neuralgic  pains,  and  the  presence  of  a  trans- 
verse tumor  in  the  epigastrium.  Abdominal  dropsy  and  signs  of  intestinal 
obstruction  may  be  caused  by  the  pressure  of  the  hard  gland  which  acts  as 
an  abdominal  tumor.     A  peculiar  cachexia  is  usually  present. 

FATTY    DEGENEEATION. 

Two  forms  are  recognized  : 

I.  Fatty  infiltration  of  the  connective-tissue  investing  the  gland  and  sur- 
rounding the  acini,  where  the  new  growth  of  fat-tissue  causes  atrophy  and 
disappearance  of  the  gland  cells  by  its  pressure.  The  whole  gland  may 
look  like  a  mass  of  fat  with  only  a  central  canal. 

II.  Fatty  degeneration  affects  the  gland  cells  and  ultimately  destroys 
them ;  the  acinous  structure  is  preserved  in  the  midst  of  a  soft,  flaccid  and 
wasted  gland.  A  more  or  less  abundant  fatty  emulsion  is  found  in  the 
ducts. 

Etiology. — The  first  form  occurs  in  general  obesity  and  in  chronic  alco- 
holismus.  The  second  is  due  to  the  same  causes,  and  a^so  to  heart  disease 
or  obstruction  to  the  outflow  of  the  pancreatic  secretion. 

WAXY    DEaENEEATION. 

The  vessels  of  the  pancreas  and  the  cells  of  the  acini  may  exhibit  amy- 
loid change.     This  is  the  rarest  disease  of  the  pancreas. 

CANCER    OF   THE   PANCREAS. 

This  is  the  most  frequent  form  of  primary  disease  of  the  pancreas.  In 
one  hundred  cases  of  cancer  the  pancreas  was  found  involved  in  five. 
Scirrhus   is   the   most  frequent  variety  of  cancer  found   here.     Pancre- 


412  DISEASES    OF   THE    DIGESTIVE    SYSTEM. 

atic  cancer  tends  to  involve  adjacent  organs ;  the  bile-duct  and  left 
ureter  may  be  pressed  upon  and  obstructed,  and  the  mass  may  com- 
press the  splenic  or  superior  mesenteric  vessels,  the  vena  portge,  the  in- 
ferior cava,  or  even  the  aorta.  The  cancer  may  ulcerate  into  neighboring 
structures.  The  canal  of  Wirsung  may  be  obstructed,  and  then  cysts  will 
form. 

Etiology. — It  occurs  chiefly  in  men  after  the  fortieth  year ;  further  than 
this  little  can  be  said. 

Symptoms. — -The  symptoms  are  varied,  because  the  neighboring  organs 
are  so  frequently  and  extensively  involved.  Neuralgic  and  paroxysmal 
pain,  is  an  important  symptom.  The  presence  of  a  tumor  with  enlarge- 
ment of  the  adjacent  lymphatic  glands  is  essential  for  a  diagnosis.  Vom- 
iting, jaundice,  dyspepsia,  dropsy,  oedema  of  the  feet, — all  may  be  present. 
Sometimes  the  stools  may  be  fatty.  There  may  be  constipation  or  diarrhoea, 
or  the  two  may  alternate.     The  general  symptoms  are  those  of  anaemia. 

Differential  Diagnosis. — A  pancreatic  cancerous  tumor  may  pulsate  and 
have  a  bruit  conducted  from  the  aorta,  and  therein  simulate  aortic  aneu- 
rism. 

Prognosis. — Cancer  of  the  pancreas  usually  causes  death  within  a  year. 
The  treatment  is  symptomatic. 

Small-celled  Sarcoma  usually  occurs  as  a  melanotic  tumor.  It  is  very 
rare,  and  clinically  indistinguishable  from  carcinoma. 

Tuberculosis  of  the  pancreas,  secondary  to  that  of  the  lungs  and  peri- 
toneum, develops  in  the  connective-tissue  between  the  acini.  Caseous 
nodules  are  oftener  met  with  than  diffuse  miliary  tubercles.  It  is  denied 
that  the  pancreas  ever  is  involved  in  acute  miliary  tuberculosis. 

Syphilitic  Gummata  are  usually  found  in  connection  with  syphilitic  in- 
terstitial pancreatitis.  They  have  been  described  by  Eostan  and  Rokitansky. 
It  is  believed  that  more  frequent  examinations  of  the  gland  would  reveal  a 
larger  number  of  gummata. 

CYSTS   IN   THE   PANCEEAS. 

Cysts  in  the  pancreas  are  due  to  retention  of  the  pancreatic  secretion, 
from  obstruction  of  the  duct  by  calculi,  or  from  external  pressure  of  tumors. 
Hemorrhagic  cysts  are  very  rarely  found.  When  the  duct  is  closed  near 
its  mouth,  the  canal  and  its  branches  look  like  a  bunch  of  currants.  Atro- 
phy and  cirrhosis  of  the  gland  may  result  from  these  cysts,  which  at  first 
contain  a  normal  secretion  which  afterward  becomes  purulent,  hemorrhagic, 
or  albuminous.  Hgematoidin  crystals,  lime-salts  and  urea  have  been  found 
in  these  cysts.  The  cyst-walls  thicken  from  connective-tissue  develop- 
ments. 

Etiology. — Any  tumor,  either  of  the  pancreas  itself  or  of  neighboring 
parts,  calculi,  cirrhosis  of  the  pancreas,  or  angular  displacements  of  the 
pancreas  may  cause  it. 

Symptoms. — The  only  symptom  is  the  discovery  of  a  smooth  lobulated  tu- 
mor in  the  region  of  the  pancreas. 


HYPEREMIA    OF   THE   SPLEEN".  4-13 


CALCULI    OF   THE   PANCEEAS. 

Calculi  of  the  pancreas  are  usually  gray-white,  rounded  masses  of  car- 
bonate or  phosphate  of  lime.  They  are  situated  anywhere  in  the  pancreas, 
are  either  free  or  embedded,  vary  in  size  from  microscopic  dust  to  a  walnut, 
and  also  vary  in  number,  but  rarely  exceed  fifteen  or  twenty.  Laminated 
protein  concretions  are  described  by  Virchow. 

Etiology. — Anomalies  in  the  pancreatic  juice  itself,  catarrh  of  the  ducts, 
and  retention  cysts  are  the  most  frequent  causes. 

Symptoms. — There  will  be  no  symptoms  except  when  interstitial  inflam- 
mation is  excited,  or  the  common  duct  is  pressed  on  so  as  to  cause  jaundice. 
Round  worms  have  been  found  in  the  pancreas. 

DISEASES  OF  THE  SPLEEN. 

Diseases  of  the  spleen  will  be  considered  in  the  following  order  : 

I.  Hyper wmia.  IV.  Degenerations,  Waxy  or 

II.  Inflammation,  or  Splenitis,  includ-  Sago-spleen. 

ing  EmhoUsm  and  Infarction.  V.  Morbid  Growths. 

III.  Hypertrophy,  or  Chronic  Enlarge-    YI.  Parasites, 
ment. 

HYPEREMIA. 

Splenic  hypersemia  may  be  active  or  passive. 

Morbid  Anatomy. — The  accumulation  of  blood  in  the  vessels  and  inter- 
vascular  spaces  of  the  spleen,  causes,  the  enlargement  which  occurs  in 
hypersemia  ;  the  organ  may  be  increased  to  five  or  six  times  its  normal  size 
and  yet  retain  its  normal  shape.  Its  color  is  darker  than  normal,  its  cap- 
sule is  usually  tense  and  shining,  and  its  consistency  is  often  diminished, 
being  sometimes  as  soft  as  pulp.  A  microscopic  examination  shows  no  new 
elements  in  the  spleen,  only  an  increase  in  the  number  of  its  normal  ones. 

Etiology. — A  physiological  congestion  of  the  spleen  takes  place  after  every 
meal.  A  pathological  engorgement  occurs  :  (1)  when  there  is  any  ob- 
struction to  the  venous  flow  from  the  spleen,  as  happens  in  certain  cardiac, 
hepatic,  and  pulmonary  diseases  ;  (2)  in  the  acute  infectious  diseases,  such 
as  typhus,  malarial  fevers,  and  pyaemia ;  (3)  at  the  menstrual  epoch,  de- 
pending upon  an  abnormality  of  menstruation  ;  (4)  as  the  result  of  inju- 
ries and  inflammation,  when  the  hypersemia  will  be  circumscribed. 

Symptoms. — The  symptoms  of  simple  hypersemia  of  the  spleen  are  usually 
not  well  marked  ;  the  patient  may  complain  of  a  sense  of  weight  in  the 
left  hypochondrium  and  more  or  less  tenderness  on  pressure  over  the 
splenic  region.  Palpation  and  percussion  will  discover  a  tumor  in  this 
region  of  greater  or  less  size  ;  this  tumor  extends  obliquely  downward  to- 
ward the  umbilicus,  rises  and  falls  with  each  respiratory  movement,  and 
has  the  outline  of  the  spleen,  with  the  characteristic  notches  on  its  lower 
rounded  edge.     The  pale  and  anaemic  appearance  often  met  with  in  those 


414  DISEASES    OF   THE    DIGESTIVE    SYSTEM. 

having  splenic  hypersemia  is  dne  to  the  overloading  of  the  spleen  with 
blood  at  the  expense  of  the  rest  of  the  body,  rather  than  to  any  change  in 
the  composition  of  the  blood. 

Prognosis. — The  prognosis  is  good,  although  in  certain  rare  cases  death 
has  occurred  from  rupture  of  the  distended  organ. 

Treatment. — The  treatment  is  directed  rather  to  the  disease  which  gives 
rise  to  the  hyperaemia  than  to  the  condition  itself.  Quinine  in  large  doses 
has  been  found  in  most  instances  to  remove  the  splenic  congestion  and 
relieve  the  accompanying  symptoms. 

IlSrFLAMMATIO]!^    OF    THE    SPLEEIST. 

{Splenitis.) 

Primary  splenitis  is  exceedingly  rare  ;  it  is  generally  due  to  injury,  em- 
bolism, or  infarction,  especially  when  occurring  with  pyaemia  or  septic 
diseases.  It  may  occur  in  connection  with  morbid  growths  and  abscesses 
in  the  spleen.  There  is  a  condition  of  the  spleen  resembling  cirrhosis  of 
the  liver,  called  by  some  chronic  or  interstitial  splenitis. 

Morbid  Anatomy. — The  anatomical  arrangement  of  the  splenic  arteries 
renders  the  spleen  a  favorable  seat  of  metastatic  inflammation.  In  acute 
splenitis  a  part  or  all  of  the  organ  may  be  attacked  ;  the  involved  portions 
are  congested  and  swollen;  and  the  peritoneum  over  them  is  injected  and 
covered  with  a  fibrinous  exudation.  The  spleen  is  of  a  deep  purplish  color 
and  friable,  being  broken  down  as  easily  as  coagulated  blood.  When  a 
hemorrhagic  infarction  is  formed  in  the  spleen,  it  is  usually  without  rupt- 
ure of  the  blood-vessels,  and  is  encircled  by  a  zone  of  sero-hemorrhagic 
infiltration.  These  infarcts  are  at  first  of  a  brownish  red  color  and  of  a 
firm  consistency  ;  later,  they  become  dirty  yellow  in  color,  and  either  under- 
go fatty  degeneration  and  become  absorbed,  or  remain  as  cheesy  and 
calcareous  masses  ;  or,  lastly,  the  infarctions  soften  and  abscesses  form, 
wliich  are  single  or  multiple,  sometimes  fusing  together,  and  again  in- 
creasing by  peripheral  extension. 

In  a  few  instances  these  abscesses  are  found  incapsulated  in  a  proliferation 
of  connective-tissue,  but  in  most  cases  this  is  not  the  case  ;  the  connective- 
tissr.e  breaks  and  a  large  sac  is  formed  filled  with  pus  ;  as  much  as  thirty 
pounds  have  been  found  in  one  of  these  sacs.  At  last  the  capsule  becomes 
mvoWed,  perisplenitis  is  set  up,  and,  adhesions  having  formed  between  the 
spleen  and  adjacent  parts,  the  abscess  may  open  into  some  adjacent  organ, 
as  the  stomach  and  colon,  into  the  thorax  or  abdominal  cavity,  or  an 
external  fistulous  opening  may  be  formed.  Localized  suppurative  inflam- 
mation of  the  small  Malpighian  bodies  in  the  spleen  has  been  found  to  occur 
in  typhus  and  other  fevers. 

"  Necrotic  splenic  softening "  may  occur  from  an  infarction  caused  by 
atheroma  and  endocarditis :  here  the  latter  is  not  ulcerative.  In  these 
cases  the  lymph-cells  in  the  fibrinous  reticulum  of  the  clot  become  fatty, 
and  then  they  mass  themselves  into  spheres  of  fat-crystals.  The  whole 
infarction  softens  and  becomes  a  fatty,  pulpy  mass.    The  capsule  over  such 


INFLAMMATION    OF  THE   SPLEEN.  415 

a  spot  is  villous  and  appears  covered  with  vegetations.  A  gangrenous  con- 
dition of  the  left  lower  lobe  of  the  lung  has  been  caused  by  such  a  form  of 
metastatic  splenitis  ;  with  the  intense  engorgement  which  accompanies 
acute  splenitis,  hemorrhage  into  the  organ  may  occur,  the  capsule  may 
be  ruptured,  and  a  fatal  peritonitis  may  be  induced. 

Chronic  splenitis  is  the  result  of  long-continued  splenic  congestion.  The 
spleen  is  of  a  brownish-red  or  slate  color,  its  capsule  is  thickened,  and 
covered  with  very  firm  vegetations  and  new  connective-tissue  formations, 
which  are  highly  vascular.  The  organ  is  more  or  less  pigmented,  owing 
to  the  pigmentary  deposit  in  tlie  endothelia  of  the  veins.  This  whole  proc- 
ess is  analogous  to  that  which  occurs  in  cirrhosis  of  the  liver,  except 
that  a  spleen  which  is  the  seat  of  interstitial  inflammation  is  larger  than 
normal. 

Etiology. — It  is  very  doubtful  whether  idiopathic  splenitis  ever  occurs. 
Blows  and  severe  muscular  exercise  are  said  to  have  caused  it.  Splenitis 
is  usually  metastatic,  the  embolic  plug,  the  result  of  endocarditis  and 
valvular  disease,  most  often  having  its  origin  in  the  left  heart,  although  it 
may  be  induced  by  thrombotic  changes  in  the  aorta.  Earely  the  embolus 
comes  from  the  lungs,  having  passed  through  the  pulmonary  vein  and  left 
heart.  In  pyaemia  and  its  allied  states  hemorrhagic  infarctions  of  the  sj^leen 
are  of  frequent  occurrence,  and  a  similar  condition  has  been  noticed  in 
Bright's  disease  and  in  the  infectious  diseases.  Extension  of  inflammation, 
especially  the  result  of  ulcerative  changes  in  the  stomach,  is  an  occasional 
cause  of  acute  splenitis. 

Symptoms. — These  are  vague ;  often  there  is  nothing  except  the  local 
changes  to  direct  attention  to  the  spleen  as  the  seat  of  disease.  There  is 
no  pain,  unless  the  capsule  is  involved ;  if  pain  is  present  it  will  be  in- 
creased by  a  full  inspiration.  There  may  be  hectic  fever,  but,  as  splenitis 
is  secondary  to  some  febrile  disease,  the  fever  may  be  attributed  solely  to 
the  latter.  There  may  be  a  sense  of  weight  and  pain  in  the  left  hypo- 
chondrium,  and  even  shooting  pains  in  the  left  shoulder  and  arm. 

Vomiting  of  blood  and  pus,  or  the  simultaneous  passing  of  blood  and  pus 
with  the  fgeces  is  indicative  of  rupture  of  a  splenic  abscess  into  the  stomach; 
this,  however,  is  an  exceedingly  rare  event.  The  recognition  of  a  splenic 
abscess  will  depend  upon  its  attaining  a  sufficient  size  to  form  an  appreciable 
fluctuating  tumor  in  the  splenic  region. 

Physical  Signs.— Inspection  will  show  a  marked  enlargement  in  the  splenic 
region. 

Palpation  may  discover  a  fluctuating  mass.  The  ''notchings"  on  the 
anterior  margin  of  the  spleen  are  usually  readily  made  out.  The  mass  is 
more  or  less  movable,  unless  adhesions  have  formed  between  the  splenic 
capsule  and  adjacent  parts. 

Differential  Diagnosis.— Acute  splenitis  may  be  mistaken  for  cancer  of 
the  stomach,  disease  of  the  pancreas,  or  hepatic  disease,  especially  that  in- 
volving the  left  lobe  of  the  liver.  Ooarian  tumors  will  rarely  be  con- 
founded with  it.  In  stomach  diseases  the  absence  of  fever,  the  vomiting, 
pain  and  discomfort  dependent  on  the  ingestion  of  food,  the  long  dura- 


416 


DISEASES   OF   THE   DIGESTIVE   SYSTEM. 


tion,  and  the  peculiar  haematemesis  will  readily  distinguish  them  from 
acute  splenitis. 

Cancer,  abscess,  or  cirrhosis  of  the  liver  would  give  physical  signs  which 
could  hardly  be  confounded  with  those  of  acute  splenitis — the  position  of 
the  area  of  dulness  would  of  itself  be  sufficient  for  a  diagnosis.  The  con- 
dition of  the  stools,  the  urine,  and  the  color  of  the  skin  are  often  sufficient 
to  lead  to  a  diagnosis  of  hepatic  diseases.  If  the  tumor  is  of  considerable 
size,  the  diagnosis  of  splenic  abscess  can  always  be  safely  reached  by  the 
aid  of  the  exploring  trochar. 

Prognosis. — Suppurative  splenitis  is  always  a  dangerous  disease,  and  is 
rarely  recovered  from,  even  when  an  extensive  opening  is  established. 

Treatment. — No  special  treatment  is  called  for  unless  the  pain  is  severe, 
when  anodynes  and  fomentations  may  be  used.  When  an  abscess  can  be 
made  out  it  should  be  treated  in  the  same  manner  as  an  hepatic  abscess. 


HYPERTKOPHY    OF   THE    SPLEElf. 

(Enlarged  Spleen.) 

Enlargements  of  the  spleen  are  of  two  kinds  :  (1)  acute  and  transient ; 
and  (2)  chronic  and  permanent.  The  first  class  occurs  in  f fevers,  e.  g., 
typhoid  ;  the  second  from  long-continued  and  repeated  congestion,  as  in 
chronic  malarial  infection. 

Morbid  Anatomy. — In  acute  enlargement,  the  spleen  may  reach  four  or 
five  times  its  normal  size.  The  capsule  becomes  thin  and  tense.  The 
spleen  pulp  varies  in  consistence,  and  may  even  be  completely  diffluent ; 
its  color  varies  from  a  bright  pink  to  a  red  black.  Hemorrhagic  foci  in- 
dependent of  embolism  may  occur.     Many  lymphoid  cells  contain  one  or 

more  red  corpuscles,  the  latter  either  being 
normal  in  size  or  smaller  (1-8000  of  an 
inch).  This  microscopical  appearance  is 
best  marked  in  typhoid  fever.' 

Chronic  Enlargement  of  the  Spleen. — The 
organ  is  enlarged  without  any  obvious 
change  in  texture  ;  there  is  an  increase  in  all 
its  elements,  and  it  acquires  a  more  or  less 
fleshy  consistency.  It  sometimes  reaches  a 
very  great  size,  filling  the  left  side  of  the 
abdominal  cavity  from  the  ribs  to  the  pelvis; 
it  may  be  increased  to  twenty  pounds  in 
weight.  Its  normal  shape  is  unchanged  and 
the  notches  on  its  edges  are  distinctly  re- 
FiG.  87.  tained.    In  rare  cases  chronic  enlargement 

Diagram  illustrating  the  abdominal  areas  of  ii.'i  nii„„i- 

plrcussiou-duinessin  Splenic  Enlargement,  occurs  as  a  multiple  nodular  hyperplasia. 


1  The  color  of  the  spleen  in  congestive  enlargement  is  always  paler  than  that  of  the  other  viscera,  on 
account  of  the  presence  of  a  larger  quantity  of  white  blood  corpuscles  than  are  found  elsewhere  in  the 
body. 


AMYLOID    DEGENERATION   OF   THE   SPLEEN".  417 

Etiology. — Acute  enlargement  of  the  spleen  is  met  with  most  frequently 
in  acute  infectious  diseases.  Many  regard  the  accumulation  of  micrococci 
in  the  spleen  and  their  retention  within  the  splenic  protoplasm  as  a  cause 
of  acute  swelling.'  Of  all  the  diseases  that  cause  sudden  and  gi-eat  enlarge- 
ment of  the  sj)leen,  the  most  frequent  are  typhoid  and  intermittent  fevers. 

Chronic  enlargement  of  the  spleen  is  frequently  associated  with  cirrhosis 
and  other  chronic  affections  of  the  liver,  and  with  chronic  cardiac  and 
pulmonary  diseases  that  induce  long-continued  or  repeated  congestion  of 
the  organ.  But  chronic  malarial  infection  is  its  most  common  and  constant 
cause.  Chronic  enlargement  of  the  spleen  is  part  of  the  history  of  leucocy- 
thsemia ;  it  is  never  idiopathic.  Chronic  mercurialism  disposes  to  en- 
largement of  the  spleen. 

Symptoms. — Acute  enlargement  of  the  spleen  is  jDart  of  the  history  of 
acute  general  diseases ;  its  natural  symptoms  are  few  :  pain  on  pressure, 
dyspnoea,  and  an  increased  area  of  splenic  dulness  are  the  most  constant 
and  prominent.  Chronic  enlargement  of  the  spleen  is  attended  by  no 
symptoms  except  the  physical  signs  of  sjDlenic  enlargement. 

Treatment. — Quinine  and  iron  are  always  indicated,  but  they  should  be 
given  alternately  and  never  at  the  same  time;  they  may  be  combined  with 
arsenic  and  cod-liver  oil.  In  malarial  hypertrophy  of  the  spleen  the  patient 
should  reside  in  a  non-malarial  district.  Inunctions  of  the  biniodide  of 
mercury  are  strongly  recommended  by  English  authorities,  but  I  have 
never  seen  any  beneficial  results  from  their  use. 

AMYLOID    DEGENEEATIOlSr    OF    THE   SPLEEl^. 

{Sago  Spleen.) 
s 

Waxy  or  lardaceous  degeneration  of  the  spleen,  also  called  the  "sago 
spleen,"  is  a  part  of  a  general  cachexia  in  which  other  organs  are  primarily 
involved. 

Morbid  Anatomy. — It  occurs  in  two  forms ;  in  one  it  is  limited  to  the 
Malpighian  bodies,  in  the  other  it  is  diffused.  In  both  the  organ  is  en- 
larged, rounded  and  doughy.  The  capsule  is  tense,  but  not  thickened,  and 
is  usually  smooth  and  glistening. 

On  section  the  first  variety  presents  the  appearance  of  a  number  of  sago 
granules,  the  Malpighian  bodies  being  enlarged  to  1-25  or  1-12  of  an  inch 
in  diameter,  and  filled  with  waxy  material  which  gives  the  characteristic 
reaction  with  iodine.  The  corpuscles  through  which  the  arteries  pass  are 
involved,  but  the  wall  of  the  in-going  vessels  may  remain  normal.  The 
"adenoid"  or  "cytogenic"  tissue,  the  lymph-corpuscles,  and  the  capilla- 
ries of  the  spleen  are,  however,  infiltrated  with  waxy  material,  massed  to- 
gether, and  channelled  by  healthy  capillaries.  The  veins  near  the  diseased 
Malpighian  bodies  are  sometimes  involved.  In  diffuse  lardaceous  degenera- 
tion, the  spleen,  on  section,  is  pale,  homogeneous,  glistening  and  anaemic ;, 
all  the  vessels,  the  trabeculse,  and  capsule  are  involved.^ 

Etiology. — The  causes  of  waxy  spleen  are  identical  with  those  of  waxy 

'  MohIct  and  Birch-Hirschfeld. 

2  Rokitansky  regards  this  form  as  but  a  later  stage  of  "  sago  spleen." 

26 


418  DISEASES    OF   THE    DIGESTIVE    SYSTEM. 

liver  ;  it  is  met  with  in  chronic  bronchitis  with  bronchiectasis,  in  phthisis, 
chronic  Bright's  disease,  chronic  peritonitis,  cirrhosis  of  the  liver,  chronic 
alcoholismus,  and  intermittent  fever.  Sago  spleen  frequently  accompanies 
chronic  intestinal  catarrh  in  children.  Syphilis  is  probably  its  most  fre- 
quent cause. 

Symptoms. — As  the  liver  and  intestines  are  generally  involved  in  the  same 
change,  the  waxy  cachexia  will  not   be  characteristic  of  splenic  changes. 
There  will  be  anaBmia,  accompanied  by  a  great  increase  in  the  area  of  splenic 
dulness.     Late  in  the  disease  there  is   usually   anorexia,   vomiting,    and 
hemorrhages,  but  it  is  not  possible  to  determine  to  what  extent  these  vari- 
ous symptoms  depend  on  the  splenic  disease. 
The  diagnosis  rests  mainly  on  its  etiology. 
The  prognosis  is  unfavorable- 
Treatment. — It  never  calls  for  independent  treatment.    Niemeyer  regards 
iodide  of  iron  as  the  most  efficacious  drug.     Our  first  efforts  should  be  to 
cure  or  remove  the  causes  or  conditions  which  have  led  to  its  development, 
and  to  improve  the  general  condition  of  the  patient  by  tonics,  hygienic 
measures,  and  a  carefully  regulated,  nutritious  diet. 

MORBID    GEOWTHS    OF   THE    SPLEEN. 

Cancer  of  the  spleen  is  very  rare  ;  it  may  be  secondary  to  cancer  of  the 
stomach,  mamma,  liver,  or  brain.  When  disseminated,  it  is  generally  of 
the  encephaloid  variety.  It  may  develop  in  the  hilum  by  contiguity  of  can- 
cer in  the  other  organs.  Secondary  isolated  growths  may  be  scattered 
through  its  substance,  or  in  many  more  instances  it  may  be  the  seat  of  pri- 
mary cancer.  In  pigment-cancer  of  the  spleen,  the  organ  rapidly  enlarges 
to  nearly  double  its  size  ;  in  other  forms  it  is  but  slightly  enlarged.  The 
symptoms  are  obscure  and  of  little  clinical  importance. 

Gummata,  or  syphilitic  tumors  of  the  spleen,  are  only  met  with  in  con- 
nection with  amyloid  changes,  and  are  accompanied  by  similar  develop- 
ments in  the  liver.  Syphilis  thus  shows  itself  in  the  spleen  in  one  of  four 
-ways, — waxy  degeneration,  gummata,  inflammation  of  the  spleen- pulp,  or 
hypertrophy  of  the  spleen  with  increase  in  interstitial  tissue.  Syphilomata 
are  of  no  clinical  importance. 

Tubercles  in  the  spleen  develop  in  the  spleen-pulp.  The  nodules  may  be 
small  and  gray,  or  large,  yellow  and  cheesy.  In  acute  tuberculosis,  the 
spleen  rapidly  enlarges  as  the  tubercles  develop.  Tubercular  formations 
are  very  common  in  young  children.  Yellow  tubercular  masses,  varying 
in  size,  are  frequently  found  in  the  spleen  in  connection  with  similar  form- 
ations in  other  parts  of  the  body ;  occasionally  they  soften  and  form  ab- 
scesses. The  small  splenic  vessels  are  often  clogged  with  lymph  and  fibrin. 
Tubercles  of  the  spleen  cannot  be  recognized  during  life. 

Cysts  have  been  found  in  the  spleen.  They  are  associated  with  cystic 
developments  in  the  liver  and  omentum. 

Hydatids,  when  occurring  in  the  spleen,  usually  accompany  similar  de- 
velopments in  the  liver  and  peritoneum.     The  enlargement  of  the  spleen 


MOEBID    GROWTHS   OF   THE    SPLEEN.  419 

may  cause  a  sense  of  weight  in  the  splenic  region,  and  if  the  splenic  capsule 
becomes  inflamed  their  development  will  be  accompanied  by  sharp  pains  in 
the  left  side.  An  hydatid  tumor  in  the  spleen  usually  fluctuates,  but  it 
rarely  gives  the  hydatid  fremitus.  An  exploratory  puncture  decides  its 
character. 

The  prognosis  and  treatment  are  the  same  as  in  hydatids  of  the  liver. 


SECTION    III. 

DISEASES  OP  THE  HEART,  BLOOD-VESSELS  AND  KIDNEYS. 

Diseases  of  the  heart  may  be  classified  as  follows  : 

I.    Pericarditis.  VIII.  Cardiac  Atrophy. 

II.  Endocarditis.  IX.  Cardiac  Thrombosis. 

III.  Valvular  Lesions.  X.  Cardiac  Aneurisin. 

IV.  Cardiac  Hypertrophy.  XI.  Morbid  Growths  and  Parasites. 
V.   Cardiac  Dilatation.  XII.  Tuberculosis  of  the  Pericardium. 

VI.  Myocarditis.  XIII.    Cardiac  Neuroses. 

VII.   Cardiac  Degenerations.         XIV.  Hydro-pericardium. 
XV.  Pneumo-hydro-perioardium. 

PEEICAEDITIS. 

The  pericardium  is  a  fibro-serous  sac  ;  the  fibrous  layer  is  firmly  adherent 
to  the  diaphragm  and  is  attached  to  the  large  vessels  about  two  inches 
above  the  heart ;  it  forms  a  closed  sac.  The  serous  layer  is  in  close  appo- 
sition to  the  internal  surface  of  the  fibrous  layer,  is  reflected  from  the  large 
vessels,  and  completely  invests  the  heart  itself.  This  shut  serous  sac,  when 
diseased,  behaves  in  all  respects  like  the  pleura.  Inflammation  of  the 
pericardium  may  be  acute  or  chronic.  Chronic  pericarditis  is  usually  the 
sequel  of  acute. 

ACUTE    PERICARDITIS. 

Acute  pericarditis  is  perhaps  more  frequently  overlooked  than  any  other 
acute  disease,  for  its  subjective  symptoms  are  rarely,  if  ever,  well  marked. 

Morbid  Anatomy. — At  its  commencement,  the  serous  surface  of  the 
pericardium  becomes  more  or  less  reddened,  with  here  and  there  ecchy- 
motic  spots  of  irregular  shape.  The  reddening  may  be  circumscribed  about 
the  roots  of  the  great  vessels,  or  it  may  involve  the  whole  visceral  and 
parietal  pericardium.  The  reddening  is  due  to  hyperaemia  of  the  sub- 
serous capillary  vessels.  With  the  redness  there  are  swelling  and  infil- 
tration of  its  serous  and  sub-serous  tissue.  Following  the  hyperaemia 
and  infiltration  the  epithelium  desquamates  and  the  membrane  loses  its 
natural  glistening  appearance.  If  the  inflammatory  action  is  continued, 
an  exudation  is  poured  out  on  its  free  surface  :  it  may  consist  of  but  a  few 
shreds  of  lymph,  or  a  fibrinous  layer  may  cover  the  whole  of  its  car- 
diac or  parietal  surface.    It  varies  in  thickness  from  a  line  to  three-fourths 


ACUTE   PERICARDITIS. 


431 


of  an  inch,  or  even  more.  This  exudation  is  composed  of  fibrin,  a  few  pua 
cells  and  detached  epithelia  ;  it  causes  the  free  surface  of  the  pericardium 
to  assume  a  roughened  appearance ;  it  is  this  appearance  which  has  given 
rise  to  the  expression  "hairy  heart."  When  there  is  only  a  very  small 
amount  of  plastic  exudation,  it 
will  usually  be  confined  to  that 
portion  of  the  pericardium  which 
covers  the  blood-vessels. 

With  or  following  the  plastic 
exudation  there  may  be  a  fluid 
effusion  which  varies  in  quantity 
and  in  quality.  It  may  be  sero- 
albuminous,  sero-fibrinous,  hem- 
orrhagic, or  purulent.  It  varies  in 
quantity  from  three  fluid  ounces 
to  several  pints.  In  most  instances 
it  will  be  sero-fibrinous  in  char- 
acter ;  it  is  rarely  sero-albuminous. 
When  it  is  small  in  amount  it  will 
gravitate  to  the  most  dependent 
portion  of  the  pericardial  sac. 
When  it  is  large  in  quantity,  the  ^^^  gg 

entire  pericardial  sac  is  filled,  and  Diagram  illustrating  the  Morbid  Anatomy  and  Physical 
thp       adiaCPuf       lllUJir  fissno     oom-  Signs  of  Sero-plastic  Pericarditis. 

tne     aajacent     lung-tissue    com       a.  Line  of  diaphragm. 

pressed,  and  the   surfaces  of  the     b.  Heart.  ^     .     ^.  , 

r  ^  .  C  Serous  effusion  into  Imver  portion  of  pericardial  sac. 

membrane    have    a   reticulated    or       B.  Plastic  exudation  upon  both  viscerai  and  parietal 

_      .  layers  of  the  pericardium. 

honey-combed  appearance,     it  is 

always  turbid  from  the  molecular  fibrin   suspended  in  it,   and  may  be 

yellow,  green,  brown,  or  red  in  color. 

Hemorrhagic  pericarditis  is  rare,  except  with  purpura,  scurvy,  cancer  of 
the  lung,  and  tuberculosis.  In  this  variety  the  line  of  demarcation  between 
the  false  membrane  and  the  pericardium  is  very  indistinct. 

Tuberculous  pericarditis  is  attended  by  the  development  of  tubercles  in 
the  pericardium  and  in  the  substance  of  the  heart ;  the  blood  effused  forms 
ochre-colored  masses  in  the  exudate.  The  exudations  and  effusions  in 
pericarditis  may  all  undergo  absorption.  The  serous  effusion  is  removed 
rapidly,  the  hemorrhagic  with  less  facility,  the  plastic  and  purulent  with 
still  greater  difficulty.  The  fluid  disappears  first,  then  the  granular,  and 
last  the  coagulated  fibrin.  The  lymph  and  purulent  exudations  may 
undergo  fatty  metamorphosis  and  be  absorbed,  or  remain  in  a  cheesy, 
mortar-like  mass,  and  finally  become  calcareous  after  the  absorption  of  the 
more  fluid  portion  of  the  degenerated  mass.  The  calcareous  material  with 
connective-tissue  formations  may  form  ossified  plates  upon  the  surface  of 
the  heart  and  pericardium. 

New  connective-tissue  formations  may  take  place  upon  the  surface  of 
the  pericardium  under  the  layer  of  plastic  exudation  ;  if  the  inflamma- 
tory process  is  continued  sufficiently  long,  these  are  converted  into  a  firm 


422  DISEASES   OF   THE    HEART. 

fibrinous  mass,  causing  either  a  permanent  thickening  of  the  pericardium, 
or  adhesions  between  its  two  surfaces.  Sometimes  these  adhesions  are  by 
bands  stretching  across  from  one  portion  to  the  other ;  at  others  there  is 
complete  agglutination  of  the  two  surfaces,  and  an  entire  obliteration  of  the 
pericardial  cavity  ;  in  either  case  more  or  less  complete  organization  takes 
place.  The  adhesions  about  the  base  are  the  most  dense.  Those  at  the 
apex  are  drawn  out  into  fibrinous  strings. 

With  infiammatory  changes  in  the  visceral  pericardium,  there  will  be 
more  or  less  inflammatory  change  developed  in  the  muscular  tissue  of  the 
heart  immediately  beneath  the  pericardium.  If  the  pericarditis  has  been 
extensive  and  long  continued,  the  walls  of  the  heart  will  become  weakened  ; 
indeed,  they  are  somewhat  weakened  in  every  attack  of  pericarditis.  The 
development  of  myocarditis  will  be  considered  more  fully  under  its  appro- 
priate head.  Dilatation  of  the  cavities  of  the  heart  may  take  place  in  con- 
sequence of  the  weakened  condition  of  the  cardiac  walls,  and  cardiac  hy- 
pertrophy may  be  developed  as  a  result  of  this  weakening  and  dilatation. 
Upon  post-mortem  examination  not  infrequently  smooth,  opaque,  pearly- 
white  patches  are  found  upon  the  external  surface  of  the  heart.  They  are 
slightly  elevated,  variable  in  size,  have  irregular  sinuous  margins,  and  are 
usually  located  on  the  anterior  surface  of  the  ventricle.  As  to  the  nature 
of  these  spots  there  has  been  considerable  discussion.  These  "  milhy 
patches  "  are,  however,  nothing  more  than  growths  of  white,  laminated  con- 
nective-tissue with  elastic  fibres,  immediately  beneath  the  cardiac  pericar- 
dium, and  indicate  the  previous  existence  of  a  localized  pericardial  inflam- 
mation which  has  been  recovered  from  without  adhesions.  In  rare  instances 
the  two  surfaces  of  the  pericardium  will  become  firmly  agglutinated  through- 
out their  entire  extent,  and  the  pericardial  sac  will  remain  completely  oblit- 
erated, and  if  attempts  are  made  to  separate  them  the  cardiac  muscle  is 
torn.  Under  such  circumstances,  the  movements  of  the  heart  carry  with 
them  the  pericardium,  and  with  each  cardiac  pulsation  there  is  a  lifting  of 
the  diaphragm. 

Etiology. — Acute  pericarditis  rarely  occurs  as  a  primary  affection,  but  is 
usually  secondary,  or  is  developed  during  the  course  of  some  other  disease. ' 
It  may  be  produced  by  injuries  to  the  pericardium, — by  extension  of  inflam- 
mation from  neighboring  organs,  as  when  it  occurs  with  pleuro-pneumonia, 
pleurisy,  necrosis  of  the  sternum,  ribs,  rupture  of  abscesses,  etc.  It  occurs 
most  frequently  in  connection  with  that  class  of  diseases  which  depend  upon 
well-recognized  blood -changes  ;  under  this  head  are  included  pericarditis 
which  accompanies  acute  rheumatism,  Bright's  disease,  acute  infectious 
diseases,  as  scarlatina,  small-pox,  typhus  and  typhoid  fever,  pneumonia, 
tuberculosis,  syphilis,  chronic  alcoholismus,  etc.  Occasionally  it  is  devel- 
oped in  connection  with  scurvy  and  purpura  ;  then  it  is  of  the  hemorrhagic 
variety.  Cancer  of  the  lung  and  tuberculosis  also  cause  *' hemorrhagic 
pericarditis." 

When  pericarditis  occurs  in  connection  with  pyaemia  and  septic  condi- 
tions, the  effusion  is  purulent  in  character  and  accumulates  rapidly.     It  is 

1  A  case  of  "  Idiopaihic  Pericarditis.''''    Glasgow  Med.  Journal,  Sept.,  1878. 


ACUTE    PERICARDITIS.  423 

of  most  frequent  occurrence  in  connection  with  acute  articular  rheumatism, 
Bright's  disease  and  pneumonia.  Often  in  rheumatic  pericarditis,  the  ar- 
ticular rheumatic  development  occurs  subsequent  to  the  pericarditis.  In 
rheumatism  it  is  an  early,  in  Bright's  disease  a  late  occurrence.  Pericar- 
ditis occurring  in  connection  with  scarlet  fever  is  especially  liable  to  be 
overlooked,  for  its  presence  is  not  revealed  until  a  large  fluid  effusion  takes 
place. 

Symptoms. — The  symptoms  cf  acute  pericarditis  are  rarely  well  defined. 
It  is  very  difficult  to  give  a  clear  description  of  the  rational  symptoms  which 
attend  its  development,  for  it  is  usually  associated  with  some  other  affection 
whose  symptoms  tend  to  obscure  those  of  pericarditis  ;  more  than  one-half 
of  the  cases  are  latent,  and  come  on  so  insidiously  that  they  would  go  un- 
recognized were  it  not  for  the  physical  signs  which  attend  them. 

The  two  prominent  rational  symptoms  are  pain  in  the  precordial  region 
and  cardiac  palpitation.  The  joain  is  usually  confined  to  the  precordial 
space  ;  occasionally  it  involves  the  brachial  plexus,  and  extends  down  the 
left  arm  ;  under  such  circumstances  it  is  probably  reflex  in  character.  The 
pain  may  be  increased  in  severity  by  pressing  the  left  lobe  of  the  liver 
against  the  diaphragm.  It  varies  in  severity  ;  sometimes  it  is  very  slight, 
again  it  is  of  a  sharp,  lancinating  character,  and  sufficiently  severe  to  de- 
mand immediate  relief.  With  the  pain  there  is  always  more  or  less  cardiac 
palpitation,  a  dry  irritable  cough,  and  a  sense  of  constriction  over  the  whole 
chest,  with  more  or  less  dyspnoea  ;  the  intensity  of  the  dyspnsea  will  vary 
with  the  amount  of  the  fluid  effusion.  When  the  effusion  is  considerable 
and  there  is  orthopnoea  the  patient  becomes  restless  and  the  countenance 
assumes  an  anxious  expression,  with  a  painful  look  of  suffering  somewhat 
characteristic  ;  he  assumes  the  half-sitting  posture,  leaning  somewhat 
toward  the  left  side.  Lying  on  the  back  with  the  head  elevated,  is  the 
position  usually  preferred  when  the  effusion  is  not  large.  The  face  is  often 
livid. 

At  first  the  pulse  is  full  and  strong,  ranging  from  90  to  120  beats  in  the 
minute,— after  the  fluid  effusion  has  taken  place,  it  becomes  feeble,  sup- 
pressed and  sometimes  delayed.  If  the  effusion  is  abundant  the  pulse  has 
a  tendency  to  become  irregular,  and  not  infrequently  intermitting ;  it  is 
always  out  of  proportion  to  the  activity  of  the  heart  and  strongly  dicrotic. 
The  temperature  usually  rises  one  or  two  degrees,— in  some  cases  it  may 
rise  as  high  as  10^°  F.  In  fatal  cases  the  temperature  falls  toward  the 
close  of  life,  sometimes  below  normal.  Jaundice  sometimes  occurs  and 
headache  and  dizziness  are  frequently  present ;  in  the  severe  forms  of  the 
disease  there  is  often  delirium,  the  patient  sometimes  becoming  so  furious 
as  to  require  restraint ;  at  other  times  it  is  low  and  muttering.  The  de- 
lirium is  often  accompanied  by  delusions,  tetanic  or  clonic  spasms,  and  in 
rare  cases  convulsions  occur,  rapidly  passing  into  coma  and  followed  by 
death.  Usually  Avhen  the  fluid  effusion  takes  place,  the  acuteness  of  the 
symptoms  subsides,  and  the  patient  experiences  a  sensation  of  op23ression 
referaljle  to  the  precordium, — he  is  disinclined  to  make  any  movement,  for 
the  least  motion  of  the  body  gives  rise  to   a  sinking  sensation   with  a 


424  DISEASES   OF  THE   HEAET. 

tendency  to  syncope.  Painful  hiccough,  accompanies  this  symptom.  The 
patient  is  now  constantly  in  danger  of  sudden  and  fatal  syncope  from  press- 
ure of  the  pericardial  accumulation  upon  the  heart.  Some  maintain  that 
sudden  and  fatal  syncope  never  occurs  in  primary  pericarditis,  but  that  it 
is  met  with  only  after  several  attacks  have  occurred,  and  more  or  less  ex- 
tensive pericardial  adhesions  have  taken  place.  This  is  not  necessarily  the 
case,  for  whenever  large  fluid  effusions  are  developed,  with  the  attendant 
weakening  of  the  cardiac  walls  from  superficial  myocarditis,  patients  are 
constantly  in  danger  from  sudden  syncope. 

The  severity  of  the  symptoms  in  pericarditis  corresponds  to  the  intensity 
of  the  inflammation  and  the  amount  of  the  effusion  ;  if  the  inflammation 
is  slight  and  the  effusion  moderate,  the  plastic  exudation  predominating, 
none  of  these  symptoms  will  be  present,  and  the  subjective  symptoms  will 
only  serve  to  attract  attention  to  the  heart  as  the  seat  of  disease. 

The  subjective  symptoms  in  many  cases  of  pericarditis  being  so  obscure, 
often  altogether  wanting,  the  physical  signs  become  all  important.  In  fact, 
in  all  cases  of  acute  articular  rheumatism,  for  the  first  two  weeks  ifc  is  an 
imperative  duty  each  day  to  make  a  careful  physical  examination  of  the 
heart,  especially  if  its  action  becomes  irritable  and  the  apex-beat  is  increased 
in  force.  Delirium  in  acute  rheumatism  ought  at  once  to  direct  attention 
to  the  heart.  The  same  care  in  examination  should  also  be  exercised  in 
Bright's  disease  when  convulsions  or  coma  occur  ;  and  in  severe  acute  infec- 
tious disease  the  heart  will  often  be  found  implicated. 

Physical  Signs. — These  vary  with  its  different  stages.  In  the  early  stage 
the  only  sign  furnished  by  inspection  and  palpation  is  an  irritable,  turbulent, 
forcible,  and  sometimes  irregular  action  of  the  heart. 

Palpation  gives  a  friction-fremitus  in  a  few  cases.  There  is  no  change 
in  the  normal  area  of  precordial  dulness. 

On  auscultation  the  first  positive  physical  signs  of  pericarditis  are  the 
pericardial  friction  sounds.  They  may  be  grazing,  rubbing,  or  creaking 
in  character.  These  friction  sounds  may  be  single  or  double,  and  may 
accompany  the  heart  sounds  or  occur  independently  of  them.  They  are 
always  superficial  in  character  and  are  generally  restricted  to  the  precordial 
space.  Their  point  of  maximum  intensity  is  usually  at  the  junction  of  the 
fourth  rib  with  the  sternum  on  the  left  side  ;  occasionally  they  will  not  be 
audible  at  this  point,  but  will  be  heard  over  the  large  vessels  at  the  base  of 
the  heart  ;  when  this  is  the  case  it  indicates  that  only  a  small  extent  of  the 
pericardium  is  involved,  and  that  the  inflammatory  changes  are  confined 
to  that  portion  of  the  pericardium  which  covers  the  large  vessels.  When 
absent,  as  they  sometimes  are,  their  absence  may  be  due  to  softness  of  the 
fibrin,  feebleness  of  heart  action,  or  alteration  in,  or  abnormal  position  of, 
the  lungs.  Pericardial  friction  sounds  may  be  increased  in  intensity  by 
changing  the  position  of  the  patient :  when  the  body  is  thrown  forward 
-the  heart  will  be  brought  nearer  to  the  anterior  wall  of  the  chest  and  the 
friction  sound  will  be  more  distinctly  audible.  These  friction  sounds  will 
also  be  increased  in  intensity  by  a  full  inspiration,  for  the  distended  lung 
will  press  the  two  pericardial  surfaces  together  and  thus  intensify  the  rub- 


ACUTE    PERICARDITIS. 


425 


bing  sounds.  In  this  way  a  single  friction  sound  may  become  double. 
These  sounds  are  usually  of  short  duration,  disappearing  after  a  few  hours, 
or  at  most  in  a  few  days. 

As  soon  as  the  stage  of  effusion  is  reached  and  liquid  is  poured  into  the 
pericardial  sac,  the  friction  sounds  disappear  and  another  class  of  physical 
signs  are  developed  which  mark  the  effusive  stage  of  pericarditis. 

Inspection  now  shows  a  diminution  in  the  respiratory  movements  over 
the  precordial  space,  and  if  the  pericardial  sac  is  distended — especially  in 
children  and  young  persons — there  will  be  arching  forward  of  the  precordial 
region  ;  this  arching  forward  may  extend  from  the  second  to  the  sixth  in- 
tercostal space.  On  lying  down  the  apex-beat  often  becomes  more  promi- 
nent. This  bulged  portion  does  not  move  with  the  rest  of  the  thorax  in 
respiration. 

Palpation  shows  the  point  of  the  apex-beat  to  be  raised  and  carried  to  the 
left  of  its  normal  position.  This  raising  of  the  apex-beat  is  never  actual 
— only  apparent— for  as  the  fluid  accumulates  the  apex  is  jDUshed  further 
back  from  the  anterior  wall  of  the  chest,  and  the  portion  of  the  heart  that 
is  nearest  to  the  chest  wall  appears  to  strike  it  and  cause  an  "apex- 
beat,"  which  is  nearer  the  base  the  more  fluid  there  is  in  the  pericardium 
■ — a  simj)le  physical  phenomenon  dependent  upon  the  "  conicity  "  of  the 
heart  and  the  pear-shaped  sac  in  which  it  hangs.  The  cardiac  excitement 
and  friction-fremitus  which  might  have  been  j^resent  before  the  effusion 
occurred  disappear,  and  if  the  effusion  is  large  the  apex-beat  becomes  im- 
perceptible. Sometimes  in  extreme  pericardial  effusion  an  undulating 
impulse  is  communicated  to  the  hand  as  it  rests  on  the  chest  walls,  by 
the  action  of  the  heart  in  the  fluid. 

On  percussion,  if  the  pericardium  is  distended  with  fluid,  the  area  of 
precordial  dulness  is  found  to  be 
increased  in  every  direction,  espe- 
cially laterally  and  vertically.  The 
shape  of  the  enlarged  area  corre- 
sponds to  the  pyramidal  form  of 
the  pericardial  sac.  Eecent  experi- 
ments prove  that  the  triangular 
or  pyramidal  dulness  is  not  due  to 
the  shape  of  the  pericardial  sac, 
but  to  the  retraction  of  the  edges 
of  the  lung.  In  a  lateral  direc- 
tion the  precordial  dulness  may 
extend  from  one  nipple  to  the 
other ;  it  may  extend  upward  as 
high  as  the  second  or  the  first  rib, 
or  above  the  clavicle,  and  down- 
ward somewhat  beyond  the  nor- 
mal limits.  A  small  amount  of 
effusion  isdenoted  by  an  increase  ^^'^'  ^^' 

,1  .,,1        „,i  ,.,  Diagram  illustrating  the  Pliysical  Signs  of  Pericarditis 

in  the  width  OI  the  precoraial  area  when  the  ijencardial  sac  is  distended  with  fluid. 


426  DISEASES   OF  THE   HEART. 

of  dulness  at  the  lower  portion  of  the  precordial  region ;  if  emphysema 
exists  the  changes  in  the  area  of  dulness  will  be  less  marked. 

Upon  auscultation  an  absence  of  respiratory  murmur  is  noticed  over  all 
that  space  which  is  normally  occupied  by  lung  tissue,  the  lungs  being 
pushed  to  the  right  and  left  by  the  distended  pericardial  sac.  The  friction 
sound  which  may  have  been  present  before  the  occurrence  of  the  effusion 
disappears  and  the  heart  sounds  become  feeble  or  indistinct.  In  most 
cases  the  fluid  disappears  rapidly  within  a  week  or  ten  days. 

Stage  of  Absorption. — As  recovery  takes  place  and  the  effusion  is  absorbed, 
the  area  of  precordial  dulness  decreases  and  the  pericardial  surfaces  again 
come  in  contact  and  the  friction  sound  reappears,  the  heart  sounds  will  be- 
come more  distinct,  the  apex  will  assume  its  normal  position,  the  cardiac 
impulse  will  regain  its  normal  force,  and  the  respiratory  and  vocal  sounds  are- 
again  heard  over  the  space  formerly  occupied  by  the  distended  pericardium. 
If  the  anatomical  changes  developed  in  the  substance,  and  on  the  surface  of 
the  pericardium,  have  been  extensive,  as  the  two  pericardial  surfaces  come 
together  they  may  become  firmly  adherent  and  all  motion  between  the 
heart  and  pericardium  cease.  This  condition  cannot  be  recognized  by  phys- 
ical examination — it  is  only  to  be  inferred  from  the  history  of  the  case. 
If  one  who  has  had  all  the  symptoms  of  pericardial  effusion  which  has 
been  followed  by  a  friction  sound  that  has  gradually  disappeared,  leaving 
a  slight  intermittent  action  of  the  heart,  suffers  on  active  exertion  from  a 
sense  of  constriction  above  the  precordial  region,  it  may  be  inferred  that 
the  two  surfaces  of  the  pericardium  have  become  adherent.  Pericardial  ad- 
hesions, whether  general  or  in  bands,  may  undergo  absorption,  and  if  a  sec- 
ond attack  of  pericarditis  is  not  developed  motion  between  the  two  surfaces 
will  be  restored,  and  the  only  evidence  of  the  disease  will  be  the  milky 
patches  on  the  pericardial  surface  found  at  the  autopsy. 

Differential  Diagnosis. — The  existence  of  pericarditis  can  never  be  positive- 
ly determined  except  by  its  physical  signs ;  even  when  attention  has  been 
directed  to  the  heart  it  is  not  always  easily  recognized.  Its  physical  signs  may 
be  confounded  with  those  of  endocarditis,  pleurisy,  and  cardiac  hypertrophy. 

The  friction  murmurs  of  pericarditis  may  be  distinguished  from  endocar- 
dial murmurs  -.—first,  by  their  superficial  character.  Second,  by  their  lim- 
ited area  of  diffusion,  their  maximum  area  of  intensity  being  over  the  right 
ventricle  and  the  junction  of  the  fourth  rib  with  the  sternum  ;  while  endo- 
cardial murmurs  are  audible  beyond  the  pericardial  limits  to  the  right  and 
left,  upward  along  the  course  of  the  vessels  and  sometimes  in  the  back. 
Third,  the  intensity  of  a  pericardial  friction  sound  may  be  increased  or  di- 
minished by  inclining  the  body  of  the  patient  forward  or  backward,  and 
it  is  rendered  more  distinct  by  a  full  inspiration  ;  whereas  endocardial 
murmurs  are  not  changed  in  intensity  by  a  change  in  the  position  of  the 
patient,  nor  by  the  period  of  time  of  the  respiratory  movement.  Fourth, 
pericardial  friction  sounds  are  not  necessarily  synchronous  with  the  heart 
sounds  and  may  be  double;  while  endocardial  murmurs  always  pre- 
cede, take  the  place  of,  or  follow  heart  sounds.  Pericardial  sounds  are 
more  grating,  rubbing  or  creaking  in  character  than  endocardial. 


ACUTE    PERICAEDITIS.  427 

Pericardial  friction  sounds  may  be  distinguished  from  the  friction 
sounds  of  pleurisy  when  the  j)leurisj  occurs  over  the  precordial  space,  by 
directing  the  patient  to  hold  his  breath  for  a  moment ;  if  the  friction 
sound  is  pericardial  it  will  continue  during  the  suspension  of  the  respira- 
tory act — if  it  is  pleuritic  the  friction  sound  will  cease  during  the  arrest  of 
resjDiration.  Occasionally,  however,  where  there  is  consolidation  of  the 
lung  directly  over  the  heart,  accompanied  by  a  pleuritic  friction,  and  firm 
adhesions  having  taken  place  between  the  two  surfaces  of  the  pericardium,  a 
distinct  friction  sound  may  be  produced  in  the  pleura  by  the  motion  of  the 
heart.  This  is  of  rare  occurrence  and  is  hardly  to  be  taken  into  considera- 
tion. In  this  case  the  general  bodily  condition  and  the  state  of  the  pulse 
may  aid  us. 

The  abnormal  area  of  percussion  dulness  produced  by  liypertropliy  or 
dilatation  of  the  right  ventricle  very  closely  resembles  that  produced  by  peri- 
cardial effusion,  and  it  is  often  exceedingly  difficult  to  draw  a  distinct  line 
between  them.  There  is  one  point  which  may  be  regarded  as  diagnostic  : 
that  is,  in  enlargement  of  the  right  heart  the  precordial  dulness  never  ex- 
tends to  the  left  beyond  the  apex-beat,  while  in  pericardial  effusion  it  may 
extend  one  or  two  inches  beyond  the  apex-beat.  The  fact  that  cardiac 
dulness  extends  to  the  left  of  the  apex-beat  proves  that  there  is  more  or 
less  fluid  in  the  pericardial  sac.  The  outline  of  dulness  is  quadrilateral 
in  dilatation,  and  triangular  in  pericardial  effusion.  Besides,  in  cardiac 
hypertrophy  there  is  an  increase  in  the  force  of  the  apex-beat,  and  an  ab- 
normal intensity  to  the  heart  sounds  ;  in  pericarditis  both  will  be  dimin- 
ished in  intensity.  Pericardial  effusion  is  distinguished  from  hypertrophy 
or  dilatation  of  the  left  heart  by  the  fact  that  in  left  cardiac  hyj)ertrophy  the 
apex- beat  is  carried  downward  and  to  the  left,  and  the  area  of  precordial 
dulness  is  increased  in  the  same  direction  and  not  to  the  right.  The 
force  of  the  heart's  action  is  greatly  increased  in  left  ventricular  hypertrophy. 

Prognosis. — In  most  instances  pericarditis  ends  in  complete  recovery. 
The  exceptions  to  this  rule  are  met  with  almost  exclusively  in  connection 
with  Bright's  disease  and  septic  or  pysemic  conditions.  In  connection  with 
either  of  these  diseases  there  is  always  more  or  less  danger  ;  if  it  occurs  in 
connection  with  pysemia,  the  danger  is  very  great,  for  the  exudation  in 
such  cases  is  usually  purulent  and  its  absorption  can  hardly  be  expected, 
although  it  does  occur.  A  large  amount  of  fluid  may  compress,  and  cause 
paralysis  of  the  heart,  death  resulting  in  a  few  hours.  The  nature  of  the 
exudation  determines  to  a  great  extent  the  prognosis  ;  when  it  is  hemor- 
rhagic or  purulent,  the  prognosis  is  bad.  Eheumatic  pericarditis  is  rarely 
fatal.  Occasionally,  acute  pericarditis  passes  into  chronic,  or  rather  is  ac- 
companied by  a  large  serous  effusion,  which  disappears  slowly,  and  is  es- 
pecially  liable  to  be  accompanied  by  relapse,  and  thus  the  disease  goes  on 
for  months.  During  its  progress  the  patient  suffers  from  repeated  attacks 
of  extreme  dyspnoea  ;  in  rare  instances  a  fatal  syncope  occurs. 

As  a  result  of  the  long  continuance  of  the  fluid  effusion  the  substance  of 
the  heart  becomes  softened  and  its  muscle  undergoes  more  or  less  degener- 
ation, on  account  of  which  its  propelling  power  is  diminished,  and  death 


428  DISEASES   OF   THE   HEART, 

by  oedema  of  the  lungs  may  occur  ;  or  any  sudden  effort  may  result  in  in- 
stant death.  This  form  of  subacute  or  chronic  pericarditis  is  generally  as- 
sociated with  blood  changes  attended  by  a  loss  of  red  corjDuscles  and  fibrin, 
and  must  always  be  regarded  as  a  grave  disease.  The  most  frequent 
sequelas  of  acute  pericarditis  are  adhesions  of  the  two  surfaces  of  the  peri- 
cardium, cardiac  dilatation,  and  hypertrophy.  Cardiac  dilatation  occurs 
as  the  result  of  the  weakening  of  the  cardiac  walls  from  myocarditis.  The 
hypertrophy  of  the  cardiac  walls  which  follows  this  dilatation  is  compensa- 
tory. .  Occasionally  the  pericardial  exudation  is  abundant,  and  extensive 
pericardial  adhesions  take , place  at  the  base  of  the  heart,  which,  by  their 
contraction  and  pressure,  interfere  with  the  current  of  blood  through  the 
coronary  arteries,  and  as  a  result  the  nutrition  of  the  heart  is  impaired  and 
fatty  degeneration  of  its  walls  may  be  developed.  The  duration  of  peri- 
carditis is  from  one  to  three  weeks  ;  some  cases  end  fatally  in  a  few  hours 
from  sudden  heart  failure. 

Treatment. — We  have  to  deal  with  an  inflammation  of  considerable  sever- 
ity, yet  from  our  knowledge  of  its  etiology  and  morbid  anatomy  we  are  not 
warranted  in  the  use  of  a  single  antiphlogistic  measure.  Blood-letting, 
hydragogue  cathartics,  diuretics  and  blisters,  which  at  one  time  were 
almost  universally  employed,  are  now  abandoned  ;  the  tendency  is  toward 
a  supporting  plan  of  treatment.  As  soon  as  it  is  discovered  that  peri- 
carditis exists,  endeavor  to  determine  its  cause,  and,  if  possible,  remove  it ; 
if  this  is  not  possible,  endeavor  to  counteract  it.  If  the  pericarditis  is  due 
to  uraemia,  employ  those  means  which  favor  elimination  of  urea.  If  it  ac- 
companies articular  rheumatism  it  must  be  treated  as  a  rheumatic  affection. 
In  those  acute  diseases  marked  by  great  depression  the  occurrence  of  peri- 
carditis is  an  indication  for  an  increase  in  stimulants.  Under  all  such  cir- 
cumstances, especially  in  connection  with  septic  and  pysemic  developments, 
supporting  measures  are  early  called  for.  The  favorite  local  applications 
in  its  early  stage  are  hot  anodyne  poultices  over  the  precordial  space  in  con- 
nection with  the  internal  administration  of  opium  ;  absolute  rest  in  bed 
must  be  enjoined.  If  the  pulse  exhibits  dicrotism,  stimulants  in  small 
quantities  may  be  given. 

Opium  is  the  most  valuable  internal  agent.  It  should  never  be  given  in 
large  doses,  but  only  in  sufficient  quantities  to  relieve  pain  and  arrest  or  al- 
lay an  irritable  action  of  the  heart.  The  largest  doses  administered  should 
be  given  at  night,  in  order  that  the  patient  may  secure  quiet  sleep ;  the 
heart  is  more  liable  to  become  irritable  at  night,  and  the  patient  usually  be- 
comes more  restless.  Great  care  should  be  exercised  in  the  administration 
of  opium  ;  it  should  never  be  carried  to  semi-narcotism.  Chloral  is  thought 
to  be  equally  good,  since  it  does  not  interfere  with  secretions  ;  my  expe- 
rience is  against  its  use. 

The  means  usually  employed  for  removal  of  the  fluid  are  hydragogue 
cathartics,  diuretics  and  blisters.  I  am  convinced  that  this  plan  of  treat- 
ment will  not  hasten,  but  will  rather  delay  the  removal  of  the  fluid.  Ex- 
perience teaches  that  pericarditis  is  an  inflammation  which  occurs  in  the 
weak  and  feeble,  and  not  in  the  strong  and  vigorous  ;  it  is  met  with  among 


CHRONIC    PERICARDITIS.  4:39 

the  young  rather  than  in  healthy  persons  in  the  prime  of  life.  In  almost 
all  instances  it  is  associated  with  those  diseases  that  are  especially  marked 
by  a  loss  of  vitality ;  consequently  all  measures  that  have  a  tendency  to 
depress  the  patient  are  to  be  avoided.  Blisters  are  apt  to  accelerate  the 
heart's  action  and  should  never  be  applied  directly  over  the  precordial 
space  ;  leeches  are  less  painful  and  more  efiBcacious,  and  may  be  applied 
over  the  precordial  space.  The  same  general  rules  which  were  given  as 
guides  in  promoting  the  absorption  of  the  inflammatory  product  in  pleu- 
risy are  to  be  followed  in  the  treatment  of  pericarditis.  Iron,  stimulants, 
and  a  highly  nutritious  and  readily  digestible  diet  are  the  most  efficient 
remedies.  Anything  which  accelerates  the  heart's  action  should  be 
avoided. 

The  surface  of  the  chest  must  be  carefully  protected  from  changes  in  tem- 
perature ;  any  exposure  incident  to  a  physical  examination  of  the  chest  must 
be  carefully  avoided.  The  Germans  advocate  cold  to  the  precordia  ;  it  is  said 
to  diminish  pain  and  frequency  of  the  heart's  action.  They  direct  that  an 
ice-bag  shall  be  kept  over  the  precordial  space  until  all  evidences  of  peri- 
carditis have  disappeared. 

During  the  period  of  convalescence  the  patient  must  be  very  strictly 
guarded,  for  the  walls  of  the  heart  are  in  a  weakened  condition,  and 
should  not  be  overtaxed.  Everything  which  will  have  a  tendency  to 
increase  the  action  of  the  heart  must  be  carefully  avoided.  Children 
should  not  be  allowed  to  go  up  and  down  stairs  or  to  play  with  other 
children  during  the  period  of  convalescence.  Patients  convalescing  from 
pericarditis  must  be  placed  under  the  very  best  hygienic  conditions  for  two 
or  three  months  after  the  disappearance  of  the  pericardial  symptoms. 

Sometimes  the  symptoms  which  attend  a  large  fluid  effusion  become  very 
urgent,  and  the  question  presents  itself  : — shall  aspiration  of  the  pericar- 
dium be  performed  ?  It  has  been  claimed  that  little  danger  attends  its  per- 
formance, but  it  should  never  be  rashly  undertaken.  When  it  is  positively 
determined  that  pus  is  in  the  pericardium  aspiration  should  be  practised. 
When  the  effusion  is  sero-fibrinous  it  must  be  remembered  that  the  urgent 
symptoms,  for  the  relief  of  which  aspiration  would  be  resorted  to,  are  usu- 
ally of  short  duration,  and  patients  rarely  die  from  the  pressure  produced 
by  the  effusion.  Whether  aspiration  shall  be  performed  under  .such  cir- 
cumstances is  a  question  for  most  careful  consideration.' 

CHEOlSriC    PEEICAEDITIS. 

Chronic  pericarditis  is  rare  except  as  a  sequela  of  acute  ;  occasionally  it 
may  be  sub-acute  from  its  commencement.  When,  after  three  or  four 
weeks,  acute  pericarditis  does  not  terminate  in  recovery,  it  becomes  chronic. 
In  some  cases  of  chronic  pericarditis  the  pericardial  sac  contains  several 
pounds  of  fluid.    In  others  firm  adhesions  form  between  the  pericardial  sur- 

'  In  a  monograph  by  Dr.  Roberts,  who  gives  an  account  of  sixty  cases  with  twenty-four  recoveries 
(forty  per  cent.),  he  states  that  the  best  points  to  tap  are  in  the  fossa  between  the  ensiform  and  costal 
cartilages  on  the  left  side,  or  in  the  fiftli  left  interspace  near  the  junction  of  the  sixth  rib  with  its  carti- 
lage. In  Huidenlang's  case  1000  c.  c.  were  withdrawn  at  two  tappings  and  recovery  followed.  (Archiv.  f. 
klin.  Med.  24,  p.  452.)      . 


430  DISEASES   OP   THE   HEART. 

faces,  binding  them  more  or  less  closely  to  each  other  ;  mingled  with  these 
adhesions  are  chalky  debris  and  calcareous  plates.  The  adhesions  which 
form  in  acute  pericarditis  are  not  regarded  as  a  part  of  the  history  of 
chronic  pericarditis.  The  fibrous  changes  of  chronic  pericarditis  only 
occur  when  the  sub-pericardial  tissue  is  involved.  The  heart  may  then  be 
encased  in  a  calcareous  wall,  and  a  fibrous  degeneration  of  the  cardiac 
muscles  result,  which  may  lead  to  local  aneurismal  dilatation. 

The  Symptoms  of  chronic  pericarditis  are  those  which  give  evidence  of 
obstructed  circulation  with  signs  of  enlargement  of  the  heart — there  is  dysp- 
noea sometimes  amounting  to  orthopnoea  and  uneasiness  or  a  sense  of  weight 
in  the  precordial  region.  In  some  instances  this  condition  is  associated 
with  attacks  of  angina  pectoris.  The  heart's  action  is  easily  disturbed,  and 
cardiac  palpitation  is  present  on  slight  physical  exertion  or  mental  excite- 
ment. 

The  Physical  Signs  of  chronic  pericarditis  closely  resemble  those  of  eccen- 
tric cardiac  hypertrophy  ;  in  both  cases  there  is  increased  dulness  in  the  pre- 
cordial region,  but  in  pericarditis  the  apex-beat  is  indistinct  and  is  raised 
above  its  normal  position  ;  while  in  hypertrophy  the  apex-beat  is  distinct 
and  is  carried  downward  and  to  the  left  of  its  normal  position.  A  friction 
murmur  is  usually  present  even  when  large  quantities  of  fluid  are  present. 
There  is  no  murmur  present  in  hypertrophy.  Bulging  sometimes  occurs, 
and  there  may  be  fluctuation  when  the  fluid  is  large  in  amount.  If  the 
two  surfaces  of  the  pericardium  are  closely  agglutinated,  and  the  pericar- 
dium is  adherent  to  the  costal  pleura,  so  that  firm  adhesions  are  formed 
between  it  and  the  chest  wall,  there  will  be  more  or  less  depression  of  the 
precordial  region — so-called  "systolic  depression;" — ^the  cardiac  impulse 
will  be  permanently  displaced  upwards,  and  will  be  unaltered  either  by 
change  of  posture  or  by  a  full  inspiration,  and  there  will  be  an  irregular 
Jogging  motion  of  the  heart  during  both  its  systole  and  diastole.  Some- 
times there  is  a  depression  over  the  scrobiculus  cordis  caused  by  adhesion 
of  the  two  layers  of  the  pericardium  to  each  other  and  to  the  pleura  cover- 
ing the  diaphragm,  and  concomitant  adhesion  of  the  diaphragm  with  the 
liver. 

Although  the  Diagnosis  of  chronic  pericarditis  is  always  difficult  and  its 
existence  is  rarely,  if  ever,  positively  determined  unless  there  is  a  large 
amount  of  fluid  effusion  in  the  pericardial  sac,  still,  if  the  symptoms  and 
physical  signs  already  detailed  follow  an  attack  of  acute  pericarditis,  there 
is  presumptive  evidence  of  its  existence. 

The  Prognosis  in  this  affection,  as  regards  complete  recovery,  is  always 
unfavorable,  and  when  it  accompanies  degeneration  of  the  cardiac  walls 
and  valvular  insufficiency  life  will  not  be  prolonged. 

The  Treatment  consists  in  limiting  physical  exercise  so  as  not  to  overtax 
the  embarrassed  heart ;  at  the  same  time  to  furnish  the  patient  with  a 
most  nutritious  but  non-stimulating  diet,  and  to  administer  daily  some 
preparation  of  iron.  Ccncerning  paracentesis,  the  same  rules  apply  here 
as  in  acute  pericarditis.  Perhaps  the  operation  will  be  resorted  to  in 
chronic  cases  with  better  success  than  in  acute. 


ACUTE   EXUDATIVE   ENDOCARDITIS. 


431 


Ein)OOAKDITIS, 

Endocarditis  is  an  Inflammation  of  the  endocardium.  I  shall  describe 
it  under  three  heads  : — 

I.  Acute  Exudative  Endocarditis. 
11.    Ulcerative  Endocarditis. 
III.  Interstitial  Endocarditis. 

In  most  instances  this  disease  depends  upon  a  constitutional  dyscrasia, 
characterized  by  alterations  in  the  vital,  physical,  or  chemical  properties 
of  the  blood.  Etiologically,  all  the  different  varieties  are  closely  con- 
nected ;  clinically  and  pathologically,  they  are  distinct.  They  cannot  be 
classified  as  acute  and  chronic  in  the  ordinary  acceptation  of  the  terms,  for 
some  cases  are  at  no  time  acute,  and  even  in  so-called  chronic  endocarditis 
the  changes  are  but  an  advanced  stage  of  an  acute  process. 

So-called  acute  endocarditis  is  accompanied  by  a  fibro-cellular  exudation 
into  the  substance  of  and  underneath  the  endocardium,  causing  elevations 
of  its  surface.  A  better  term  for  this  variety  is  "acute  exudative  endo- 
carditis," it  being  understood  that  no  exudation  occurs  on  its  free  surface, 
but  underneath  it.  This  form  may  be  entirely  recovered  from,  or  may 
lead  to  interstitial  formative  changes. 
Acute  exudative  endocarditis  may  be 
stamped  with  an  ulcerative  process, 
the  result  of  septic  infection,  giving 
rise  to  changes  known  as  acute  ulcera- 
tive endocarditis. 

Chronic  or  interstitial  endocarditis 
is  the  form  in  which  the  endocardial 
and  myocardial  tissues  are  involved  in 
sclerotic  or  cirrhotic  changes,  giving  /J 
rise  to  the  many  varieties  of  valvular 
disease.  It  may  be  a  sequela  of  the 
acute  exudative  variety,  or  the  inflam- 
mation may  have  been  interstitial  from 
its   commencement,    for   the  valvular  Fis.  90. 

changes  due  to  this  form   are   often  ^ -i'^^i^s  «i^T>?ri.l^'^T^„^r£?.lJ^^ 
found  in  those  who  never  have  had  a,  a 
either  acute  articular  rheumatism,  or 
acute  exudative  endocarditis,  but  who  are  subjects  of  chronic  rheumatism, 
syphilis,  or  gout. 

ACUTE   EXUDATIVE    ENDOCARDITIS 

This  variety  is  met  with  most  frequently  in  connection  with  acute  articu- 
lar rheumatism.  In  adults,  the  left,  and  in  intra-uterine  life  the  right, 
heart  is  oftenest  affected.  The  process  rarely  extends  beyond  the  valves 
and  valvular  orifices  ;  but  it  may  involve  the  whole  or  any  part  of  the  ven- 
tricular or  auricular  portions  of  the  endocardium. 


theritic  Endocarditis. 

Thickening  of  the  Endocardium  on  the  free 

harder  of  the  mitral  valve,  imth  papillary 

elevatiom  surmounted  by  fibrinous  deposit. 


432 


DISEASES   OP  THE   HEAET. 


Morbid  Anatomy. — The  endocardium  becomes  infiltrated  with  cells,  the 
process  beginning  in  the  layer  of  flat  cells.  The  new  formative  cells  are 
developed  in  the  layer  underneath  the  endocardium.  This  hyperplasia  is 
accompanied  by  softening  of  the  intercellular  structure,  which  is  soon  de- 
stroyed. The  endothelial  elements  take  part  in  the  process.  The  masses 
of  new  cells  push  out  the  endocardium,  and  papillary  elevations  are  formed. 

These  conical  elevations  are  sur- 
rounded in  the  deeper  layers  of 
the  endocardium  by  a  zone  of  pro- 
liferation which  is  never  distinctly 
limited,  but  which  exhibits  pro- 
gressive hyperplasia  from  the 
periphery  toward  the  centre.  All 
these  changes  may  have  taken  place 
in  non-vascular  tissue.  Where  the 
capillaries  are  most  numerous  a 
punctate  or  aborescent  vascularity 
is  seen,  after  which  the  part  be- 
comes opaque.  There  is  no  exu- 
dation upon  the  papillary  eleva- 
tions, but  fibrin  from  the  blood  is 
deposited  on  them  as  on  foreign 
bodies.  These  coagula  are  most 
numerous  on  the  surface  opposed 
to  the  blood  current.  They  have 
a  cauliflower-like,  bulbous  ex- 
tremity connected  by  a  constricted 
neck  with  a  firm,  hard  base  which 
is  continuous  with  the  subjacent 
tissue.  Each  mass  is  covered  by  a  thin  hyaline  layer.  At  first  these  vege- 
tations are  so  small  and  numerous  that  the  membrane  has  a  granular  look. 
Later,  they  enlarge,  sometimes  to  the  size  of  a  pea,  and  have  a  conical  or 
raspberry-like  shape.  They  are  arranged 
on  the  borders  of  the  aortic  valve  near 
the  edge,  their  seat  being  determined  by 
the  limit  of  the  vascular  net-work.  The 
bands  of  tissue  passing  from  the  attached 
valvular  border  to  the  corpus  Arantii  in 
the  centre  show  the  granulations  most 
distinctly.  Near  the  insertion  of  the 
tendons  upon  the  auricular  surface  of  the 
mitral  valve  are  irregular  wreaths  of  vege- 
tations enclosing  attachments  of  the 
chordse  tendineae.  Friction  of  the  coagula 
upon  them  may  excite  the  vegetations  or 
of  endocarditis  at  points  remote  from 
the  valves.      The  chordae  tendineae  may  adhere  to  one  another.      From 


Fig.  91. 

Drawing  from  the  previous  case  showing  simUar  changes 
upoij  the  Aortic  Valves. 

A,  A.  Aortic  Valves  showing  papillae,  and  fibrimms  de- 
posit. 


Vertical  Section  of  an  Aortic  Valve  in  Acute 
Endocarditis. 

A.  Endocardium. 

B.  Papillary  elevation. 

C.  Fibrinous  deposit,     x  60. 


ACUTE   EXUDATIVE   ENDOCARDITIS.  433 

these  adhesions  stenosis  may  result,  by  the  flaps  becoming  agglutinated 
to  each  other,  or  regurgitation  by  their  adhering  to  the  heart-walls.  As 
a  result  of  these  changes,  new  vessels  appear  in  the  substance  of  the  mitral 
valve  or  existing  ones  become  more  apparent.  The  more  rajiid  the  course, 
the  more  marked  are  these  changes.  The  largest  vegetations  are  found 
on  the  valves.     Young  vegetations  are  translucent,  soft  and  friable. 

UlcerativeEndocarditis. — Ulcerative  endocarditis  occurs  in  those  diseases 
where  there  is  great  vital  depression.  It  is  oftenest  met  with  in  pyaemia, 
puerperal  fever,  scarlatina  and  diphtheria,  ;  it  has  been  called  "septic," 
"diphtheritic,"  and  "  infectious"  endocarditis.  The  margins  of  the  valves 
are  irregular,  but  well  defined.  The  edges  are  swollen  and  thick,  and  their 
floor  is  infiltrated  with  pus.  In  some  cases  the  apices  of  the  vegetations 
which  are  formed  are  swept  off  by  the  blood-current,  and  an  ulcerated  sur- 
face is  left.  If  their  removal  causes  great  loss  of  substance,  perforation  of 
the  valve  may  occur.  These  perforations  are  sometimes  closed  or  hidden 
by  a  fibrinous  exudation.  It  is  claimed  that  the  ulceration  or  suppuration 
of  these  elevations  is  the  result  of  granular  degeneration  ;  micrococci  and 
bacteria  are  often  found  in  ulcerative  endocarditis  of  a  septic  or  diphtheritic 
origin,  and  have  given  to  it  the  name  of  "mycosis  endocardii.''^ '  It  is  more 
probable  that  these  minute  organisms  are  developed  by  the  aid  of  the  ulcera- 
tive process,  rather  than  that  they  are  the  cause  of  it. 

The  valvular  ulcerations  in  this  form  of  endocarditis  may  give  rise  to 
various  lesions.  If  small  masses  are  detached  from  the  cardiac  orifices,  ei- 
ther from  deposits  on  the  valves  or  from  ulcerations,  and  enter  the  blood- 
current,  they  originate  morbid  processes  in  the  organs  to  which  they  are 
carried.  It  is  important  to  distinguish  between  the  results  produced  by 
displacements  into  the  blood-current  of  large  masses,  and  those  arising  from 
the  entrance  of  molecular  fragments.  Masses  from  the  vegetations,  or  from 
the  ulcerated  valves  in  ulcerative  endocarditis,  being  stamped  with  a  septic 
element,  lead  to  the  development  of  suppurative  infarctions  in  different  or- 
gans. The  size  and  site  of  the  emboli  are  important ;  they  may  be  so  large 
as  to  obstruct  vessels  of  the  largest  size,  as  the  external  iliac.  When  arte- 
ries in  the  lungs  are  thus  plugged,  the  result  is  generally  an  ischmmia,  often 
terminating  in  gangrene.  Capillary  embolism  may  occur  in  a  number  of 
organs  simultaneously. 

Wlien  the  cutaneous  capillaries  are  obstructed,  ecchymotic  spots  are 
formed,  followed  by  cellulitis.  If  in  cerebral  embolism  the  occluded  ves- 
sel is  large,  instantaneous  hemiplegia  and  secondary  softening  will  result ; 
if  it  is  very  small,  softening  develops  without  evidence  of  obstructed  circu- 
lation. Infarctions  and  suppuration  of  the  spleen  (sjolenitis,  so-called)  are 
not  uncommon.  The  kidneys  may  be  similarly  affected.  Septic  phenom- 
ena are  very  important.  When  typhoid  symptoms,  deep  jaundice,  and 
symptomatic  intermittent  fever  are  associated  with  endocarditis,  it  estab- 
lishes its  "  ulcerative  "  character.  When  the  inflammation  develops  rapidly, 
the  valves  soften,  lose  their  resisting  joower,  and  in  time  become  stretched,, 
bulged  or  torn  by  the  blood- current.     A  rupture  of  the  mitral  valves  will 

'  Jaccoud.    Klebs. 

28 


434  DISEASES    OP   THE   HEART. 

open  into  the  auricular,  and  tliat  of  the  aortic  into  the  yentricular 
cavity. 

If  the  blood  penetrates  a  rent  in  the  flap  of  the  valves,  the  endocardium 
is  puifed  out  and  a  "valvular  aneurism"  is  formed;  round  or  funnel- 
shaped  aneurismal  sacs  may  project  from  the  valves  ;  the  bottom  of  one  of 
these  sacs  may  be  perforated,  and  long,  ragged,  gray  shreds  covered  vs^ith 
fibrin  may  hang  into  the  ventricular  cavity.  When  the  ulceration  is  situ- 
ated in  the  ventricular  wall,  the  pressure  of  the  blood  may  bulge  out  the 
heart- wall  and  give  rise  to  ''partial  cardiac  aneurism."  Communication 
between  the  various  heart  cavities  may  thus  be  established.  The  results  of 
both  varieties  of  acute  endocarditis  will  be  considered  under  the  head  of 
''interstitial  endocarditis." 

Etiology. — Acute  exudative  endocarditis  is  rarely  if  ever  idiopathic.  It 
is  closely  connected  with  those  diseases  and  dyscrasiae  in  which  the  blood  is 
altered  either  in  the  relative  proportion  of  its  constituents  or  in  its  phys- 
iological elements.  Endocarditis  is  so  frequently  associated  with  acute 
articular  rheumatism,  that  they  are  often  described  as  one  disease.  It  is 
said  to  occur  in  fifty  per  cent,  of  all  cases,  but  the  statistics  of  Bellevue 
Hospital  show  that  it  complicates  only  thirty- three  and  one-third  per  cent. 
of  the  cases.  The  irritation  caused  by  blood,  the  salts  of  which  are 
changed,  or  which  contains  excrementitious  products,  or  a  specific  poison, 
is  shown  most  markedly  upon  the  valvular  surface  of  the  endocardium ; 
and  for  this  reason  the  parts  most  exposed  to  friction  are  those  which  first 
and  most  extensively  exhibit  its  pathological  changes,'  There  is  no  disease 
characterized  by  a  morbid  condition  of  the  blood  in  which  endocarditis  may 
not  occur  :  thus  it  often  complicates  the  essential  fevers,  the  exanthemata, 
diphtheria,  Bright's  disease,  and  syphilis.  When  an  individual  who  is 
already  suffering  from  valvular  disease  of  the  heart  is  attacked  with  acute 
rheumatism,  the  liability  to  acute  endocarditis  is  much  increased.  Even 
when  rheumatism  and  chorea  are  absent,  acute  endocarditis  is  liable  to 
occur  when  valvular  disease  exists. 

Some  regard  myocarditis,  pericarditis,  pleurisy  and  pneumonia  as  capa- 
ble of  exciting  endocarditis  by  the  extension  of  the  inflammatory  process 
from  the  surface  of  the  heart ;  this  is  questionable,  but  that  it  can  result 
from  traumatism  is  possible.^ 

Wunderlich  ranks  measles  next  to  rheumatism  as  a  cause  of  endocarditis. 
We  must  remember  that  not  every  "  blowing  "  murmur  is  indicative  of 
endocarditis.  Bamberger  and  Niemeyer  think  that  the  excited  and  irregu- 
lar action  of  the  heart  in  children,  by  inducing  irregular  tension  of  the 
valves,  will  bring  about  a  "blowing"  sound  during  acute  rheumatism 
without  endocarditis. 

Acute  ulcerative  endocarditis  is  met  with  in  pyaemia,  puerperal  fever, 
scarlatina,  diphtheria,  and  it  may  occur  secondarily  to  a  septic  inflammatory 
process  located  in  any  part  of  the  body — "  septic  endocarditis,"     It  may 

1  Charcot  records  a  large  number  of  observations  in  which  endocarditis  was  developed  in  patients  with 
chronic  rheumatism,  and  in  which  it  never  assumed  an  acute  form.  It  thus  seems  evident  that  organic 
valvular  lesions  from  endocarditis  may  arise  during  chronic  as  well  as  acute  articular  rheumatism. 

*  Bamberger  records  two  traumatic  cases. 


ACUTE    EXUJ)ATiVE    EJSJ J)OCATlDITIS.  435 

also  appear  without  any  obvious  cause, — spontaneously, — or  in  connection 
with  some  siJecific  form  of  inflammatory  disease,  as  croupous  pneumonia. 
Wicks  calls  it  then  arterial  pycemia. 

Symptoms. — The  subjective  symptoms  of  acute  exudative  endocarditis  are 
more  obscure  than  those  of  any  other  cardiac  disease.  They  are  few, 
ill-defined,  and  without  any  regular  order  of  development ;  when  the  heart- 
muscle  is  not  involved  the  disease  cannot  be  appreciated  by  a  single 
rational  symptom,  for  the  urgency  of  the  symptoms  of  the  diseases  in  which 
it  occurs  often  masks  the  few  symptoms  which  attend  its  development. 
But  when  it  is  extensive  and  the  muscular  tissue  of  the  heart  is  involved, 
palpitation  and  a  sense  of  discomfort  in  the  precordial  region  are  present, 
and  there  may  be  attendant  dyspnoea  and  decubitus  on  the  left  side.  Sel- 
dom is  the  palpitation  appreciable  to  the  physician,  for  the  heart  may  beat 
with  force  and  be  tumultuous  and  yet  the  pulse  remain  unchanged.  At 
first  the  pulse  is  strong  and  forcible  ;  later  it  becomes  rapid,  small,  feeble, 
and  irregular  ;  it  is  frequent  from  the  onset.  As  a  rule,  the  force  of  the 
pulse  does  not  correspond  to  the  cardiac  activity,  for  as  the  heart-muscle 
becomes  involved,  its  propelling  power  is  diminished  and  the  pulse  becomes 
feeble,  compressible  and  sometimes  dicrotic.  The  respirations  are  accele- 
rated and  sometimes  labored  ;  there  may  be  paroxysmal  dyspnoea,  the  face 
may  be  flushed,  or  it  may  be  dusky,  pallid,  ashy-gray,  or  even  cyanotic. 
Sleeplessness  and' nocturnal  delirium  are  rare.  When  the  muscular  tissue 
of  the  heart  is  extensively  involved,  nausea,  vomiting,  giddiness  and  syn- 
cope may  be  present,  yet  slight  pain  or  a  ''tightness"  is  not  an  infre- 
quent symptom  when  endocarditis  occurs  in  those  who  have  chronic  val- 
vular disease.     The  temperature  seldom  exceeds  103°  F. 

When  in  acute  ulcerative  endocarditis^  a  valve  ruptures,  a  typhoid  state 
rapidly  supervenes.  The  patient  is  forced  to  assume  the  upright  j)os- 
ture  on  account  of  dyspnoea  ;  cyanosis  is  sudden  and  extreme,  and  the 
symptoms  of  multi]3le  embolism  ajDpear.  The  temperature  rises  to  106°- 
107°  F.  There  is  jaundice  and  frequent  rigors  which  with  the  parox- 
ysms of  fever  simulate  the  icteric  form,  of  malarial  fever.  The  spleen 
becomes  enlarged  and  tender  ;  the  urine  is  scanty,  dark  colored,  albumi- 
nous, and  of  high  specific  gravity.  Delirium  and  coma  occur  in  severe  cases. 
Some  cases  are  marked  by  nausea,  vomiting,  and  diarrhoea.  The  frequency 
with  which  this  form  of  endocarditis  is  associated  with  pneumonia  suggests 
the  presence  of  a  blood  poison  of  great  intensity.  Although  it  rarely  occurs 
except  with  septic  diseases,  yet  it  may  occur  late  in  severe  forms  of  rheu- 
matic and  traumatic  endocarditis  or  when  there  has  been  pre-existing  sup- 
purative bone-disease. 

The  symptoms  of  embolism,  are  due  to  the  arrest  of  a  detached  portion  of 
the  endocardium  in  some  artery.  The  spleen  is  much  oftener  the  seat  of 
such  embolisms  than  the  kidney  or  brain.  The  occurrence  of  hemiplegia 
with  aphasia  or  of  severe  cerebral  disturbance  during  the  course  of  an  en- 
docarditis is  indicative  of  cerebral  embolism. 

Physical  Signs. — Inspection  sometimes  shows  the  area  of  cardiac  impulse 
greater  than   normal  ;   the   impulse  is  irregular  and   often   tumultuous. 


436  DISEASES    OF   THE   HEART. 

Later  the  apex-beat  and  the  impulse  grow  more  distinct,  but  never  so  sud- 
denly or  so  markedly  as  in  pericarditis.  In  children  the  vessels  of  the  neck 
may  exhibit  venous  stasis. 

Palpation. — At  the  onset  of  the  disease,  the  cardiac  impulse  is  more 
forceful  than  normal,  and  the  heart's  action  is  frequently  irregular.  Some- 
times the  heart  thumps  violently  against  the  chest- walls.  The  force  of  the 
cardiac  impulse  varies  from  day  to  day,  being  stronger  when  pain  is  present. 
If,  during  the  disease,  there  is  no  increase  in  the  force  of  the  apex-beat,  we 
infer  that  the  muscular  power  of  the  heart  is  deficient.  When  acute  en- 
docarditis supervenes  upon  long-standing  valvular  disease,  there  is  alter- 
nate increase  and  diminution  in  the  area  and  force  of  the  impulse.  When 
the  heart-walls  are  weakened  by  myocarditis,  or  when  the  endocarditis  is  it- 
self very  extensive,  the  force  of  the  apex-beat  is  diminished  ;  an  endocar- 
dial thrill  is  often  present. 

Percussion. — The  area  of  cardiac  dulness  is  normal  unless  changes  at 
the  valvular  orifices  retard  the  outflow  of  blood  from  the  lungs,  and  then 
the  cavities  in  the  right  heart  become  engorged  and  the  area  of  dulness 
will  be  abnormally  increased.  But  this  increase  is  always  slight,  except  in 
those  cases  where  sudden  and  extreme  distention  of  the  heart  cavities  re- 
sults from  the  presence  of  masses  of  fibrin.  Extensive  myo-  or  endo-car- 
dial  inflammation  may  so  weaken  the  heart  that  dilatation  results,  and 
then  percussion  will  show  marked  increase  in  the  area  of  cardiac  dulness. 

Auscultation  reveals  a  murmur,  or  murmurs,  over  the  various  cardiac  ori- 
fices. The  fact  that  valvular  disease  may  have  pre-existed  makes  it  impor- 
tant to  carefully  examine  the  heart  at  the  first  visit  to  one  suffering  with 
acute  rheumatism,  chorea,  Bright's,  etc.,  etc.  When  hyj)ertrophy  and  old 
valvular  disease  of  the  heart  exist,  the  advent  of  an  attack  of  acute  exu- 
dative endocarditis  generally  passes  unrecognized  and  even  its  presence  is 
often  undetermined.  The  most  important  constant  sign  of  endocarditis  is 
2i  systolic  murmur,  heard  with  greatest  intensity  at  the  apex  ;  this  soft,  blow- 
ing, or  "  bellows  "  murmur  may  be  ventricular  or  valvular.  In  all  cases, 
it  is  due  to  roughening  or  tMchening  of  the  endocardium.  It  often  changes 
its  point  of  maximum  intensity  during  the  acute  period  of  the  disease.  It 
is  developed  early,  and  when  one  is  on  the  lookout  for  endocarditis  this 
will  be  the  first  evidence  of  it.  In  some  instances  no  murmur  is  at  any 
time  present. 

A  mitral  murmur  alone  occurs  in  fifty  per  cent,  of  cases  of  rheumatic 
endocarditis  ;  it  is  developed  early  and  is  preceded  by  j^rolongation  of  the 
first  sound,  a  "  transition  "  sound,  so  to  speak,  feeble  and  wavering  in  char- 
acter, extending  over  the  slight  interval  which  normally  exists  between  the 
first  and  second  sounds.  Other  changes,  not  murmurs,  but  which  precede 
them  in  many  cases— are  loud,  ringing  normal  sounds  ;— muffled  first 
sound  ; — feeble  first,  intensified  second  sound  ;— doubling  of  the  first  sound  ; 
— "roughening"  of  the  first  sound  ;— and  a  "humming"  over  the  right 
heart.  Complete  absence  of  the  heart  sounds  is  a  rare  but  possible  ante- 
cedent of  an  endocardial  murmur.  A  mitral  murmur,  in  acute  endocar- 
ditis, is  usually  audible  over  a  limited  area.     It  is  the  exception  to  hear  it 


ACUTE    EXUDATIVE    ENDOCARDITIS.  437 

both  in  front  and  at  the  back  ;  very  frequently  it  is  heard  most  distinctly 
over  the  stom;ich.  Wlien  the  joulmonary  circulation  is  greatly  obstructed, 
it  causes  an  extra  strain  on  the  pulmonary  valves  and  then  the  second 
sound  will  be  accentuated,  while  the  first  j^ulmonic  sound  may  be  feeble  or 
absent.  A  subdued  or  absent  sound  shows  tension  of  the  artery.  Eedu- 
plication  of  the  second  sound  in  mitral  endocarditis  is  probably  due  to  the 
difference  in  time  occupied  by  the  ventricles  in  emptying  themselves. 

A  tricuspid  murmur  occurs  in  fifty  per  cent,  of  the  cases  of  acute  mitral 
endocarditis  :  o, pulmonic  murmur  in  about  one-third  of  the  cases.  They 
are  superficial  and  "  scratchy"  in  character,  and  indicate  a  relaxed  condi- 
tion of  the  vessels  and  a  thin  state  of  the  blood.  They  are  never  perma- 
nent. Mitral  endocarditis  is  accompanied  by  aortic  murmurs  in  about 
sixteen  per  cent,  of  the  cases,  and  these  murmurs  are  usually  soft  and 
blowing,  but  maybe  "musical,"  ''whistling,"  or  "  twangy." 

In  aortic  endocarditis  the  second  sound  is  usually  lost  over  the  carotids. 
In  about  twelve  per  cent,  of  all  cases  of  acute  (rheumatic)  endocarditis  a 
regurgitant  murmur  will  be  heard  over  the  tricuspid  orifice.  Tricusj)id 
murmurs  are  present  in  fifty  per  cent,  of  all  cases  of  recent  mitral  mur- 
murs, in  forty  per  cent,  of  recent  aortic  murmurs,  and  in  twenty-five  per 
cent,  of  mifcro-aortic  murmurs.  They  are  due  to  an  increase  in  the  slight 
(normal)  insufficiency  of  the  tricuspid  valves.  Such  murmurs  are  of  short 
duration,  vibrating  in  character,  and  heard  over  the  right  ventricle.  In 
children  aortic  endocarditis  is  rare ;  at  this  period  obstruction  at,  and  re- 
gurgitation through,  the  mitral  orifice  commonly  occur  together. 

DifFerential  Diagnosis. — Acute  exudative  endocarditis  may  be  mistaken 
for  pericarditis,  and  its  murmur  may  be  mistaken  for  that  produced  by 
aortitis  or  for  those  friction  murmurs  that  develop  during  fevers.  The 
friction-sounds  oi pericarditis  are  superficial  and  limited  to  the  precordial 
space,  while  those  of  endocarditis  are  distant,  and  each  murmur  will  have 
its  area  of  diffusion  beyond  the  precordial  space.  A  pericardial  sound  is 
distinctly  a  friction,  creaking,  or  rubbing  sound,  and  it  has  a  "to-and- 
fro "  character,  while  that  of  endocarditis  is  soft  and  blowing.  Endocar- 
dial murmurs  accompany  the  heart  sounds,  while  pericardial  friction 
sounds  are  not  rhythmical  with  the  heart-sounds.  The  intensity  of  a  peri- 
cardial sound  is  increased  when  the  patient  bends  forward,  at  the  end  of 
a  full  inspiration,  or  when  the  stethoscope  is  pressed  firmly  over  the  pre- 
cordial region,  and  in  the  last  instance  it  becomes  "grazing"  and  "rub- 
bing "  in  character.  As  soon  as  effusion  occurs  in  pericarditis,  alteration 
in  the.  character  of  the  pulse,  increase  in  the  area  of  precordial  dulness,  and 
the  disappearance  of  adventitious  sounds  will  decide  the  diagnosis. 

Aortitis  has  many  of  the  symptoms  of  endocarditis,  but  in  addition  the 
pulse  is  more  rapid,  the  respirations  are  more  hurried,  and  pain  is  present 
in  the  precordial  region,  shooting  down  the  spine  and  increased  by  motion. 
Aortitis  is  often  accompanied  by  cutaneous  hypersesthesia.  Acute  aortitis 
is  very  rare.' 

The  functional  murmurs  which  occur  in  fevers  are  usually  heard  only 

1  Lebert  and  Rindfleisch  doubt  its  existence. 


438  DISEASES    OF   THE   HEART. 

at  the  base  of  the  heart ;  while  those  of  endocarditis  are  most  frequent  and 
dibiinct  at  the  apex.  There  are  no  signs  of  obstruction  present  with  fe- 
brile murmurs,  while  they  are  frequent  with  endocarditis 

It  is  difficult  to  tell  whether  a  murmur  is  of  old  or  recent  origin.  If, 
during  an  attack  of  rheumatism,  a  murmur  is  developed  under  daily  exam- 
ination, it  indicates  acute  exudative  endocarditis.  If  a  murmur  exists 
at  the  first  examination,  systolic,  soft,  blowing,  and  unaccompanied  by  car- 
diac hypertrophy,  there  is  reason  to  believe  that  it  is  due  to  an  acute 
endocardial  inflammation  ;  but  should  it  be  rough,  diastolic,  and  accom- 
panied by  cardiac  hypertrophy,  ,it  is  probably  not  due  to  acute  endo- 
carditis. 

Prognosis. — Acute  exudative  endocarditis  is  rarely  a  direct  cause  of 
death,  and  is  seldom  completely  recovered  from.  Acute  mitral  endocar- 
ditis ends  in  permanent  valvular  disease  in  twenty-five  per  cent,  of  the 
cases.  The  prognosis  is  rendered  unfavorable  when  the  signs  of  embolism 
or  metastasis  occur.  Sudden  splenic  enlargement  with  tenderness,  albu- 
minuria, or  hemiplegia,  when  accompanied  by  the  physical  signs  of  acute 
insufficiency  or  perforation  of  a  valve,  with  cyanosis,  dyspnoea  and  disturb- 
ance of  the  cardiac  rhythm  will  render  the  prognosis  bad.  All  these  symp- 
toms indicate  acute  ulcerative  endocarditis,  so  that  when  the  symptoms  of 
this  disease  appear  during  the  course  of  septic  diseases,  the  liability  to  its  oc- 
currence must  be  borne  in  mind.  Typhoid  symptoms  in  acute  endocarditis, 
render  the  prognosis  unfavorable.  In  children,  bronchitis,  lobular  pneu- 
monia, and  intercurrent  diarrhoea  may  cause  death.  It  may  result  from 
acute  insufficiency  of  the  heart. 

In  cardiac  aneurism  death  may  result  from  rupture  of  the  sac,  apo- 
plexy, or  from  secondary  disease  in  organs. 

Treatment. — The  treatment  of  both  varieties  of  acute  endocarditis  must 
be  determined  by  the  conditions  under  which  they  occur.  The  patient 
must  have  absolute  rest  in  bed,  in  a  room  whose  temperature  is  never 
below  70°  to  75°  F.  The  chest  should  be  covered  with  flannel,  and  during 
the  physical  examination  it  should  be  exposed  as  little  as  possible.  Some 
claim  that  an  ice-bag  over  the  heart  during  the  acute  period  will  arrest  or 
limit  the  inflammation,  but  my  own  experience  does  not  sustain  this  state- 
ment. In  rheumatic  endocarditis  anti-rheumatic  remedies  are  indicated. 
The  joints  must  be  kept  absolutely  at  rest  in  the  most  comfortable  position 
and  the  pain  relieved.  If  the  urine  is  kept  alkaline,  the  liability  to  endo- 
carditis is  diminished.  To  insure  rest  small  doses  of  opium  may  be  given, 
but  opium  cannot  be  administered  as  freely  as  in  pericarditis.  The  pa- 
tient's strength  must  be  sustained  by  the  judicious  use  of  concentrated 
nutriment  with  some  preparation  of  iron. 

"When  endocarditis,  accompanied  by  typhoid  symptoms,  occurs  with 
septic  lesions,  or  when  it  is  of  the  "ulcerative"  variety,  alcohol,  quinine 
and  iron  must  be  freely  administered  ;  when  it  complicates  Brighi,'s  dis- 
ease the  rapid  elimination  of  urea  must  be  established.  The  pain  over  the 
precordium  is  often  relieved  by  the  application  of  a  few  leeches.  The 
(internal)  use  of  mercury,  with  the  external  application  of  blue  ointment 


INTERSTITIAL   ENDOCARDITIS.  439 

to  "lessen  the  plasticity  of  the  blood,"  and  even  the  use  of  iodide  of 
potassium — "for  the  absorption  of  the  fibrinous  exudation" — are  harmful, 
and  the  theory  of  their  use  has  no  foundation. 

ESTTEESTITIAL    ENDOCARDITIS. 

Kreizing  first  traced  the  relationshij)  between  chronic  valvular  diseases  of 
the  heart  and  interstitial  endocarditis. 

Morbid  Anatomy. — Interstitial  (or  chronic)  endocarditis  may  be  a  sequela 
of  the  acute,  or  it  may  be  interstitial  from  its  commencement,  and  be  so 
insidiously  evolved  as  to  escaj)e  notice.  Sometimes  its  lesions  are  con- 
fined to  the  edges  or  base  of  the  valves ;  at  others  the  entire  valve  may  be 
involved. 

The  affected  valves  may  be  thichened,  indurated,  contracted,  adherent, 
or  degenerated.  It  is  more  closely  allied  to  rheumatism,  gout,  and  chronic 
interstitial  changes  in  other  organs  than  either  of  the  other  varieties ; 
no  part  of  the  endocardium  is  exempt  from  interstitial  changes,  but  the 
endocardium  over  the  valves  and  that  at  the  apex  of  the  left  ventricle  are 
its  favorite  sites.  The  mitral  valves  may  become  three  or  four  times  thicker 
than  normal.  Sometimes  their  functional  activity  is  unaffected  even  after 
they  have  undergone  extensive  ]3athological  changes.  White,  thickened, 
oi^aque  spots,  the  results  of  interstitial  endocarditis,  are  often  found  irregu- 
larly scattered  over  the  internal  wall  of  the  heart  cavities.  When  vegeta- 
tations  are  developed  in  interstitial  endocarditis,  they  differ  from  those  of 
the  acute  form,  for  they  are  firmer  and  less  prominent,  and  rest  upon  an 
indurated  base.  In,  and  u.nderneath,  the  endocardium  there  is  tissue- 
increase,  and  fibrin  is  deposited  on  any  prominence  of  the  endocardium. 
These  deposits  are  of  various  forms,  and  may  extend  for  one-half  an  inch 
or  more  into  adjacent  vessels  or  cavities.  They  are  usually  globular  or 
wart-like  in  form,  and  are  situated  on  the  ventricular  surface  of  the  aortic, 
and  upon  the  auricular  surface  of  the  mitral  and  tricuspid  valves. 

A  microscopical  examination  of  a  cross  section  of  an  indurated  valve 
shows  flat  cells  arranged  in  irregular  layers,  having  between  them  a  fibrinous 
material,  which  has  in  it,  here  and  there,  a  few  elastic  fibres.  The  new 
formation  always  originates  in  the  layer  of  flat  cells.  These  changes  are 
best  marked  in  the  fibrous  zone  of  the  valvular  orifices,  upon  the  surfaces  of 
the  valves,  and  in  the  chordae  tendinese.  After  a  time  the  new  tissue  be- 
comes organized,  and  contracts,  and  this  contraction  is  progressive.  Gradu- 
ally the  rigid  valves,  whose  edges  are  rounded  and  hard,  are  drawn  together 
toward  their  base,  and  thus  assume  a  puckered  appearance.  Similar  proc- 
esses in  the  chordae  tendinese  cause  them  to  hypertrophy,  become  rigid  and 
shortened.  In  this  way  the  valves  are  diminished  in  depth,  and  sometimes 
their  free  edges  become  approximated  to  the  cardiac  walls,  so, that  exten- 
sive valvular  insufficiency  is  the  result.  This  does  not  always  happen  ;  for 
a  thickened  cartilaginous  valve  may  have  so  much  fibrinous  or  papillary 
groAvth  upon  it,  that  the  inward  current  is  obstructed  and  stenosis  results 
without  insufficiency.  As  this  thickening  and  rigidity  increase  the  mobility 


440  DISEASES   OF   THE    HEART. 

of  the  valvular  flaps  is  diminished,  and  adhesions  occur  between  their 
edges,  beginning  at  their  base  and  extending  toward  their  apex.  So  ad- 
herent may  they  become  that  all  evidences  of  a  valvular  outline  is  lost  and 
a  fibrous  diaphragm  is  stretched  across  the  orifice,  having  only  a  small  slit 
at  its  centre,  looking  and  feeling  like  a  button- hole,  hence  the  term 
" hutton-hole  slit."  The  mitral  opening,  which  normally  will  admit  the 
ends  of  three  fingers,  may  be  so  narrowed  that  the  end  of  the  little  finger 
will  scarcely  pass  through  it,  and  the  aortic  opening  may  not  even  admit 
a  small  quill.  These  retractions  and  adhesions  cause  the  mitral  valves 
with  their  columns  and  cords,  to  assume  the  form  of  a  perforated  cone. 

Long  gelatinous  vegetations  on  the  aortic  valve  sometimes  form  adhesions 
with  the  aortic  walls,  and  thus  a  sudden  and  extensive  regurgitation  is  in- 
duced. Insufficiency  and  stenosis  are  often  found  at  the  same  valvular 
orifice  as  the  result  of  the  valvular  thickening,  adhesion,  and  retraction. 
Such  changes  at  the  aortic  orifice  usually  occur  after  middle  life,  and  cause 
more  thickening,  adhesion,  and  retraction  than  those  at  the  mitral  valve. 
In  children  and  early  adalt  life,  the  mitral  valves  are  the  most  frequent  seat 
of  interstitial  endocarditis.  The  tendency  of  this  lowly  organized  tissue  is 
to  undergo  fatty  and  calcareous  changes.  The  minute  patches  of  fatty  de- 
generation in  the  imperfectly  organized  tissue  underneath  the  endocardium 
sometimes  form  atheromatous  masses,  containing  more  or  less  granular 
debris.  The  endocardium  over  these  patches  may  be  destroyed,  or  they 
may  soften,  ulcerate,  and  cause  extensive  destruction  of  the  valves. 

A  valvular  aneurism  may  form  in  the  same  manner  as  has  been  described 
in  ulcerative  endocarditis.  The  formation  of  calcareous  granules  and 
plates  is  a  very  frequent  termination  of  interstitial  endocarditis.  The 
aortic  orifice  is  the  most  frequent  seat  of  these  calcareous  degenerations. 
So  extensive  may  this  process  become  that  little  beads  of  chalky  material 
are  seen  studding  the  free  edges  of  the  valve  and  even  extending  into  the 
cardiac  cavities. 

"When  interstitial  endocarditis  has  its  seat  in  the  endocardium  of  the 
heart  cavities,  it  will  undergo  changes  similar  to  those  of  the  valves,  and 
the  muscular  walls  of  the  heart  will  become  the  seat  of  interstitial  changes. 
As  a  result  the  walls  of  the  heart  become  thin  and  less  resistant  than  nor- 
mal, and  depressions  occur  on  its  inner  surface.  The  process  is  a  fibrous 
overgrowth,  which  occurs  in  spots  varying  in  size  from  one-half  an  inch  to 
one  inch  in  diameter.  When  it  extends  through  the  entire  heart-wall,  the 
columns  and  cords  may  be  so  shortened  as  to  cause  valvular  insufficiency. 
If  the  cardiac  walls  yield  to  the  internal  blood  pressure,  a  well-defined 
pouch  is  produced.  This  condition  is  called  ''  aneurism  of  the  heart,"  and 
is  usually  situated  at  the  apex  of  the  left  ventricle  ;  the  pouch  may  be  as 
large  as  the  closed  fist,  and  may  communicate  with  the  ventricle  by  a  fun- 
nel-shaped or  ring-like  aperture.  The  walls  of  the  sac  are  firm  and  rigid, 
the  internal  surface  is  generally  smooth,  but  it  may  be  irregular,  in  which 
case  clots  adhere  to  its  walls.  Cardiac  muscular  fibres  are  found  in  the 
walls  of  the  aneurismal  sac.  Aneurisms  at  the  base  and  in  the  interven- 
tricular septum  may  result  from  the  extension  of  a  valvular  aneurism. 


CAKDIAC    MURMURS.  441 

These  may  destroy  the  septum  and  establish  a  communication  between  the 
two  ventricles. 

Etiology.— As  has  already  been  stated,  the  majority  of  cases  of  interstitial 
endocarditis  are  the  sequelae  of  the  acute,  and  the  affection  is  more  fre- 
quently associated  with  articular  rheumatism  than  with  any  other  disease. 
When  it  occurs  with  gout,  chronic  rheumatism,  in  alcohol  drinkers,  or 
in  the  aged,  it  is  interstitial  from  its  onset. 

Symptoms. — There  are  no  positive  subjective  symptoms  of  interstitial 
endocarditis.  There  may  be  palpitation  and  a  sense  of  uneasiness,  some- 
times amounting  to  pain,  in  the  pericardium.  There  may  be  irregularity 
in  the  action  of  the  heart ;  but  all  of  these  when  taken  together  are  not 
sufficient  for  a  diagnosis.  It  can  only  be  determined  by  the  changes  it  pro- 
duces in  the  valves  and  valvular  orifices,  causing  abnormal  changes  in  the 
heart-sounds. 

The  physical  signs  s^xidi  differential  diagnosis  are  those  of  the  murmurs 
or  valvular  disease  induced  by  the  chronic  interstitial  process,  and  will  be 
next  considered. 

The  prognosis  in  interstitial  endocarditis  will  depend  upon  the  seat  and 
the  extent  of  the  valvular  lesions  which  it  produces. 

CAEDIAC    MURMURS    AND    THEIR  RELATIOJSTS  TO    VALVULAR   DISEASE 

OF   THE    HEART. 

A  cardiac  murmur  is  an  adventitious  or  abnormal  sound  produced  within 
the  heart  or  blood-vessels,  either  by  obstruction  to  the  blood-current,  an 
abnormal  direction  of  the  blood-current,  or  a  change  in  the  blood  constit- 
uents. The  study  of  cardiac  murmurs  dates  from  Laennec's  discovery  of 
auscultation,  although  forms  of  valvular  diseases  had  been  described  by 
Vieussens  as  early  as  1716.  Aortic  disease  was  the  form  first  brought  to 
notice,  from  the  changes  it  induced  in  the  radial  pulse  ; '  John  Hunter, 
Laennec,  and  Allan  Burns  were  among  the  pioneers  in  this  branch  of  in- 
vestigation.'' 

Corvisart  was  the  first  to  mention  the  importance  of  what  we  call  to-day 
the   "  purring  thrill ."  ^ 

Many  advocate  the  "  tension  theory,^'  viz.,  that  an  increase  in  the  ten- 

1  In  Virchow's  "  Handbuch  "  Meckel's  ess^y  of  1756  is  given  as  the  first  paper  on  endocardial  disease.— 
Art.  by  Friedrichs. 

2  The  last  named  supposes  "  that  a  reflux  current  can  produce  a  hissing  noise,  something  like  what  is 
described  as  audible  palpitation  in  some  diseases  of  tlie  heart,"  1809. 

3  He  said  :  "It  probably  came  from  a  difficulty  experienced  by  the  blood  hi  going  through  an  orifice 
disproportionate  to  the  amount  of  fluid."  Laennec  regarded  murmurs  or  '■'■bruits"  as  due  to  spasmodic 
contraction  of  the  heart  or  arteries.  Corrigan  said  that  murmurs  are  "the  result  of  the  development  of 
currents — the  intrinsic  collision  of  the  moving  liquid."  In  1842  Gendrin  established  the  '■'■friction  theory  " 
^bruits  de  frottements  endocardiaques),  and  first  called  attention  to  the  fact  that  alteration  in  the  con- 
stituents of  the  blood  will  produce  murmurs  audible  in  arteries  of  medium  calibre.  Bouillaud  describes 
a  murmur  as  an  "  exnggeration  of  the  normal  bruit  caused  by  blood  friction  airainst  the  segments  of  the 
heart."  Chauveau  states  that  a  tjrnit  de  souffle  is  produced  by  the  vibration  of  a  "  reine  fiuide  "  always 
formed  when  blood  rushes  throui^h  a  part  of  the  circulatory  system  actually  or  relatively  dilated.  This 
veine  fluidehas  its  best  development  in  aiicemia  (then  called  brnit  de  diable),  for  the  jugular  veins  do  not 
collapse  and  the  volume  of  blood  in  anaemia  is  diminished.  Chauveau's  theory  is  applicable  to  anaemic 
murmurs,  but  not  to  other  cardiac  murmurs.  It  is  claimed  that  valve  murmurs  are  produced  by  collision 
of  the  blood  particles  against  one  another  ;  or  that  either  the  liquid  alone  or  the  liquids  and  solids  con- 
jointly may  develop  murmurs. 


442 


DISEASES   OF   THE   HEART. 


sion  and  force  can  so  exaggerate  a  normal  sound  as  to  produce  a  murmur. 
Tins  theory  has  clinical  foundation ;  for  valve  lesions  may  exist,  and  the 
blood  current  and  propulsive  force  may  be  so  feeble  that  there  is  no  au- 
dible murmur.  Spasm  of  the  papillary  muscles  and  chordae  tendinese  and 
vi^eakening  of  these  structures  by  fatty  degeneration  are  by  some  regarded 
as  causes  of  temporary  murmurs.'  The  same  vibration  that  produces  a 
murmur  may  produce  an  endocardial  thrill,  called  the  ''purring  thrill." 
Far  more  important  than  the  loudness,  pitch  or  quality  of  a  murmur  are 
its  rhythm,  point  of  maximum  intensity,  and  area  of  diffusion,  all  of 
which  will  be  considered  in  connection  with  the  physical  signs  of  each  lesion. 
At  the  end  of  a  cardiac  diastole  all  the  heart  cavities  are  filling ;  just 
before  the  cardiac  systole,  blood  is  forced  from  the  lungs  and  cavse  through 
the  auricles  and  ventricles,  while  the  mitral  and  tricuspid  valves  are  pressed 
against  the  ventricular  walls,  thus  offering  no  obstruction  to  the  blood 
current.  Should  any  obstruction  exist  at  either  of  the  auriculo-ventricular 
orifices,  the  blood  while  passing  through  the  opening  will  impinge  on  such 
obstruction  and  cause  a  presystolic  murmur.  During  a  cardiac  systole, 
the  filled  ventricles  contract  and  blood  is  thrown  through  the  arterial 
openings,  the  flaps  of  whose  yalves  are  pressed  against  the  walls  of  the 
vessels  so  that  no  obstruction  is  offered  to  the  outgoing  current.  At  the 
same  instant,  the  auriculo-yentricular  valves  close  their  orifices,  so  that 

blood  may  not  flow  back  into  the 
auricles.  If  the  semilunar  valves 
obstruct  the  outgoing  current,  or 
if  the  mitral  or  tricuspid  valves  do 
not  wholly  close  the  auriculo-ven- 
tricular orifices,  then,  in  the  one 
case,  the  blood-current  as  it  passes 
over  the  obstruction  at  the  semi- 
lunar orifices,  will  produce  a  sys- 
tolic murmur,  and  in  the  other  a 
systolic  murmur  will  be  produced 
by  the  backward  current  through 
the  abnormal  opening  at  the  au- 
riculo-ventricular orifices.  If  the 
pulmonary  and  aortic  system — 
which  are  filled  at  the  systole — 
have  back  of  them  a  semilunar 
valve  that  does  not  completely 
close  that  end  of  the  circuit,  the  blood  will  regurgitate  into  the  ventricles 
during  the  period  of  cardiac  rest,  so  that  semilunar  incompetence  causes 
a  diastolic  murmur. 


Fig.  93. 
Diagram  illustrating  the  mode  of  producticm  of  Car- 
diac Murmurs  in  the  Left  Heart,  with  the  cmidition 
qf  the  valves  and  cavities.  By  svhstituting  tlie  words 
Tri  cuspid  a.7id  Pulmonary  for  Mitral  aiid  Aortic,  the 
diagram  will  illustrate  Murmurs  occurring  in  the 
Bight  Heart. 


1  The  factors  that  determine  the  character  of  a  murmur— its  pitch,  quality  and  intensity— are  physical, 
as  the  force  with  which  the  jet  is  propelled,  and  the  physical  properties  of  the  media  of  conveyance  ;  and 
they  are  the  same  as  those  which  determine  the  quality  of  other  sounds. 


ENDOCARDIAL   MURMURS. 


443 


ENDOCARDIAL   MURMURS. 


TIME. 

SITUATION. 

ORIFICE. 

NATURE. 

Systolic,       1 

Basic. 

Aortic. 

Obstructive. 

2 

" 

Pulmonary. 

" 

3 

Apical. 

Mitral. 

Regurgitant. 

4 

" 

Tricuspid. 

a 

Diastolic,     1 

Basic. 

Aortic. 

" 

Presystolic,  1 

Apical. 

Mitral. 

Obstructive. 

Pulmonary  (diastolic)  regurgitant  murmurs  and  tricuspid  (presystolic)  obstructive  mur- 
murs are  so  rare,  clinically,  that  they  may  be  disregarded. 

The  following  is  the  order  of  relative  frequency  of  cardiac  murmurs  : 
(1)  mitral  regurgitation  ;  (2)  aortic  obstruction  ;  (3)  aortic  regurgita- 
tion ;  (4)  mitral  obstruction  ;  (5)  tricuspid  regurgitation  ;  (6)  tricuspid 
obstruction  ;  (7)  pulmonary  obstruction  ;  and  (8)  pulmonary  regurgita- 
tion. 

The  most  frequent  combinations  of  murmurs  are  :  (1)  aortic  obstruction 
and  regurgitation ;  (3)  mitral  obstruction  and  regurgitation  ;  (3)  mitral 
obstruction  and  tricuspid  regurgitation  ;  (4)  aortic  obstruction  and  mitral 
regurgitation  ;  (5)  double  valvular  disease  at  aortic  and  mitral  orifices  (four 
murmurs). 

Having  appreciated  the  existence  of  a  cardiac  murmur,  it  is  often  very 
difficult  to  determine  its  rhythm.  This  difficulty  may  be  lessened  by  re- 
membering that  the  first  sound  of  the  heart  is  synchronous  with  the  carotid 
and  radial  pulse  and  the  apex-beat,  and  that  it  may  be  wholly  replaced  by 
a  systolic  murmur  ;  the  second  sound  is,  however,  almost  always  heard,  for 
the  pulmonic  and  aortic  valves  are  rarely  diseased  at  the  same  time. 

After  determining  the  rhythm,  pitch,  intensity,  and  quality  of  a  cardiac 
murmur,  we  next  find  the  point  of  its  maximum  intensity.  Murmurs 
arising  at  the  mitral  valve  are  loudest  at  the  apex  of  the  heart,  ov  just  alove 
it ;  tricuspid  murmurs  are  loudest  over  the  lower  part  of  the  sternum  ; 
pulmonary  murmurs,  in  the  second  left  intercostal  space  close  to  the 
sternum,  and  aortic  murmurs  in  the  second  right  intercostal  space  at  the 
edge  of  the  sternum. 

Valvular  diseases,  causing  murmurs,  consist  in  a  condition  of  the  valves 
allowing  either  of  regurgitation  or  obstruction. 

Valvular  insufficiency  results  when  extensive  retraction,  perforation,  or 
partial  detachment  of  the  valves  prevents  them  from  completely  closing 
their  respective  orifices  ;  or  when  the  chordge  tendinese  have  been  rupt- 
ured, or  calcareous  degeneration  has  made  the  valves  rigid,  the  backward 
current  in  such  conditions  giving  rise  to  a  regurgitant  murmur. 


444 


DISEASES   OF   THE   HEART. 


"When  the  valves  are  thickened,  retracted,  adherent,  hypertrophied,  or 
degenerated,  they  obstruct  the  outward  current  of  blood  and  give  rise  to 
obstructive  murmurs.^     Both  conditions,  viz.,  stenosis  and  insufficiency, 

are  often  found  co-existing,  but 
rarely  to  the  same  extent.  The 
lesions  which  induce  these  mur- 
murs are  acute,  when  they  occur 
during  the  course  of  acute  endocar- 
ditis, and  chronic  when  they  de- 
pend upon  the  presence  of  some 
firm  tissue,  such  as  connective, 
fibroid,  calcareous,  or  atheromatous 
tissue,  which  alters  the  form  and 
impairs  the  function  of  the  valves. 
Both  the  above  varieties  may  pro- 
duce the  same  murmurs. 

Since  physical  signs  are  here  the 
most  important  factors  in  diagnosis, 
the  normal  (physical)  relation  of 
the  heart  must  be  borne  in  mind: 
the  apex  of  the  heart  is  normally 
felt  between  the  fifth  and  sixth 
ribs  on  the  left  side,  about  two 
inches  below  the  nipple  and  one 
inch  to  its  sternal  side.  The  highest  part  of  the  base  of  the  heart  is  on  a 
level  with  the  third  costal  cartilage.  The  tricuspid  orifice  is  situated  at 
the  junction  of  the  fourth  left  costal  cartilage  with  the  sternum.  The 
mitral  orifice  is  to  the  left  of  the  tricuspid,  immediately  behind  the  left 
border  of  the  sternum,  at  the  junction  of  the  third  costal  cartilage  with 
that  bone.  The  aortic  orifice  is  one-half  an  inch  lower  than  and  to  the 
right  of  the  pulmonary  orifice,  behind  the  sternum  on  a  level  with  the  third 
interspace.  The  tricuspid  orifice  is  the  most  superficial,  then  the  pulmonary, 
next  the  aortic,  and  deepest  of  all  the  mitral.  Eanged  from  above  down- 
wards, the  pulmonary  orifice  comes  first,  then  the  aortic,  then  the  mitral, 
lastly  the  tricuspid. 


Fig.  94. 

Diagram  showing  the  Areas  of  Cardiac  Murmurs. 

A.  Area   of  Aortic  Murmurs;   M.  3Iitral ;    T.  Tri- 
cuspid ;  P.  Pulmonary. 


AORTIC    OBSTEUCTION,    OE    STENOSIS. 

This  is  a  common  cardiac  lesion,  and  is  always  accompanied  by  more  or 
less  hypertrophy  of  the  left  ventricle. 

Morbid  Anatomy. — The  valves  will  be  found  to  present  some  or  all  of  the 
changes  described  in  the  history  of  interstitial  endocarditis,  together  with 
degenerative  changes  due  to  atheromatous,  calcareous,  fibroid,  fatty,  or  con- 
nective-tissue metamorphosis ;  they  may  be  covered  with  thick,  warty, 
irregular  excrescences,  that  cause  loud  murmurs  and  yet  do  not  seriously 


1  Some  call  obstructive  murmurs  direct ;  and  regurgitant  murmurs  indii'ect,  from  the  current  that  causes 
the  sound. 


AORTIC    OBSTRUCTION,    OR   STENOSIS. 


445 


Fig.  95. 

Vegetations  on  the  Aortic  Valves  giving 

rise  to  Aortic  Obstruction. 


obstruct  the  out-going  blood-current.  Or  the  aortic  orifice  may  be  almost 
completely  occluded,  and  then  the  extent 
of  the  lesion  is  measured  more  by  the  re- 
sulting hypertrophy  and  its  effects  on  the 
systemic  circulation,  than  by  the  loudness 
or  harshness  of  the  murmur.  The  A^alves 
are  often  so  rigid  that  they  cannot  be 
pressed  back,  and  then  they  present  greater 
obstruction  to  the  outgoing  current  than 
when  vegetations  exist ;  as  the  result  of 
adhesions,  the  valves  may  become  fused 
into  a  mass,  so  that  they  project  into  the 
blood-stream  in  the  form  of  a  funnel,  ir- 
regular in  shape  and  studded  with  calcare- 
ous nodules.  The  line  of  attachment  of 
the  valves  to  the  aorta  frequently  becomes 
obliterated. 

Aortic  stenosis  is  frequently  accompanied 
by  atheromatous  changes  in  the  aorta,  called  "Arteritis  deformans."  As 
a  result  of  aortic  stenosis,  hypertrophy  of  the  left  ventricle  occurs,  which  is 
gradual  in  its  development  and  called  ''compensatory"  hypertrophy,  be- 
cause it  is  due  to  the  increased  force  required  to  propel  the  blood  through 
the  constricted  orifice.  Mitral  insufficiency  is  apt  to  occur  later,  either 
from  extension  of  the  inflammation  from  the  aortic  valves,  or  from  forcible 
pressure  of  blood  upon  the  ventricular  surface  of  the  mitral  flaps.  Slight 
thickening  and  roughening  of  the  aortic  valves  lead  to  no  serious 
results. 

Etiology. — Aortic  stenosis  is  most  frequently  met  in  middle  and  ad- 
vanced life  ;  the  mean  age.  being  forty-seven  years,  and  the  extreme  limits 
twenty  to  sixty.  It  is  occasionally  met  with  in  children  under  two  years 
of  age.  It  may  be  the  result  of  defective  aortic  development  and  perhaps 
of  imperfect  development  of  the  trachea,  causing  imperfect  expansion  of 
the  chest.'  Interstitial  endocarditis  of  rheumatic  origin  is  its  most  fre- 
quent cause.  Chorea  and  chronic  Bright's  disease  may  cause  it.  Atheroma 
or  arteritis  deformans  extending  to  the  valves  sometimes  gives  rise  to  it. 
Increased  aortic  tension  indirectly  causes  aortic  stenosis.^  Men  suffer  from 
aortic  stenosis  oftener  than  women,  for  in  them  the  valves  are  subject  to 
greater  tension,  and  hence  non-rheumatic  aortic  valvular  disease  is  common 
in  men  and  rare  in  women.  Occupations  that  involve  re^Dcated  sudden  and 
severe  muscular  effort  induce  it.  In  old  age,  the  aortic  walls  are  weak- 
ened, and  when  aortic  disease  is  met  with  in  the  young,  it  is  often  the 
result  of  premature  vascular  senility.'     Disease  of  the  aortic   valves   is 

1  Guy's  Hosp.  Reports,  S.  I.,  vol.  vi.,  p.  2,35. 

2  The  coexistence  of  cardiac  valvular  disease  and  cancer  is  a  remarkable  coincidence,  possibly  with  a 
causal  relation. 

'  Dr.  Allbutt  says  that  in  Leeds  quite  young  men  have  aortic  valvular  disease  ;  and  Dr.  Peacock  men- 
tions sevf.ral  cases  wliere  it  has  occurred  in  young  girls  who  have  been  placed  at  service  before  they  were 
fully  developed.  Corvisart  and  Virchow  both  admit  the  possibility  of  syphilis  being  a  cause  of  aortic 
valvular  disease,  but  clinically  this  is  not  yet  proven. 


446  DISEASES   OF   THE   HEART. 

oftener  non-rheumatic  in  origin  than  mitral  lesions.     It  is  slower  in  its 
development,  and  is  more  frequently  met  with  in  advanced  life. 

Symptoms. — The  subjective  symptoms  of  aortic  stenosis  are  rarely  well 
marked.  Although  extensive,  it  may  cause  no  discomfort,  for  as  the  ob- 
struction increases,  compensatory  hypertrophy  relieves  pulmonary  pressure  ; 
but  when  this  no  longer  compensates  for  the  obstruction,  the  arteries  are 
inadequately  filled,  the  left  auricle  cannot  empty  itself,  and  consequently 
the  pulmonary  vessels  and  the  venous  system  are  abnormally  full.  The 
scanty  arterial  supply  causes  pallor  of  the  face,  and  syncope  may  occur 
from  cerebral  ansemia,  but  these  are  late  symptoms,  not  usually  appearing 
until  after  the  mitral  valve  has  become  secondarily  involved.  The  pulse  is 
normal  in  frequency,  diminished  in  volume  and  fulness,  and,  as  a  rule, 
regular  in  rhythm,  though  it  may  be  intermittent,  compressible,  and 
''  jerky  "  in  character.  Signs  of  arterial  anasmia  usually  precede  those  of 
venous  engorgement.  The  sphygmograph  gives  a  slanting  or  oblique  up- 
stroke, showing  that  the  influence  of  percussion  is  lost,  and  the  tracings 

may  show  considerable  sep- 
aration between  the  "percus- 
sion "  and  "  tidal "  waves. 
The  pulse  is  rarely  slowed. 
There  may  be  slight  palpita- 
tion and  paroxysmal  pain  in 
the  chest. 

Aortic  stenosis  is  more  often 
'^^^■^^-  associated  with  cerebral  em- 

Sphygmographictracing  in  a  case  of  Aortic  Obstruction,  with    ^   j-  ^^  ^j  j_ 

marked  separation  of  the  percussion  and  tidal  waves.  J 

vular  lesion,  and  the  splenic 
and  renal  vessels  are  frequently  the  seat  of  emboli.  The  left  middle 
cerebral  artery  is  the  most  common  seat  of  cardiac  emboli  ;  and  the  left 
lower  limb  is  more  subject  to  embolism  from  aortic  valvular  disease  than 
the  right.  Embolism  may  be  due  to  small  auricular  or  ventricular  clots 
that  form  behind  the  obstruction  ;  such  clots  have  occluded  the  aortic  ori- 
fice and  caused  sudden  death.' 

Physical  Signs. — The  physical  signs  of  aortic  stenosis  are  usually  distinc- 
tive and  easily  appreciated. 

Inspection  shows  the  area  of  cardiac  impulse  to  be  abnormally  increased. 
Very  extensive  increase  of  this  area  is  often  accompanied  by  lifting  of  the 
chest  over  the  precordial  region. 

Palpation. — The  impulse  is  felt  to  be  forcible,  and  may  be  accompanied 
by  a  heaving  or  lifting  sensation.  The  apex  is  displaced  to  the  left  and 
slightly  downward.  An  indistinct  thrilling  sensation  is  often  imparted  to 
the  hand  during  the  systole.  This  systolic  fremissement  is  nothing  more 
than  an  intensified  endocardial  thrill,  and  it  generally  radiates  to  the  ensi- 
form  process,  being  most  intense  in  the  second  right  intercostal  space. 

Percussion. — The  area  of  cardiac  dulness  increases  in  proportion  to  the 
displacement  of  the  apex  beat  to  the  left. 

1  Path.  Tran!^.,  vol.  ix.,  p.  9. 


AORTIC   OBSTRUCTION",    OR   STENOSIS.  447 

Auscultation. — Aortic  obstructive  murmurs  are  loudest  and  most  distinct 
at  the  second  right  intercostal  space  and  at  the  sternal  insertion  of  the  third 
left  costal  cartilage.  They  are  systolic,  and  oftener  accompany,  than  replace 
the  first  sound  ol  the  heart.  The  maximum  intensity  of  this  murmur  is  at 
the  second  sterno-costal  articulation  of  the  right  side,  but  it  may  be  heard 
with  equal  intensity  over  the  whole  upper  part  of  the  sternum,  and  may  be 
audible  at  the  xiphoid  cartilage.  It  is  always  a  harsh  murmur,  heard  most 
distinctly  at  the  commencement  of  the  systole.  In  uncomplicated  aortic 
stenosis,  the  aortic  second  sound  may  be  inaudible  ;  it  is  always  feeble,  but 
the  pulmonic  second  sound  is  always  audible.  The  area  of  diffusion  of  this 
murmur  follows  the  law  that  a  murmur  is  propagated  in  the  direction  of 
the  blood-current.  It  is  conveyed  along  the  aorta  into  the  carotids,  and 
one  of  its  characteristics  is  that  it  is  heard  in  the  great  vessels  of  the  neck. 
It  may  be  heard  in  the  thoracic  and  abdominal  aorta.  When  an  aortic  ob- 
structive murmur  is  heard  at  the  apex,  its  intensity  is  diminished,  and 
when  heard  behind  it  is  most  distinct  at  the  left  of  the  third  and  fourth 
dorsal  vertebrae,  near  their  spines,  and  frequently  extends  downward  along 
the  spine  in  the  course  of  the  aorta,  but  with  diminished  intensity.  It  is 
to  be  noted  that  a  systolic  murmur,  audible  at  the  base  and  traceable  along 
the  ascending  arch  toward  the  end  of  the  right  clavicle,  is  by  no  means 
limited  to  cases  of  aortic  stenosis,  although  this  lesion  always  produces  a 
murmur  with  these  characteristics.  When  the  mitral  or  tricuspid  valves 
are  thickened  or  incompetent,  or  when  the  myocardium  undergoes  fatty  de- 
generation, this  murmur  will  entirely  replace  the  first  sound  of  the  heart. 

DiiFerential  Diagnosis. — Aortic  obstruction  may  be  mistaken  for  mitral 
and  tricuspid  regurgitation,  an  aticBinic  h'uit,  or  the  murmur  of  a  tlioracic 
aneurism.  Both  mitral  and  tricuspid  regurgitation  and  aortic  stenosis  pro- 
duce a  systolic  murmur.  The  murmur  of  aortic  stenosis  is  heard  with  its 
maximum  intensity  at  the  third  left  sterno-costal  articulation,  and  dimin- 
ishes in  intensity  toward  the  apex  of  the  heart.  The  murmur  of  mitral 
regurgitation  is  heard  loudest  at  the  apex-beat.  The  murmur  of  aortic 
stenosis  is  conveyed  into  the  vessels  of  the  neck  ;  that  of  mitral  regurgita- 
tion to  the  left,  in  the  direction  of  the  apex-beat,  and  is  heard  behind,  be- 
tween the  fifth  and  eighth  dorsal  vertebrse,  at  the  left  of  the  spine,  with 
very  nearly  the  same  intensity  as  at  the  apex.  The  pulse  in  aortic  stenosis 
is  hard,  firm,  wiry,  but  regular  ;  while  in  mitral  regurgitation  it  is  irregu- 
lar in  rhythm  and  force,  but  never  incompressible,  and  is  easily  increased 
in  frequency.  Gastric,  intestinal,  renal,  hepatic,  and  bronchial  symptoms 
are  present  in  mitral  regurgitation,  while  the  subjective  symptoms  of  aortic 
obstruction  are  cerebral  in  character.  The  pulmonic  second  sound  is  feeble 
in  aortic  stenosis,  but  in  mitral  regurgitation  it  is  intensified.  The  mur- 
mur of  aortic  stenosis  is  harsh,  that  of  mitral  regurgitation  soft,  and  often 
musical. 

Tricuspid  regurgitation  is  accompanied  by  a  systolic  murmur  which  is 
rarely  heard  above  the  third  rib  ;  while  that  of  aortic  stenosis  has  its  point 
of  maximum  intensity  at  the  right  second  sterno-costal  articulation.  Tri- 
cuspid regurgitation  is  accompanied  by  jugular  pulsation  ;  while  the  mur- 


448 


DISEASES   OF  THE   HEAET. 


mur  of  aortic  obstruction  is  heard  in  the  arteries  of  the  neck/  The  area  of 
transmission  of  tricuspid  regurgitant  murmurs  is  not  more  than  two  inches 
from  the  point  of  their  maximum  intensity,  while  aortic  stenotic  murmurs 
are  conveyed  into  the  vessels  of  the  neck.  The  pulse  in  tricuspid  disease 
is  normal ;  in  aortic  stenosis  it  is  hard  and  wiry. 

Anmmia  produces  a  murmur  heard  loudest  in  the  carotids  and  accom- 
panied by  a  venous  hum,  which  is  continuous  and  best  heard  on  the  right 
side  of  the  neck.  Thus,  in  anaemia  there  are  three  murmurs  :  cardiac, 
venous,  and  arterial.  In  aortic  disease  the  point  of  maximum  intensity 
and  the  absence  of  a  ''venous  hum"  will  aid  in  the  diagnosis;  besides, 
there  will  be  cardiac  hypertrophy  and  an  increase  in  the  force  of  the  apex- 
beat,  while  the  impulse  is  feeble  in  anaemia.  The  murmur  is  soft  and 
blowing  in  anaemia,  and  harsh  in  aortic  obstruction.  The  pulse  is  charac- 
teristic in  aortic  stenosis,  in  anaemia  it  may  have  a  thrill,  but  is  never 
hard  and  wiry.  The  etiology  and  subjective  symptoms  of  these  two  are 
strikingly  dissimilar. 

In  tlioracic  aneurism  the  dilating  impulse  on  palpation,  the  normal  force 
of  the  heart-beat,  the  single  and  double  bruit,  and  the  pain  are  all  impor- 
tant signs,  which  are  absent  in  aortic  stenosis. 

The  prognosis  and  treatment  of  ''  valvular  diseases  of  the  heart"  will  be 
considered  at  the  end  of  their  history. 


AOETIC    INSUFFICIENCY,    OR    REGUEGITATIOlSr. 

This  is  an  abnormal  condition  of  the  aortic  valves,  which  prevents  their 

complete  closure,  and  allows  a  backward  current  of  blood  to  flow  from  the 

aorta  into  the  left  ventricle  during  its  diastole.     It  is  usually  associated 

with  more  or  less  aortic  stenosis. 

Morbid  Anatomy. — In   aortic   insufficiency,  the  flaps  of  the  valves  may 

be  thickened,  puckered,  or  shortened,    so  that 
they  do  not  meet.     If  the  centre  of  a  valve  is 
indurated,  it  will  curl  up,  either  toward  the  ori- 
fice or  back   against  the  aortic  wall.      In  the 
former  case,  there  is  insufficiency  with  great  ob- 
struction ;  in   the  latter,  insufficiency  with  only 
slight   obstruction.      This   valvular   thickening 
or  shortening  may  be  due  to  endocarditis.     In 
some  cases,  the  flaps  of  the  valves  may  become 
adherent  to  the  walls  of  the  aorta,  or  a  diseased 
valve  may  be  torn   or  ruptured,  which  will  al- 
low a  free  opening  for  the  regurgitant  blood. 
View  of  Aortic  Semiinnar  Valves  FoUowing  stenosis,  little  tunucls  may  form  by 
torvtirs'trlhfcke^^^^^^^        the  side  of  the  vaWes  and  permit  of  a  regurgi- 
Z^^^to^^tXl^LKT^;.^^^'^^^^^^^'^'     The  aortic  valves   are  more  lia- 
tic  orifice.  I^lg   |-Q   laceration   than   any  other  valves.      In 

aortic  regurgitation,  during  a  cardiac  diastole, 

1  To  distinguish  between  intrinsic  pulsation  of  the  jugular  vein  and  throbbing  of  the  carotids,  press 
fightly  on  the  vein  above  the  clavicle  ;  this  arrests  pulsation  when  due  to  tricuspid  disease,  while  if  due 
to  aortic  stenosis,  the  result  is  negative. 


Fig.  97. 


AORTIC    INSUFFICIENCY,    OR   REGUEGITATION.  449 

there  is  added  to  the  blood,  which  normally  flows  from  the  auricle  into 
the  ventricle,  a  regurgitant  current  from  the  aorta,  and  so  over-distention 
of  the  left  ventricle  results.  Thus,  after  a  time,  the  left  ventricle  becomes 
permanently  dilated.  To  overcome  this  distention  compensatory  hyper- 
trophy takes  place.  The  left  heart  is  often  greatly  enlarged.  As  a  result, 
the  arterial  system  is  over-distended  at  each  cardiac  systole. 

The  extra  ventricular  power  and  the  abnormal  quantity  of  blood  thrown 
against  the  arterial  walls  lead  to  endarteritis  and  subsequent  atheroma, 
and  the  degeneration  of  the  vessels  predisposes  to  apoplexy  and  to  aneu- 
rism. Since,  normally,  aortic  recoil  fills  the  coronary  vessels,  aortic  regur- 
gitation must  be  followed  by  imperfect  blood-supply  to  the  heart,  and  dila- 
tation again  commences  at  the  expense  of  the  walls  of  the  heart,  the  hyper- 
trophy ceasing  to  compensate  for  the  increased  dilatation.  Atrophy  of  the 
papillary  muscles  may  allow  the  mitral  flaps  to  pass  beyond  their  normal 
line  at  the  auricles,  when  there  is  an  increase  in  blood  pressure,  and  then 
mitral  regurgitation  and  impeded  venous  circulation  will  result.  Passive 
pulmonary  hyperemia  may  be  present  wWiout  mitral  lesions,  when  the  left 
auricle  cannot  wholly  empty  itself. 

Etiology. — This  is  similar  to  that  of  aortic  stenosis.  Eheumatic  en- 
docarditis is  its  chief  source ;  but  it  may  follow  sudden  and  violent 
muscular  effort,  atheroma  of  the  aorta  or  endarteritis.  Congenital  mal- 
formation, according  to  Virchow,  is  a  frequent  cause  in  chlorotic  females. 
The  atheroma  which  causes  aortic  insufficiency  is  often  of  gouty  origin, 
especially  when  gouty  kidneys  coexist  or  when  alcoholismus  is  associ- 
ated with  a  gouty  diathesis.  Dilatation  of  the  aorta  at  its  origin  may  in- 
duce it.  Fagge  says  only  fifty  per  cent,  of  the  cases  of  aortic  insufficiency 
give  a  rheumatic  history.  The  violence  with  which  the  valves  are  closed 
during  prolonged  and  violent  physical  exertion  may  induce  an  interstitial 
endocarditis  which  will  lead  to  it- 
Symptoms. — So  long  as  hypertrophy  compensates  for  the  regurgitation, 
there  is  little  or  no  inconvenience  experienced  by  the  patient,  even 
though  the  regurgitation  is  extensive.  When  the  regurgitant  stream  is 
small,  there  is  no  disturbance  of  the  general  health,  but  in  time  the  hyper- 
trophy induces  excessive  heart-action  during  excitement  or  violent  muscu- 
lar effort.  The  heart-action  then  becomes  labored  and  the  patient  is  anx- 
ious, nervous  and  fretful,  and  knows  well  that  exercise  will  augment  his 
uncomfortable  symptoms.  The  respirations  are  accelerated  with  the  cardiac 
palpitation  ;  as  the  disease  advances  attacks  of  headache  and  vertigo  be- 
come more  and  more  prolonged  and  severe  ;  the  patient  complains  of  muscas- 
volitantes,  dyspnoea,  and  giddiness,  and  is  compelled  to  sleep  with  his 
head  elevated.  Palpitation  and  a  visible  carotid  impulse  are  now  con- 
stantly present.  A  comparatively  frequent  symptom  is  a  distinctly  par- 
oxysmal shooting  or  stabbing  pain  over  the  heart,  in  the  left  shoulder,  or 
extending  down  the  left  arm.  This  pain  may  be  accompanied  by  numb- 
ness and  a  peculiar  whiteness  of  the  skin  along  the  line  of  pain.  In  other 
cases,  the  pain  passes  from  the  middle  of  the  sternum  down  the  right  arm.. 
This  pain  is  increased  by  excitement,  physical  exercise,  and  over-distention, 

29 


450 


DISEASES    OF   THE    HEART. 


of  the  stomach.  Sometimes  these  patients  complain  of  a  sickening  flutter- 
ing of  the  heart  when  the  nutrition  of  the  heart  walls  becomes  interfered 
with  ;  and  when  mitral  insufficiency  exists,  the  systemic  veins  become  over- 
loaded and  cyanosis  and  dropsy  result ;  the  dropsy  appears  first  as  oedema 
of  the  feet,  and  gradually  extends  upward  until  there  is  general  anasarca. 
The  cyanosis  is  increased  after  slight  exertion,  and  is  accompanied  by  vio- 
lent i^aroxysms  of  dyspnoea,  carotid  pulsation,  and  puffiness  of  the  face. 

Later  in  the  disease,  there  is  orthopnoea,  sudden  startings  in  sleep, 
angina  pectoris,  and  there  may  be  albuminuria  and  enlargement  and 
tenderness  of  the  liver.  Attacks  of  syncope  at  first  occur  only  after  active 
exercise  ;  later,  they  occur  independently,  and  are  very  distressing.  These 
patients  may  die  at  any  moment,  either  when  perfectly  quiet  or  when  under 
intense  excitement ;  the  danger  is  greatest,  however,  during  exertion. 

The  pulse  is  the  most  characteristic  subjective  symptom,  and  was  first 
accurately  described  by  Sir  D.  Oorrigan,'  and  is  therefore  often  called  "Cor- 
riga7i's2nilse."  He  said  the  disease  was  indicated  by  visible  pulsation  of  the 
vessels  of  the  head,  neck  and  upper  extremities.  On  account  of  the  elonga- 
tion of  the  arteries  during  their  pulsation,  and  their  flexuosity,  the  pulse  is 
often  called  the  "piston  pulse  f'  it  is  large  and '  distinct,  and  rapidly  pro- 
jected against  the  finger,  and  the  arterial  tension  sinks  just  as  quickly  to 
a  minimum.  It  may  be  accompanied  by  a  vibrating  jar,  on  account  of  which 
it  is  called  the  '^water-hammer,"  "jerking,"  "splashing,"  or  *' col- 
lapsing "  pulse.  Its  characteristics  are  more  apparent  when  the  arm  is  raised 
above  the  head  ;  although  slightly  infrequent,  quick,  and  jerking,  it  is 
always  regular  in  rhytlim; — the  radial  impulse  is  felt  a  little  after  the  apex- 
beat.  As  soon  as  the  systemic  circulation  is  overloaded  from  insufficiency 
of  the  heart  or  from  secondary  mitral  insufficiency,  the  pulse  becomes 
feeble,  irregular,  and  sometimes  intermittent,  but  always  "  jerking."  The 
sphygmograph  shows  a  high  upstroke  and  an  absence  of  the  dicrotic  wave. 

The  pulse-tracing  of  aortic 
regurgitation  resembles  the 
senile  pulse,  but  a  senile  pulse 
gives  a  rounded  instead  of  a 
pointed  summit.  The  pecu- 
liar crochet  or  beak  is  very 
noticeable.^ 

Physical  Signs. — Inspection 
reveals  an  increase  in  the  area 
and  force  of  the  apex-beat, 
which  is  visible  over  a  wider 
area  than  in  aortic  stenosis.  The  vessels  of  the  neck  and  upj)er  extremities 
often  pulsate  ;  when  compensation  ceases  to  balance  the  forces  in  the  heart, 
the  apex-beat  becomes  feeble  and  diffused.  Pulsation  of  the  retinal  vessels 
has  been  observed. ' 

1  Edin.  Med.  Surg.  Jonr.,  April,  1832. 

2  Stokes  has  described  a  peculiar  and  characteristic  pulsation  (steel-hammer  pulse)  occurring  in  cases 
of  acute  rheumatic  arthritis,  and  supervening  iipon  aortic  insutficienc.v.  This  pulse  is  abrupt  and  ener- 
getic as  the  rebound  of  a  smith's  hammer  from  the  anvil ;  it  is  only  exhibited,  however,  in  the  arteries 
near  the  affected  joints. 

3  Lond.  Ophth.  Hosp.  Rep  ,  Feb.,  1873. 


Sphygmographic  tracing   in  Aortic  Regiirgitation,   showin: 
marked  amplitude  with  absent  dicrotic  wave. 


AORTIC    INSUFFICIENCY,    OK   REGURGITATION.  451 

Palpation. — A  heaving,  lifting  imjDulse  will  be  appreciated  which  is 
transmitted  over  a  large  area.  The  apex-beat  is  displaced  down  and  toward 
the  left,  sometimes  as  far  as  the  eighth  rib,  and  two  and  one-half  inches  to 
the  left  of  the  left  nipple.  A  continuous  diastolic  thrill  is  sometimes  felt 
over  the  site  of  the  aortic  valves.  There  may  be  slight  pulsation  in  the 
scrobiculus  cordis. 

Percussion. — The  superficial  and  deep  areas  of  dulness  correspond  to  the 
extent  of  the  cardiac  enlargement.  As  soon  as  dilatation  exceeds  hyper- 
trophy, the  area  of  dulness  will  extend  horizontally  and  slightly  upward, 
the  apex  beating  in  the  axillary  line.  Dulness  may  extend  six  and  a  half 
inches  from  right  to  left  and  from  the  third  rib  to  the  line  of  liver  dulness. 
Superficial  dulness  is  increased  horizontally  and  to  the  left. 

AuscuUatio7i.—AovtiG  regurgitation  is  attended  by  a  diastolic  murmur, 
which  may  take  the  place  of,  or  immediately  follow,  the  second  sound  of 
the  heart.  This  murmur  has  its  maximum  intensity  at  the  sternal  end 
of  the  second  right  intercostal  space,  or  at  the  sternal  junction  of  the  third 
rib  on  the  left  side.  It  is  transmitted  over  the  sternum  and  may  be  loud- 
est at  the  xiphoid  cartilage  and  is  thence  transmitted  in  the  direction  of 
the  apex.  Its  area  of  diffusion  is  greater  than  any  other  cardiac  murmur  : 
it  is  not  only  conducted  down  the  sternum  to  the  apex,  but  it  may  be 
heard  at  the  sides  of  the  chest,  along  the  spinal  column,  faintly  in  the 
ascending  and  transverse  arch,  in  the  carotids,  and  sometimes  as  far  as  the 
radial  arteries.  The  murmur  is  "substitutive"  rather  than  "accompany- 
ing," for  the  pulmonic  second  sound  is  audible  at  the  right  base.  Incom- 
petency of  the  posterior  segment  of  the  aortic  valve  induces  a  murmur 
which  is  conducted  to  the  apes,  while  inadequacy  of  the  anterior  flaps  pro- 
duces a  murmur  which  is  conveyed  toward  the  ensiform  cartilage ;  the 
former  murmur  would  indicate  a  more  favorable  prognosis,  owing  to  the 
relationship  of  the  anterior  segments  to  the  coronary  arteries.  When  the 
second  sound  of  the  heart  is  distinct,  the  murmur  immediately  follows  it. 
Some  call  this  a  " post-diastolic  aortic  murmur." 

Although  an  aortic  regurgitative  murmur  has  the  greatest  area  of  dif- 
fusion, it  is  not  the  loudest  murmur  ;  it  is  soft,  blowing,  sometimes  rough, 
and  frequently  musical.  It  is  loudest  at  the  beginning  of  diastole,  gradu- 
ally decreasing  in  intensity,  although  it  may  be  "  rushing  "  or  "  blowing  ; " 
this  murmur  may  temporarily  disappear  during  the  whole  diastole.  When 
aortic  stenosis  coexists  there  will  be  a  double  murmur,  audible  over  a  very 
large  area,  and  having  its  maximum  intensity  at  the  right  edge  of  the 
sternum  in  the  second  interspace.  Systolic  and  diastolic  murmurs  may  run 
into  each  other.  If  mitral  occurs  with  aortic  regurgitation,  each  murmur 
retains  its  own  place  of  maximum  intensity.  Earely,  when  two  segments 
of  the  valve  are  healthy,  a  clear  aortic  second  is  heard,  preceded  by  a  faint 
"reflux  "  murmur,  said  to  be  pre-diastolic  in  rhythm. 

Aortic  murmurs  are  sometimes  so  indistinct  as  to  be  heard  only  when  the 
patient  is  in  a  recumbent  posture.  A  diastolic  murmur  heard  at  or  below 
the  level  of  the  aortic  valves,  and  chiefly  audible  in  tlie  line  of  the  sternum, 
indicates  considerable  regurgitation.     When  a  diastolic  murmur  is  inaudible 


452  DISEASES   OF   THE   HEART. 

in  the  carotids,  it  is  because  preceded  by  a  systolic  murmur  which  has  its 
maximum  intensity  in  the  "  aortic  area."  Such  a  murmur  indicates  much 
more  obstruction  than  regurgitation.  When  a  diastolic  murmur  is  heard 
distinctly  in  the  carotids,  and  is  also  preceded  by  a  systolic  murmur  in 
them,  the  combination  indicates  trifling  obstruction  with  considerable  in- 
competence. 

Differential  Diagnosis. — The  diagnosis  of  aortic  regurgitation  is  generally 
not  difficult,  as  it  rests  almost  exclusively  upon  the  existence  or  non-existence 
of  a  diastolic  murniiir.  It  may  be  mistaken  for  aortic  stenosis,  mitral  ob- 
struction, pericarditis  localized  over  the  aorta,  aneurism  of  that  portion 
of  the  aorta  immediately  above  the  valves,  patency  of  the  ductus  arteriosus, 
insufficiency  of  the  pulmonic  valves,  and  occasionally  for  a  rough  and  in- 
elastic condition  of  the  ascending  aorta. 

Mitral  obstruction  gives  a  presystolic  murmur,  while  aortic  reflux  pro- 
duces a  diastolic  murmur.  Mitral  stenosis  is  accompanied  by  no  hyper- 
trophy or  dilatation  of  the  left  ventricle;  whereas  these  conditions  are 
always  present  in  aortic  reflux.  The  quality  of  a  presystolic  mitral  murmur 
is  harsh  and  rough,  and  it  has  a  churning,  blubbering  or  grinding  character  ; 
while  aortic  reflux  has  a  murmur  of  low  pitch,  and  a  soft,  blowing  or  musi- 
cal character.  Mitral  stenosis  is  accompanied  by  a  purring  thrill,  which  is 
absent  in  aortic  regurgitation.  The  murmur  of  mitral  stenosis  is  the 
longest  of  all  cardiac  murmurs,  and  is  never  heard  behind;  whereas  that 
of  aortic  regurgitation  is  heard  at  the  sides  of  the  chest  and  along  the 
spinal  column.  Finally,  mitral  stenosis  is  attended  by  well-marked  pul- 
monary symptoms  during  active  physical  exertion,  which  are  rarely  pres- 
ent in  aortic  insufficiency. 

A  pericardial  friction  sound  over  the  aorta  has  its  maximum  intensity 
over  the  seat  of  its  production,  and  is  usually  audible  during  both  the 
cardiac  systole  and  diastole.  In  aortic  regurgitation,  the  character  of  the 
pulse,  the  existence  of  hypertrophy  and  dilatation  of  the  left  ventricle,  and 
the  carotid  pulsation  will  establish  the  diagnosis. 

An  aneurism  at  the  sinuses  of  Valsalva  is  diagnosticated  by  the  history  of 
the  case,  the  presence  of  the  murmur  over  the  pulmonary  artery,  the  evi- 
dence of  arterial  degeneration,  the  absence  of  left  ventricular  dilatation  and 
hypertrophy,  and  by  the  peculiar  jerking  pulse.  An  aneurismal  murmur 
is  circumscribed,  has  a  booming  quality,  is  usually  systolic  in  rhythm,  and 
is  never  transmitted  to  the  apex  of  the  heart. 

Patency  of  the  ductus  arteriosus  is  a  rare  condition  ;  in  a  case  where  it 
was  diagnosticated '  the  murmur  was  audible  at  the  left  of  the  sternum,  was 
not  everywhere  continuous  with  the  second  sound,  was  only  transmitted 
very  feebly  to  the  left,  and  had  a  wavy  character  sufficient  of  itself  to  distin- 
guish it  from  aortic  regurgitation. 

Insufficiency  of  the  pulmonic  semilunar  valves  is  the  rarest  of  all  valvu- 
lar lesions  ;  the  murmur  should  be  diastolic,  having  its  maximum  intensity 
in  the  second  intercostal  space  of  the  left  side,  it  would  be  transmitted 
only  downward  and  toward  the  right   apex,  and  would  not  be  attended 

1  Guy's  Hosp.  Rep.    Series  3,  vol.  xviii.,  1873-3. 


MITRAL   STENOSIS. 


453 


by  arterial  pulsation,  a  jerking  pulse,  or  left  ventricular  dilatation  and  hy- 
pertrophy. 

A  diastolic  murmur  in  the  ascending  arch  due  to  roughening,  rigidity, 
and  dilatation  of  the  artery  is  also  rare,  while  the  condition,  which  some 
say  can  produce  it,  is  very  common.  Two  cases  are  recorded  in  which  the 
diagnosis  rested  upon  the  character  of  the  pulse,  throbbing  of  the  arteries 
and  the  absence  of  left  ventricular  hypertrophy  and  dilatation.' 


MITRAL    STENOSIS. 

Stenosis  or  obstruction  of  the  auriculo-ventricular  opening  of  the  left 
heart,  is  due  partly  to  constriction  at  the  base  of  the  mitral  valves,  and 
partly  to  adhesion  of  the  valve  tips  or  chordae  tendinese.  It  usually  occurs 
as  a  consequence  of  rheumatic  endocarditis, — rarely  of  atheromatous  degen- 
eration,— and  is  most  likely  to  occur  in  endocarditis  affecting  young  persons. 
Usually,  insufficiency  and  stenosis  of  the  mitral  orifice  occur  together,  and 
stenosis  probably  never  occurs  without  some  insufficiency. 

Morbid  Anatomy. — As  a  result  of  acute  exudative  or  interstitial  endo- 
carditis, the  valves  are  rendered  shorter  and  narrower,  as  well  as  thicker 
and  more  cartilaginous  than  normal.  These  rigid  valvular  projections  not 
only  obstruct  the  flow  of  blood  from  the  auricle  into  the  ventricle,  but 
allow  of  its  regurgitation  from  the  ventricle  into  the  auricle.  In  mitral 
stenosis,  there  is  not  only  thickening  and  contraction  of  the  valves,  but 
the  valve-tips  or  the  chordae  tendineae  become  adherent  and  sometimes  each 
papillary  muscle  is  changed  into  a  corrugated,  cylindrical  mass,  pierced 
with  one  or  more  slits,  indicating  the  chordae  of  which  it  was  originally 
made  up.  The  wall  of  the  valve,  especially  toward  its  free  edge,  is  greatly 
thickened,  and  these  thickened  por- 
tions are  so  dense  that  they  have  a  dis- 
tinct cartilaginous  feel.  On  the  val- 
vular flaps  that  have  undergone  this 
sclerotic  change  calcareous  masses  are 
very  frequently  developed,  and  cal- 
careous nodules  are  especially  liable 
to  form  when  a  gouty  diathesis  exists. 
When  the  chordae  tendinege  and  pap- 
illary muscles  have  become  adherent, 
the  edges  of  the  valves  are  drawn  down 
toward  the  apex  of  the  heart ;  and  since 
the  flaps  are  adherent  at  a  greater  or  less 
distance  upward  from  their  base,  the 
valve  presents  a  funnel-shaped  appear- 
ance with  its  base  looking  toward  the 
auricle,  and  its  apex  toward  the  ven- 
tricle, whose  smaller  opening,  rarely 
circular,  usually  resembles  a  slit  whose  axis  runs  with  the  line  which  unites 


Pig.  99. 
View  of  the  Mitral  Valve  in  a  case  of  Mitral  Ste- 
nosis. The  chordse  tendineae  are  thickened  and 
shortened,  and  the  edges  of  the  valve  are  calci- 
fied and  drawn  downward,  giving  the  funnel- 
shaped  appearance. 


'  Bellingham,  Dis. 
cle  by  Prof.  Law. 


of  Heart,  1875,  p.  152.     Also  Trans.  Path.  Society,  vol.  iii.,  Mar., 


p.  3.    Arti- 


454 


DISEASES   OF   THE    HEART. 


the  original  segments  of  the  valve.  This  "  button-hole  "  slit  may  scarcely 
admit  the  tip  of  the  little  finger,  while  the  normal  mitral  orifice  permits  the 
-easy  introduction  of  three  fingers.  Annular  (ring-like)  stenosis  is  far  more 
common  at  the  mitral  than  at  the  aortic  orifice.  Sometimes  the  funnel- 
shaped  appearance  is  wanting,  and  the  flaps  are  stretched  horizontally 
across,  with  a  small  opening  in  the  centre,  like  a  diaphragm ;  looked  at 
from  the  auricle,  this  slit  often  appears  crescentic. 

In  cases  of  long  standing  the  vegetations  may  become  calcified.     If  the 

new  tissue  in  the  diseased  valves  undergoes 
fatty  change  and  softens,  ulcerative  processes 
are  set  up  and  the  chordae  tendineae  may 
rupture.  On  the  floor  of  such  ulcers  cal- 
careous masses  and  debris  are  frequently 
found.  Dr  Hayden  thinks  that  '•  all  funnel- 
shaped  mitral  stenosis  is  the  result  of  primary 
acute  inflammation  of  the  valve  segments 
with  cohesions  of  their  adjacent  edges."  Out 
of  sixty-two  cases  of  mitral  stenosis,  fifty- 
nine  assumed  the  "button-hole"  form  and 
three  only  the  funnel  shaped.'  In  rare  in- 
stances the  tendons  will  adhere  to  the  wall  of 
the  heart.  Adjacent  to  the  valves,  the  endo- 
cardium will  usually  be  found  slightly  thick- 
ened. The  valves  presenting  the  roughest 
and  most  irregular  surfaces  do  not  give  rise 
to  the  harshest  or  loudest  murmurs. 

The  following  changes  are  developed  in 
the  heart  and  vessels  as  a  result  of  mitral 
stenosis.  The  left  ventricle  becomes  smaller, 
sometimes  its  walls  are  thinner  than  normal. 
The  aorta  is  also  small  and  thin-walled.  An 
almost  necessary  result  of  mitral  stenosis  is 
dilatation  with  subsequent  hypertrophy  of  the  left  auricle.  Sometimes  the 
auricular  cavity  is  enormously  dilated,  and  its  appendix  is  elongated  and 
curved.  Not  infrequently  the  left  auricular  walls  are  from  one  eighth  to 
one-seventh  of  an  inch  in  thickness.  As  soon  as  the  auricular  hypertrophy 
ceases  to  be  compensatory,  the  pulmonary  circulation  becomes  obstructed, 
causing  tension  in,  and  distention  of,  the  pulmonary  vessels.  The  walls  of 
the  pulmonary  vessels,  especially  those  of  the  main  trunk,  are  thickened 
and  hypertrophied  ;  they  have  been  found  tivice  the  thichness  of  those  of 
the  aorta.  Although  mitral  stenosis  is  a  disease  of  youth,  and  atheroma 
one  of  old  age,  yet  it  not  infrequently  happens  that,  even  before  the  age  of 
puberty,  atheromatous  degeneration  occurs  in  the  pulmonary  vessels,  espe- 
cially in  the  small  branches,  as  a  result  of  the  increased  blood  tension  in 
the  pulmonary  system.'^ 

The  passive  pulmonary  hyper^emia  which  results  from  the  obstructed 


Fig.  100. 


the 


tlie 


View  of  the  Mitral  orifice  from 
Auricle,  with  calciflcation  of 
valves  and  reduction  of  the  opening. 
In  the  above  case  the  point  of  the 
little  finger  was  barely  admitted 
through  the  "  button-hole  "  slit.  Tlie 
valves  are  stretched  horizontally 
across. 


'  Fagge  and  Hayden. 


''Trans.  Path.  Society,  xvii.,  p.  90. 


MITRAL   STENOSIS.  455 

pulmonary  circulation  may  lead  to  changes  which  collectively  constitute 
hrown  induration  of  the  lung.  Another  occasional  occurrence  directly  due 
to  extensive  mitral  stenosis  is  nodular  hemorrhagic  infarctions.  In  some 
instances  an  extensively  dilated  left  auricle  may,  by  pressing  on  a  bronchus, 
reduce  its  calibre  one-half,  and  thus  interfere  with  the  functional  activity  of 
the  left  lung.  When  the  pulmonary  hypergemia  is  extensive,  violent  physi- 
cal exertion  or  violent  coughing  may  cause  a  rujoture  of  one  of  the  larger 
pulmonary  vessels,  and  true  pulmonary  apoplexy  results.  Bronchorrhoea  is 
a  frequent  result  of  the  intense  hypergemia  of  the  mucous  membrane  of  the 
bronchial  tubes  which  may  be  produced  in  mitral  stenosis.  The  lungs  are 
always  so  liable  to  congestion  and  oedema  that  any  sudden  or  violent  exer- 
cise may  cause  sudden  death.  Again,  when  the  above  conditions  have 
existed  for  some  time,  mitral  stenosis  may  lead  to  dilatation  and  hyper- 
trophy of  the  right  heart.  In  some  rare  cases,  the  tricuspid  orifice  has 
become  slightly  insufficient. 

Etiology.— Mitral  stenosis  is  most  frequent  in  the  young ;  it  rarely  occurs 
after  fifty.  Statistics  show  it  to  be  twice  as  frequent  in  females  as  in  males. 
It  is  not  infrequently  of  congenital  origin.  Acute  rheumatic  endocarditis 
is  its.  most  frequent  cause.  In  some  few  instances  stenosis  results  from  ex- 
tension of  the  inflammatory  process  from  the  aortic  valves.  It  is  a  question  if 
endocarditis  in  scarlatina  or  diphtheria  in  children  ever  causes  mitral  stenosis. 

Symptoms. — The  subjective  symptoms  of  mitral  stenosis  are  few.  Usually 
after  violent  exercise  there  is  more  or  less  cai'diac  palpitation,  and  this  will 
cease  as  soon  as  the  auricle  can  empty  itself,  which  is  accomplished  by  the 
patient  assuming  a  recumbent  position  on  the  right  side,  with  the  head 
slightly  elevated.  This  class  of  patients  are  usually  pale  and  anaemic, 
and  frequently  experience  a  sharp  pain  in  the  region  of  the  apex-beat.  The 
pulse  is  regular  and  normal  in  character,  so  long  as  the  auricular  hyper- 
trophy compensates  for  the  auricular  dilatation.  When  the  ventricle  does 
not  receive  and  discharge  its  normal  quantity  of  blood  with  normal  regu- 
larity, the  pulse  becomes  small  in  volume,  feeble  in  force,  rapid  and  irregular 
in  rhythm.  The  sphygmograph  exhibits  a  tracing,  sometimes  called  the 
*'  mitral  pulse,"  the  nature  of  which  is  the  same  as  when  the  ventricle 
throws  a  greatly  diminished  blood  current  into  the  aorta,  i  The  auricular 
systole  commences  earlier  than 
normal  on  account  of  the  hy- 
pertrophy of  the  auricle.  This 
premature  contraction  of  the 
auricle  stimulating  ventricular 
contraction,  is  indicated  by  a 
second  ventricular  systole, 
which  is  much  less  forcible 
than  the  first.  Fre.  loi. 

TTiP    niQciira   mil  TYinnQT-^r   >.t7     Sphyf^jmographic  tracins:  in  a  case  of  Mitral  Stenosis.  The  line 
xijc    jJtis&ivt!   puiiiiuiid,i_y    xiy-         of  descent  is  broken  by  pulsations  from  premature  con- 

persemia  which  attends  the  ad-       ^'^^"*^°°  "^  '^"  over-fliied  auricle. 

'  Balfour  differs  from  other  authorities  in  the  statement  that  among  the  most  remarkable  subsidiary 
phenomena  of  mitral  stenosis  is  irrefjularily  of  cardiac  rhythm  which  is  always  present  in  a  greater  or  less 
degree. 


4-56  DISEASES   OF   THE   HEART. 

vanced  stages  of  this  form  of  cardiac  disease  causes  habitual  dyspnoea, 
which  is  exaggerated  by  physical  exertion  and  by  a  dry,  hacking,  "  teas- 
ing" cough,  which  resembles  the  so-called  ''nervous"  cough.  After 
violent  or  prolonged  exertion  there  may  be  bronchorrhcea,  a  pint  of  glairy, 
watery  mucus  often  being  expectorated  in  a  few  moments.  Severe  exercise 
sometimes  induces  attacks  of  profuse,  watery,  blood-stained  expectoration, 
indicative  of  pulmonary  congestion  and  oedema.  The  exertion  of  walking 
rapidly  against  a  strong  wind  will  often  cause  such  intense  congestion  and 
cedema  of  the  lungs  in  one  with  extensive  mitral  stenosis  as  to  induce  sud- 
den death.  Haemoptysis  is  not  infrequent,  small. quantities  of  pure,  florid 
blood  being  expectorated.  Orthopnoea  is  a  rare  symptom,  for  even  in  ex- 
tensive and  long-standing  cases  the  pulmonary  congestion  is  not  constant, 
for  the  auricle  is  ordinarily  able  to  empty  itself,  and  only  becomes  engorged 
during  active  physical  exertion  or  great  excitement. 

Physical  Signs  — Inspection.  As  the  left  ventricle  does  not  receive  its 
normal  quantity  of  blood,  the  cardiac  impulse  is  feeble.  Sometimes  it  has 
a  visible  undulating  movement. 

Palpation. — On  palpation,  although  the  apex-beat  is  less  forcible  than 
normal,  a  distinct  purring  thrill  will  be  communicated  to  the  hand  ;  this 
thrill  is  a  constant  attendant  of  mitral  stenosis.  While  mitral  stenosis  is 
always  accompanied  by  a  purring  thrill,  it  should  be  remembered  that  a 
purring  tlirill  does  not  always  indicate  mitral  stenosis.  It  is  most  distinct 
at  the  apex-beat,  although  it  may  be  diffused  over  the  whole  precordial 
space.  It  either  continues  through  the  entire  diastole,  or  is  only  present 
just  before  the  systole.  It  is  sometimes  called  a  "  presystolic  "  thrill.  It 
ceases  at  the  apex-beat. 

Percussion. — The  increased  size  of  the  left  auricle  may  cause  an  increase 
in  the  area  of  cardiac  dulness,  upward  and  to  the  left,  at  the  inner  part  of 
the  second  left  intercostal  space.  This  increased  area  of  dulness  will  only 
be  recognized  on  careful  percussion  during  expiration. 

Auscultation. — Mitral  stenosis  is  characterized  by  a  loud  "churning," 
"grinding,"  or  "blubbering"  presystolic  muraiur ;  this  murmur  is  of 
longer  duration  than  any  other  cardiac  murmur,  on  account  of  the  time  re- 
quired for  the  blood  to  pass  through  the  narrowed  and  obstructed  orifice.  It 
ends  with  the  commencement  of  the  first  sound  and  the  apex-beat,  being 
synchronous  with  the  purring  thrill.  The  murmur  is  heard  with  its  maxi- 
mum intensity  a  little  above  the  apex-beat.  It  is  louder  when  the  patient 
is  erect  than  when  in  a  recumbent  posture.  When  there  is  great  debility 
or  just  before  death,  the  murmur  becomes  indistinct.  A  presystolic  mur- 
mur is  never  present  unless  there  is  narrowing  of  the  auriculo- ventricular 
orifice,  and  then  it  is  seldom,  if  ever,  absent.  A  prolonged  murmur  and  a 
sharp  first  sound  indicate  a  "funnel-shaped"  stenosis.  The  pulmonic 
second  sound  is  intensified.  When  mitral  reflux  and  mitral  obstruction  co- 
exist, the  two  murmurs  run  into  each  other,  constituting  a  single  murmur. 
A  mitral  obstructive  murmur  is  never  soft  or  musical ;  it  is  usually  sepa- 
rated from  the  first  sound  by  a  short  interval.  In  about  one-third  of  all 
cases,  the  second  sound  is  reduplicated.    Pulmonary  congestion  sufficiently 


MITEAL   EEGURGITATIO]Sr.  457 

accounts  for  the  redaplication.'  Some  regard  the  length  of  the  pause 
between  the  murmur  and  the  first  sound  as  a  measure  of  the  stenosis  :  the 
shorter  the  pause  the  greater  the  stenosis. 

Differential  Diagnosis. — The  diagnosis  of  mitral  stenosis  is  not  difficult : 
it  depends  upon  the  existence  of  two  physical  signs,  the  "  purring  thrill  " 
and  a  loud,  long,  blubbering  jn-esystolic  murmur.  It  may  be  mistaken  for 
pericardial  friction,  for  a  prolongated  systolic  murmur  replacing  the  first 
sound  at  the  apex,  and  for  a  pre-diastolic  basic  murmur  transmitted  to  the 
apex. 

To  diagnosticate  between  local  pericarditis  and  mitral  stenosis  the  same 
methods  are  employed  and  the  same  rules  are  to  be  observed  as  in  the  diag- 
nosis between  aortic  murmurs  and  local  pericarditis  (g.  v.). 

A  prolonged  systolic  apical  murmur  reaching  to  the  second  sound  is  dis- 
tinguished from  a  presystolic  murmur  by  its  soft  and  blowing  character, 
and  its  synchronism  with  the  systolic  impulse  and  carotid  pulsation. 

K pre-diaxtolic  murmur  is  distinguished  from  a  mitral  stenotic  murmur 
by  its  progressively  diminishing  intensity,  from  the  base  to  the  apex,  by  its 
not  being  accompanied  by  hypertrophy  of  the  left  ventricle,  and  by  a  jerk- 
ing, irregular  pulse. 

MITEAL    EEGTJEGITATIO]^. 

Eegurgitation  at  the  mitral  orifice  is  due  to  a  condition  of  the  mitral 
valves  which  allows  the  blood  to  flow  back  from  the  left  ventricle  into  the 
left  auricle. 

Morbid  Anatomy. — The  most  common  lesions  are  thickening,  induration 
and  shortening  of  the  mitral  valves.  In  rare  instances,  regurgitation  may 
occur  independently  of  valvular  disease,  from  displacement  of  one  or  more 
of  the  segments  of  the  valve,  the  result  of  changes  in  the  papillary  muscles, 
chordge  tendinese,  or  the  ventricular  walls.  It  may  also  occur  in  extensive 
anaemia  or  from  relaxation  of  the  papillary  muscles  and  dilatation  of  the 
left  ventricle  without  a  corresponding  elongation  of  the  papillary  muscles, 
and  from  rupture  of  the  chordae  tendinese.  In  most  instances,  however, 
the  valves  are  shortened,  thickened,  and  indurated.  In  some  cases,  lime 
salts  and  large  masses  of  chalky  matter  are  found  embedded  in  the  in- 
durated valves.  In  such  cases  the  surface  and  edges  of  the  valves  are  so 
rough  and  jagged  that  more  or  less  obstruction  accompanies  the  regurgi- 
tation. All  these  changes,  except  calcification,  may  also  occur  in  the  chordas 
tendineae  and  columnse  carnese.  The  valves  may  also  become  adherent  to 
the  walls  of  the  ventricles,  or,  as  a  result  of  the  shrinking  and  shortening 
of  the  chordae  tendineae,  the  valve-flaps  will  not  pass  back  to  the  plane  of 
the  orifice.  Again,  the  chordae  tendinese  may  be  ruptured  so  that  the 
valves  are  pressed  back  into  the  auricle  during  the  cardiac  systole.  If  the 
chordae  tendineae  which  are  inserted  nearest  the  centre  of  the  valve  become 

>  Geigel  ascribes  it  to  "  non-coincidence  in  the  closure  of  the  valves."  Guttman  regards  it  as  originat- 
ing at  the  stenotic  orifice  itself.  Balfour  thinks  that  thrill  and  reduplication  of  the  second  sound  are  suf- 
ficient to  make  a  diagnosis  in  the  absence  of  murmur. 


458 


DISEASES   OF   THE   HEART. 


Pig.  102. 

View  of  the  Left  Heart  in  Mitral 

Regursjitation. 


lengthened,  that  part  of  the  flap  will  be  bent  upon  itself,  having  evidently 
yielded  to  the  blood  pressure,  and.  this  allows  of  regurgitation.  Sometimes 
when  the  valves  appear  perfectly  healthy  they  will 
be  found  by  the  application  of  the  "  luater  test " 
to  be  insufficient. 

The  first  effect  of  mitral  regurgitation  is  dilata- 
tion of  the  left  auricle,  due  to  the  pressure  of  the 
two  blood  currents  during  its  diastole,  one  from 
the  lungs,  and  tbe  other  from  the  left  ventricle. 
The  dilatation  leads  to  thickening  and  hypertrophy 
of  the  left  auricular  walls  ;  as  a  result,  the  pul- 
monary circulation  is  impeded.  The  pulmonary 
vessels  enlarge  and  may  undergo  degeneration,  as  a. 
result  of  the  continued  regurgitant  j)ressure.  Passive 
hypersemia  of  the  lungs,  with  brown  or  pigment 
induration,  is  an  early  pathological  sequel  of  mitral 
regurgitation.  The  constant  interference  with  the 
return  circulation  from  the  lungs,  more  or  lesa 
obstructs  the  outward  current  of  blood  to  the  lungs 
from  the  right  ventricle.  As  the  obstruction  is  a 
The  avHcrdo-ventricuiar  valves  aradual  oue,  tlic  riffht  vcntriclc  bccomcs  sufficient- 

are  thickened  with  calcareous  ^  ^  o 

deposits,  as  shown  at  B,  B.  w  hvpertrophied  to  overcome  it,  consequently  the 

The  aortic  valves  A,  A,  were     •^-'J-  t  -,      .    .  ,  ,    •    ■,  Z       j^        ±^ 

in  this  case  the  seat  of  like  de-  hypertrophicd  right  vcntricle  Compensates  lor  the 

mitral  regurgitation. 
So  long  as  the  hypertrophied  right  ventricle  is  able  to  fully  overcome 
the  abnormal  pressure  of  the  blood  in  the  lungs  from  the  mitral  regurgi- 
tation, the  patient  is  comfortable.  Sooner  or  later,  however,  the  compen- 
satory hypertrophy  of  the  right  ventricle  ceases,  and  a  secondary  dilata- 
tion occurs  which  admits  of  no  compensation.  This  final  dilatation  of 
the  right  ventricle  is  favored  by  the  myocardial  degeneration  which  occurs 
as  a  result  of  defective  nutrition  of  the  heart  walls  ;  when  this  condition  is 
reached,  the  veins  throughout  the  body  are  placed  in  a  similar  condition  to 
those  in  the  lungs.  This  general  venous  congestion  is  indicated  by  passive 
hypersemia  of  the  abdominal  viscera  and  by  cyanosis  of  the  surface  during 
active  physical  exercise.  The  liver  is  the  organ  first  affected  on  account 
of  its  great  vascularity,  and  from  the  fact  that  the  hepatic  veins  do  not  col- 
lapse readily  and  possess  no  valves.  Thus,  the  liver  becomes  enlarged  and 
has  a  stony  hardness ;  as  a  result  of  the  obstruction  to  the  emptying  of  the 
hepatic  vein  the  portal  vein  is  obstructed,  and  this  leads  to  passive  hyper- 
emia of  the  intestines  and  stomach,  and  enlargement  of  the  spleen.  The 
impediment  to  the  return  of  venous  blood  to  the  heart  causes  cerebral  con- 
gestion, renal  congestion,  and,  in  fact,  general  systemic  venous  congestion. 
In  addition  to  these  changes,  the  dilated  and  hypertrophied  left  auricle 
throws  an  abnormal  quantity  of  blood  with  abnormal  force  into  the  left 
ventricle  during  the  diastole,  which  leads  to  dilatation  of  its  cavity,  and 
necessitates  a  compensatory  hypertrophy  of  the  left  ventricular  walls;  this 
hypertrophy  increases  the  force  of  the  reflux  current,  so  that  during  ex- 


MITEAL    EEGUEGITATION".  459 

■sitement  and   active  physical   exertion,  pulmonary  congestion  and  cedema 
are  liable  to  occur. 

Etiology, — Mitral  regurgitation  may  occur  at  any  age  ;  it  is  especially 
liable  in  the  young  to  follow  rheumatic  endocarditis,  which  causes  exten- 
sive valvular  retractions  and  thickenings.  It  is  not  infrequently  second- 
ary to  changes  at  the  aortic  orifice  produced  either  by  an  extension  of  endo- 
carditis from  the  aortic  to  the  mitral  valves  and  their  appendages,  or  by 
the  secondary  mitral  valvulitis  excited  by  the  regurgitant  blood  current 
from  the  aorta.  Mitral  insufficiency  may  also  be  the  result  of  that  enlarge- 
ment of  the  left  auriculo-ventricular  orifice  which  accompanies  excessive 
dilatation  of  the  left  ventricle.  Diseases  of  the  columnae  carneae  and  chor- 
dse  tendineae,  when  their  structures  are  so  weakened  as  to  allow  the  flaps  of 
the  valves  to  pass  back  of  the  plane  of  the  orifice,  will  also  cause  miti-al 
insufficiency.  Ulcerative  endocarditis  may  also  cause  it,  either  by  perfora- 
tion and  rupture  of  the  valves  or  by  rupture  of  the  chordge  tendinese. 

Symptoms. — During  the  early  stage,  when  the  hypertrophy  of  the  right 
ventricle  compensates  for  the  regurgitation,  there  are  no  rational  symp- 
toms which  would  lead  one  to  suspect  its  existence ;  but  when  the  right 
ventricle  is  unable  to  overcome  the  obstruction  to  the  jDulmonary  circu- 
lation caused  by  the  regurgitant  blood  current,  there  will  be  more  or  less 
dyspnoea  accompanied  by  a  short,  hacking  cough  with  an  abundant  expec- 
toration of  frothy  serum.  Sometimes  the  watery  expectoration  is  blood- 
stained. Active  physical  exertion  increases  the  dyspnoea  and  causes  cardiac 
palpitation. 

In  advanced  cases,  the  extremities,  face,  and  lips  become  blue,  the  result 
of  the  interference  with  the  capillary  return  circulation.  The  liver  becomes 
enlarged  and  hardened,  a  condition  easily  recognized  by  palpation  and  per- 
cussion. The  patient  will  complain  of  a  sense  of  weight  and  fulness  in  the 
right  hypochondrium,  and  there  will  be  anorexia,  nausea,  and  a  sense  of 
oppression  in  the  epigastrium,  and  sometimes  the  hepatic  circulation  be- 
comes so  obstructed  that  the  biliary  secretion  is  interfered  with  and  a  jaun- 
diced hue  of  the  surface  will  be  added  to  the  cyanotic  discoloration,  which 
■will  give  to  the  skin  a  greenish  tint.  Headache,  dizziness,  vertigo,  stupor, 
somnolence,  and  sometimes  a  peculiar  form  of  delirium  of  short  duration, 
result  from  the  passive  cerebral  hyperaemia  induced  by  obstruction  in  the 
superior  vena  cava.  Following  the  hepatic  derangement,  are  frequent 
attacks  of  gastric  and  intestinal  catarrh,  and  evidences  of  embarrassed  renal 
circulation.  The  urine  is  diminished  in  quantity,  high  colored,  and  loaded 
with  lithates.  Sometimes  albumen  and  blood  casts  are  found  in  it.  Fre- 
quently the  blood-stained  expectoration  is  accompanied  by  free  haemoptysis  j 
a  cough  and  watery  expectoration  with  occasional  dark  blood  stains  are 
usually  present  as  advanced  symptoms  of  mitral  regurgitation.  Another 
late  symptom  of  mitral  regurgitation  is  dropsy  ;  it  first  appears  in  the  lower 
extremities,  and  gradually  extends  over  the  whole  body.  With  the  general 
anasarca  there  is  more  or  less  dyspnoea.  Late  in  the  disease,  pulmonary 
hemorrhagic  infarctions  may  occur. 

The  pulse  of  mitral  regurgitation  is,  at  first,  regular  in  force  and  rhythm; 


460  DISEASES    OF   THE   HEABT. 

later  it  becomes  diminished  in  volume,  irregular  m  rhythm,  and  diminished 
in  force ;  it  is  never  jerking   in   character.     Wlien  the  heart's  action  is 

excited,  it  becomes  feeble  and  com- 
pressible and  has  a  certain  tremu- 
lousness.  The  sphygmographic 
tracing  shows  great  depth  and 
amplitude  of  the  diastolic  notch. 
Physical  Signs.  —  Inspection. 
The  area  of  the  visible  cardiac 
impulse  is  increased,  and  not  in- 
PiG.  103.  frequently  there  is  a  slight  pulsa- 

Sphygmographic  tracing  in  Mitral  Regurgitation  show-     tiou.      Corresponding     in     rhythm 
ing  great  depth  and  amplitude  of  the  diastolic  notch.  ■   ■,        ,        -,  i       mi 

With  the  heart  beats.  The  epi- 
gastric pulsation  is  due  to  right  ventricular  hypertrophy,  which  is  a  con- 
dition always  found  with  extensive  mitral  regurgitation.  The  jugular  veins 
appear  swollen,  especially  when  the  patient  is  lying  down. 

Palpation. — The  apex-beat  is  displaced  to  the  left  and  is  felt  lower  than 
normal.  When  the  dilatation  exceeds  the  hypertrophy,  the  apex-beat  is 
carried  outward  and  often  slightly  upward.  The  impulse  is  dilfused  and 
more  or  less  forcible,  according  as  right  or  left  ventricular  hypertrophy 
predominates.  Palpation  sometimes  reveals  a  systolic  thrill,  which  is  con- 
fined to  the  region  of  the  second  left  intercostal  space  near  the  sternum. 
This  sjstoWc  fremissement  is  not  noticeable  when  the  base  of  the  heart  lies 
close  to  the  chest-wall  because  of  retraction  of  the  margin  of  the  left  lung. 
A  purring  tremor,  systolic  in  rhythm,  felt  most  intensely  at  the  apex,  and 
becoming  feebler  the  farther  the  hand  is  removed  from  that  part,  either  to 
the  right  or  upward,  is  invariably  due  to  mitral  regurgitation.'' 

Percussion. — Percussion  reveals  an  increase  in  the  area  of  cardiac  dul- 
ness,  especially  laterally  ;  it  extends  both  to  the  left  and  right  of  the  normal 
line,  as  well  as  downward.  The  area  of  the  superficial  as  well  as  of  the 
deep-seated  dulness  will  be  increased  laterally  and  downward. 

Auscultation. — Mitral  insufficiency  is  attended  by  a  systolic  murmur, 
which  either  completely  or  partially  replaces  the  first  sound  of  the  heart. 
The  quality  of  the  murmur  is  variable,  and  not  in  itself  distinctive.  It  is 
usually  soft  and  blowing ;  sometimes,  toward  its  end,  the  murmur  will 
assume  a  distinctly  musical  character.  The  first  sound  of  the  heart  may 
be  heard  distinctly  in  the  early  stages,  but  later  the  murmur  nearly  always 
takes  the  place  of  the  heart  sound.  Hence  many  English  writers  rightly 
call  this  murmur  "  post-systolic "  rather  than  "  systolic "  in  its  nascent 
stages.  It  is  heard  with  its  maximum  intensity  at  the  apex-beat.  Its  area 
of  diffusion  is  to  the  left,  on  a  line  corresponding  to  the  apex-beat.  It  is 
audible  at,  or  near,  the  inferior  angle  of  the  left  scapula.  It  can  he  heard 
between  the  lower  border  of  the  fifth  and  the  upper  border  of  the  eighth 

1  Skoda,  Bamberger  and  Leyden  record  instances  in  which  inspection  showed  a  double  impulse,  accom- 
panying, with  more  or  less  regularity,  each  cardiac  systole.  This  only  occurs  in  aggravated  cases,  and 
arises  from  non-coincidence  of  contraction  of  the  ventricles. 

^  Hayden  states  that  "  it  is  exceptional  to  have  a  puning  thrill  with  simple  mitral  reflux."  I  have  never 
found  it,  except  in  those  cases  where  left  ventricular  dilatation  greatly  exceeded  the  hypertrophy. 


MITRAL   EEGURGITATION".  461 

vertebra,  at  the  left  of  the  spine,  with  nearly  the  same  intensity  as  at  the  apex. 
The  second  sound  of  the  heart,  over  the  pulmonary  valves,  is  accentuated, 
while  at  the  junction  of  the  third  rib  with  the  sternum  on  the  left  side, 
both  heart  sounds  are  feeble.  Skoda  first  drew  attention  to  exaggeration 
of  the  second  pulmonary  arterial  sound  as  a  "positive  and  unerring"  indi- 
cation of  mitral  regurgitation.  It  is  not  always  present.  Whatever 
may  be  its  character,  the  murmur  is  generally  loudest  at  its  commence- 
ment. 

A  loud  systolic  murmur  at  the  apex,  and  not  heard  at  the  back,  is  not 
indicative  of  mitral  reflux.  If  stenosis  and  regurgitation  occur  in  the  same 
individual,  they  give  rise  to  a  combined  presystolic  and  systolic  murmur, 
which  begins  shortly  after  the  second  sound  of  the  heart,  and  continues 
until  the  second  sound  commences.  The  two  sounds,  although  mingling 
to  form  one  murmur,  can,  in  the  majority  of  cases,  be  readily  distinguished 
from  each  other,  for  the  point  of  maximum  intensity  and  the  very  limited 
area  of  diffusion  of  a  presystolic  murmur  readily  distinguish  it  from  a  mi- 
tral systolic,  which  is  audible  in  the  left  scapular  region.  It  is  important 
to  recognize  the  existence  of  both  these  murmurs  in  estimating  the  progno- 
sis in  any  case. 

DiiFerential  Diagnosis. — It  is  usually  not  diflBcult  to  recognize  mitral  re- 
gurgitation. The  seat  and  rhythm  of  the  murmur  and  its  area  of  diffusion 
are  sufficient  to  distinguish  it  from  other  cardiac  murmurs.  The  character 
of  the  pulse,  the  symptoms  referable  to  the  right  heart,  and  the  pulmonary 
complications  will  also  assist  in  its  diagnosis.  It  may,  however,  be  mis- 
taken for  aortic  olstruction,  since  each  gives  rise  to  a  systolic  murmur,  for 
tricuspid  regurgitation,  and  for  roughening  of  the  ventricular  surface  of 
the  mitral  valve,  or  of  the  ventricular  wall  near  the  aortic  orifice.  The  di- 
agnosis between  mitral  regurgitation  and  aortic  stenosis  has  already  been 
considered. 

Mitral  and  tricuspid  itisufficiencg  both  produce  a  systolic  murmur ;  a 
mitral  regurgitant  murmur  has  its  maximum  intensity  at  the  apex,  and  is 
conveyed  toward  the  left  axillary  and  scapular  regions,  while  the  maximum 
intensity  of  a  tricuspid  regurgitant  murmur  is  to  the  left  of  the  base  of  the 
xiphoid  cartilage,  and  it  is  transmitted  upward  and  to  the  right, — the  area 
of  transmission  establishes  the  diagnosis.  Pulmonary  symptoms  are  prom- 
inent in  mitral  reflux  and  absent  in  tricuspid  regurgitation.  The  pulmo- 
nary second  sound  is  markedly  enfeebled  in  tricuspid  regurgitation,  and 
markedly  intensified  in  mitral  regurgitation. 

Roughening  of  the  ventricular  wall  gives  rise  to  a  murmur  which  has  its 
maximum  intensity  at  the  base  of  the  heart,  and  is  transmitted  along  the 
aortic  arch  and  into  the  vessels  which  spring  from  it  in  the  thorax.  The 
vibration  of  an  irregular  chorda  tendinea  stretched  across  the  aortic  orifice, 
its  extremities  being  inserted  into  opposite  walls  of  the  ventricle,  may  pro- 
duce a  systolic  musical  murmur,  but  the  line  of  its  transmission  will  cor- 
respond to  that  of  an  aortic  obstruction.  A  systolic  mitral  murmur,  due  to  a 
sudden  rupture  of  one  or  a  number  of  the  valve-flaps,  of  the  papillary  mus- 
cles, or  tendons,  is  a  loud,  blowing  murmur,  usually  appearing    suddenly, 


462  DISEASES    OF   THE   HEART. 

which  is  immediately  accompanied  by  all  the  urgent  symptoms  of  acute 
pulmonary  congestion. 

TKICUSPID    STET^OSIS. 

This  lesion  is  so  rare  that  there  are  no  rules  for  its  diagnosis.  Its  rnorlid 
appearances  and  etiology  are  similar  to  those  of  pulmonic  stenosis.  Its 
symptoms  would  be  those  due  to  obstruction  to  the  entire  systemic  venous 
circulation.  The  right  auricle  would  be  dilated,  and  there  would  be  vis- 
ceral enlargements  in  the  abdomen,  cyanosis  of  the  face  and  extremities, 
scanty  and  albuminous  urine,  hemorrhoidal  tumors,  headache,  dizziness 
and  vertigo  (due  to  passive  cerebral  hyperasmia),  and  general  anasarca.  The 
few  cases  recorded  are  associated  with  mitral  stenosis,  with  one  exception,  a 
case  of  Bertin's.'  In  a  case  exhibited  by  Quain,  the  tricuspid  flaps,  thick 
and  opaque,  were  united  for  one-third  of  their  extent.  In  the  other  cases, 
the  flaps  of  the  valve  formed  a  diaphragm  whose  central  opening  admitted 
only  the  point  of  one  finger.  In  every  recorded  case  of  tricuspid  stenosis 
the  heart  was  enlarged.  Tricuspid  stenosis  (as  also  pulmonic  stenosis)  may 
be  the  result  of  the  pressure  of  a  tumor.  In  all  well-authenticated  cases, 
the  chief  symptoms  seem  to  have  been  extreme  lividity,  palpitation,  and 
dyspnoea. 

Physical  Signs. — Inspection  reveals  general  cyanosis.  The  jugulars  are 
turgescent  and  exhibit  presystolic  ^w?sa^40?i.  This  pulsation  is  sometimes 
the  only  inconvenience  the  patient  suffers. 

Palpation  may  discover  a  venous  thrill  at  the  base  of  the  neck. 

Percussion  may  show  the  right  auricle  to  be  greatly  enlarged,  and  car- 
diac dulness  will  be  increased  laterally  and  toward  the  right. 

Auscultation. — Tricuspid  stenosis  should  be  attended  by  a  presystolic 
murmur  whose  maximum  intensity  would  be  at  the  lower  portion  of  the 
sternum  just  above  the  xiphoid  cartilage.  This  murmur  may  be  propa- 
gated faintly  toward  the  base,  but  never  toward  the  apex  of  the  heart.  It 
is  sometimes  accompanied  by  fremitus.  Hayden  offers  the  following 
''diagnostic  point:" — the  murmur  of  mitral  stenosis  (without  which 
tricuspid  stenosis  never  occurs)  is  limited  to  the  apex  region  ;  a  murmur  of 
the  same  rJiytJim  is  produced  at  the  sternum  by  tricuspid  stenosis,  "and 
between  these  two  localities  there  is  a  point  where  no  murmur  can  deheard.'^ 

It  is  unnecessary  to  consider  its  differential  diagnosis.  The  lesion 
would  be  diagnosticated  (if  at  all)  by  exclusion,  and  prognosis  and  treat- 
ment would  depend  upon  the  gravity  of  the  accompanying  condition.  As 
tricuspid  stenosis  never  occurs  unless  there  is  extensive  mitral  obstruction, 
the  latter  condition  is  always  the  predominant  one. 

TRICUSPID    REGUEGITATIOIST. 

This  lesion  is  usually  secondary,  yet  it  may  be  primary.     Mitral  disease 
is,  in  nearly  every  instance,  the  antecedent  condition. 
Morbid  Anatomy. — The  lesions  are  similar  to  those  occurring  in  mitral 

1  Traite.  des  Mai.  du  Coeur,  Oba.  17. 


TEICUSPID   REGUEGITATI02S".  4G3 

insufficiency.  The  valves  are  thickened,  shrunken  and  opaque  ;  the  papil- 
lary muscles  are  shortened  and  thickened,  and  the  chordae  tendineae  under- 
go like  changes  and  are  sometimes  adherent.  The  valves,  or  the  columns 
or  cords,  may  rupture;  in  either  case  acute  and  extensive  insufficiency  re- 
sults. Acute  endocarditis  of  the  right  heart  is  rare  in  adults,  but  when  it 
occurs  the  tricuspid  valves  are  its  principal  and  primary  seat,  on  account 
of  their  anatomical  structure  and  the  tension  to  which  they  are  subject  in 
mitral  disease.  They  are  rarely  the  seat  of  rheumatic  or  calcareous  de- 
generation. Ulcerative  endocarditis  in  the  right  heart  is  seldom  met  with.' 
Any  infection  from  emboli  from  the  tricuspid  flaps  will  produce  their 
secondary  effects  in  the  lungs.  The  first  effect  of  tricuspid  regurgitation 
is  dilatation  of  the  right  auricle  ;  following  this,  there  will  be  hypertrophy 
of  its  walls.  The  auricular  hypertrophy  soon  ceases  to  compensate,  and 
then  venous  engorgement  occurs. 

As  soon  as  the  valves  in  the  subclavian  and  jugular  veins  are  no  longer 
able  to  resist  the  regurgitant  current,  jugular  pulsation  follows.  But,  be- 
fore this  occurs,  the  tributaries  of  the  inferior  cava  and  the  organs  to  which 
they  are  distributed  will  become  greatly  engorged,  for  they  have  no  valves 
to  resist  the  regurgitant  current.  The  inferior  cava  and  the  hepatic  veins 
sometimes  become  enormously  distended  under  these  circumstances,  the 
liver  showing  the  peculiar  appearance  on  section  that  has  gained  for  it  the 
name  of  nutmeg  liver.  Following  the  hepatic  changes,  the  skin  as- 
sumes a  dingy  yellow  hue.  When  this  is  combined  with  cyanosis  it  has  a 
peculiar  greenish  tint,  only  met  with  in  heart  disease.  The  spleen  enlarges 
and  hardens  ;  the  mucous  memhrane  of  the  stomach  is  congested  and 
ecchymotic,  and  often  presents  numerous  hemorrhagic  erosions.  Intestinal 
catarrh  is  subsequently  developed,  and  the  general  venous  congestix)n  with- 
in the  abdominal  cavity  is  exhibited  by  hemorrhoids  and  ascites.  The 
kidneys  become  congested  and  stony,  and  thrombi  may  form  in  the  femoral 
vein  and  induce  subsequent  pulmonary  infarctions. 

The  stasis  in  the  veins  below  the  diaphragm  is  accompanied  by  transu- 
dation of  serum,  first  in  the  ankles,  and  thence  the  dropsy  progresses  up- 
ward until  the  patient  may  finally  reach  a  condition  of  general  anasarca. 
The  resulting  obstruction  to  the  general  systemic  circulation  may  cause 
hypertrophy  of  the  left  ventricle,  and  then  we  have  the  rare  occurrence  of 
disease  of  the  left  heart  following  that  of  right.  Since  tricuspid  reflux 
has  mitral  disease  for  its  principal  cause,  the  heart  becomes  greatly  en- 
larged, and  a  condition  of  extreme  cardiac  dilatation  and  hypertrophy  is 
reached. 

Etiology. — The  most  frequent  cause  of  tricuspid  regurgitation  is  mitral 
stenosis  and  regurgitation.  Tricuspid  reflux  from  primary  endocarditis  is 
very  rare.  Any  condition  of  the  lungs  which  will  produce  hypertrophy 
and  dilatation  of  the  right  ventricle  will  lead  to  it ;  it  is  met  with  in 
extreme  pulmonary  emphysema  and  in  cirrhosis  of  the  lung  with  exten- 
sive chronic  bronchitis.     Balfour  regards  chronic  bronchitis  as  its  most 

'  Charcot  and  Vnlpian  record  a  case  where  one  of  the  tricnapid  valves  was  softened  and  perforated, 
presenting  numerous  vegetations.    Scattered  abscesses  in  the  lungs  were  found  in  this  case. 


464  DISEASES   OF   THE    HEART. 

frequent  cause  after  mitral  stenosis.  Any  valvular  disease  in  the  left  heart 
of  long  duration  may  lead  to  it.  In  all  these  causes  the  rationale  is  the 
same  :  the  abnormal  amount  of  blood  in  the  right  ventricle  presses  with 
undue  force  against  a  valve  which  physiologists  regard  as  normally  slightly 
insufficient,  and  the  stress  upon  the  valve  flaps  and  the  valvular  attach- 
ments is  such  that  endocardial  inflammation  is  excited  at  the  part  subject 
to  the  greatest  strain,  and  valvular  insufficiency  results. 

Symptoms. — As  tricuspid  reflux  is  usually  secondary  to  some  other  form 
of  valvular  disease,  or  to  some  chronic  pulmonary  affection,  the  symp- 
toms during  its  early  stages  are  vague  and  masked  by  those  of  the 
primary  disease.  But  directly  the  venous  return  is  markedly  impeded, 
a  train  of  symptoms  is  developed  which  has  its  origin  in  the  visceral  de- 
rangements. In  addition  to  these  symptoms,  there  may  be,  in  extensive  tri- 
cuspid reflux,  cardiac  palpitation,  cardiac  dyspnoea,  and  marked  irregularity 
in  the  force  and  rhythm  of  the  heart.  The  liver  is  enlarged!,  the  skin  becomes 
dingy,  and  there  is  obstinate  constipation  and  hemorrhoids.  The  liver  is 
rendered  liable  in  such  cases  to  interstitial  hepatitis.  The  spleen  is  en- 
larged. Venous  stasis  in  the  stomach  is  evinced  by  dyspepsia,  nausea,  vom- 
iting, and  hsematemesis.  The  secretion  of  the  kidneys  is  scanty,  dark 
colored,  of  high  specific  gravity,  often  containing  albumen  and  casts. 
Passive  cerebral  hypersemia  is  marked  by  headache,  dizziness,  vertigo,  and 
muscffi  volitantes  ;  there  is  a  peculiar  mental  disturbance  which  is  not 
met  with  in  any  other  form  of  heart  disease.  Placing  the  patient  in 
a  horizontal  position,  after  the  disease  has  existed  for  some  time,  causes 
the  face  to  become  turgid  and  blue,  and  if  the  position  be  retained,  stupor 
and  coma  may  supervene.  Jugular  and  epigastric  pulsation  are  its  char- 
acteristic physical  signs.  A  very  late  symptom  is  dropsy,  which  begins  at 
the  ankles,  extending  upward  until  there  is  general  anasarca.  It  is  a  no- 
ticeable point,  that  in  the  dropsy  from  tricuspid  reflux  the  genital  organs 
suffer  slightly,  if  at  all. 

Physical  Signs. — Inspection.  In  extensive  tricuspid  disease,  the  area  of 
cardiac  impulse  is  increased  more  than  in  any  other  valvular  lesion.  This 
area  sometimes  extends  from  the  nipple  to  the  xiphoid  cartilage,  and  it 
may  reach  as  high  as  the  second  right  intercostal  space.  There  is  a  visi- 
ble impulse  in  the  Jugular  veins,  more  apparent  in  the  right  than  in  the 
left.  Sometimes  the  veins  in  the  face,  arms,  and  hands  are  seen  to  pulsate, 
and  even  the  thyroid  and  mammary  veins. 

Palpation. — The  apex-beat  is  indistinct,  except  in  cases  where  there  is 
marked  hypertrophy  of  the  left  ventricle.  Pulsation  occurs  in  the  epi- 
gastrium, which  maybe  due  to  reflux  into  the  enlarged  hepatic  veins,  or  to 
the  fact  that  the  dilated  and  hypertrophied  right  ventricle  so  presses  on  the 
river,  that  the  impulse  is  conveyed  through  the  diaphragm  with  each  car- 
diac pulsation.  Early  in  the  disease,  the  impulse  in  the  jugular  is  con- 
fined to  the  lower  part  of  the  vessel.  Beyond  this  point,  the  vein  rarely 
undulates.  Later,  a  systolic  pulsation  is  felt  as  high  as  the  angle  of  the 
jaw,  and  may  be  accompanied  by  distinct,  though  feeble,  presystolic  pul- 
sation.    The  liver  may  simply  undergo  systolic  depression,  chiefly  at  the 


PULMOliriC    OBSTRUCTION".  465 

left  lobe  ;  or  the  whole  liver  may  pulsate  from  an  impulse  coming  from  an 
enormously  dilated  vena  cava  ;  or  the  systolic  pulsation  of  the  veins  within 
the  organ  may  give  rise  to  a  palpable  expanso-pulsatory  movement.  The 
hepatic  pulsation  is  synchronous  with  the  cardiac  impulse.  In  rare 
cases  it  precedes  jugular  pulsation.  Sometimes  pulsation  is  felt  in  the 
femoral  veins.  ^  Sphygmographic  tracings  of  the  Jugular  pulse  show  it  to 
be  dicrotic. 

Percussion  shows  an  increase  in  the  area  of  cardiac  dulness  to  the  right 
and  upward,  sometimes  as  far  as  the  second  intercostal  space. 

Auscultation. — The  murmur  of  tricuspid  reflux  is  heard  with,  or  takes 
the  place  of,  the  first  sound  of  the  heart ;  it  is  superficial,  of  low  pitch, 
blowing,  soft,  and  faint,  and  is  heard  with  greatest  intensity  over  the  lower 
part  of  the  sternum,  at  its  left  border  between  the  fourth  and  sixth  ribs. 
It  is  rarely  audible  above  the  third  rib,  or  to  the  left  of  the  apex-beat.  This 
murmur  is  transmitted  from  the  region  at  the  base  of  the  xiphoid  cartilage, 
upward  and  to  the  right,  from  one  to  two  inches.  Sometimes  it  is  heard 
over  a  very  limited  area,  and  then  it  may  be  overlooked. 

Differential  Diagnosis. — A  tricuspid  regurgitant  murmur  may  be  con- 
founded with  an  aortic  obstructive,  pulmonic  obstructive,  aw(}i  mitral  regur- 
gitant. A  tricuspid  regurgitant  murmur  is  never  audible  above  the  third  rib, 
is  accompanied  by  an  accentuation  of  the  second  sound  over  the  pulmonary 
artery  and  by  jugular  and  epigastric  pulsation,  and  is  heard  with  maximum 
intensity  near  the  base  of  the  ensiform  cartilage.  These  points  are  suffi- 
cient to  differentiate  it  from  an  aortic  obstructive  murmur. 

The  differential  diagnosis  between  it  and  a  mitral  regurgitant  murmur 
has  been  given. 

PULMONIC    OBSTEUCTION". 

Very  little  is  known  of  diseases  at  the  pulmonary  orifice.  Their  diagnosis 
is  arrived  at  by  exclusion,  and  they  cannot  be  recognized,  except  by  their 
physical  signs.  Endocarditis  in  the  right  heart  is  rare,  except  in  intra- 
uterine life.  Valvular  diseases  of  the  right  heart  are  usually  the  sequelae 
of  valvular  disease  in  the  left.  The  pulmonary  artery  may  become  athe- 
romatous, but,  even  then,  disease  of  the  pulmonary  valves  is  rare.  Balfour 
believes  that  constriction  of  the  pulmonary  artery  may  occur  at  various 
periods  of  intra-uterine  life  ;  as  a  rule,  the  pulmonary  valves  are  subject  to 
no  lesions  except  congenital  malformations. 

Morbid  Anatomy. — Bertin  records  an  instance  of  pulmonary  obstruction 
where  the  distorted  and  adherent  valves  formed  a  horizontal  sejotum  across 
the  orifice,  which  was  only  one-fourth  of  an  inch  wide.  A  rigid  tricuspid 
valve  has  been  found  to  be  the  cause  of  obstruction  at  the  pulmonary  ori- 
fice, the  pulmonary  valves  themselves  being  normal.  A  few  auto^Dsies  have 
revealed  obstructions  at  the  pulmonary  artery  caused  by  aneurisms,  tumors 
of  the  pericardium  or  of  the  anterior  mediastinum,  enlarged  bronchial 
glands,  or  pressure  of  a  solidified  lung.     The  pulmonary  artery  may  be  oc- 

1  Guttman  thinks  epigastric  pulsation  ib  duewliolly  to  reflusinto  the  veins  of  the  liver,  and  not  to  right 
ventricular  pulsation. 

30 


466  DISEASES   OF   THE   HEART. 

eluded  just  beyond  the  valves  by  a  cancerous  tumor,  and  there  are  exam- 
ples where  a  phthisical  process  in  the  left  lung  has  induced  it.  A  murmur 
indicative  of  pulmonary  obstruction  may  be  produced  by  a  cardiac  throm- 
bosis. 

The  above  statements  I  place  under  the  head  of  morbid  anatomy  of  the 
lesion,  as  they  cannot  be  appreciated  nor  their  pathological  significance 
realized  during  life.  Eeasoning  from  analogy,  obstruction  at  the  pulmo- 
nary orifice  ought  to  be  followed  by  compensatory  hypertrophy  of  the  right 
ventricle,  and  accompanied  by  tricuspid  regurgitation  and  dilatation  of  the 
right  auricle. '  I  have  met  with  only  two  cases  of  pulmonic  obstructive 
murmurs  in  which  autopsies  were  obtained.  In  both  cases  it  was  found 
that  the  murmur  had  been  produced  by  mediastinal  tumors  pressing  upon 
the  pulmonary  artery  so  as  to  diminish  its  calibre. 

Etiology. — Pulmonary  stenosis  is  rarely  the  result  of  endocarditis  or  of 
degenerative  changes  in  the  pulmonary  artery.  Bertin  states  that  when  ab- 
normal communication  between  the  two  sides  of  the  heart  has  existed,  the 
arterial  blood  may  excite  endocarditis  in  the  right  heart.  Syphilis  has 
been  advanced  as  a  possible  cause  of  degenerations  at  the  pulmonary  orifice. 

Symptoms. — The  only  rational  symptoms  that  have  been  noted  in  the  few 
recorded  cases  of  pulmonic  disease  admit  of  manifold  explanations,  and  no 
one  is  either  constant  or  diagnostic.  In  some  cases  ansemia  existed  ;  in 
others  there  was  cardiac  palpitation,  dyspnoea,  cyanosis,  and  dropsy,  but 
none  of  these  belong  exclusively  to  a  pulmonic  lesion,  nor  do  they  necessa- 
rily depend  upon  it. 

Physical  Signs. — Inspection,  palpation,  and  percussion  give  negative  re- 
sults. Palpation  may  give  a  systolic  thrill,  confined  to  the  second  left  in- 
tercostal articulation.  Such  a  fremissement  results  both  from  roughness 
and  contraction  of  the  pulmonic  orifice. 

Auscultation. — A  systolic  murmur  is  heard  with  its  maximum  intensity 
directly  over  the  pulmonic  valves  ;  it  is  very  superficial  and  consequently 
very  distinct,  and  is  limited  in  its  diffusion.  It  is  never  heard  at  the  xiphoid 
■cartilage,  nor  along  the  course  of  the  aorta.  If  it  has  an  area  of  diffusion, 
it  is  toward  the  left  shoulder.  The  murmur  is  loud  and  soft  in  character, 
sometimes  "  bellows  ; "  it  is  not  audible  in  the  vessels  of  the  neck,  nor  is  it 
attended  by  arterial  pulsation.  When  phthisical  consolidation  partially  oc- 
cludes the  pulmonary  artery,  a  loud  but  soft  systolic  murmur  is  heard, 
which  is  sometimes  high-pitched  and  musical,  and  which  is  often  entirely 
suspended  during  a  full  inspiration.  In  some  few  instances,  there  is  a  Iruit 
de  diahle  in  the  jugular  veins. 

DiflFerential  Diagnosis. — It  is  possible  to  confound  a  pulmonic  obstructive 
murmur  with  a  mitral  regurgitation  which  is  propagated  upward  into  the 
left  auricular  appendix.     But  the  area  of  a  mitral  regurgitant  is  also  back- 

1  Dr.  Ormerod  records  three  cases  in  which  pulmonary  obstruction  was  diagnosticated  during  life,  and 
■where  the  post-mortem  proved  the  accuracy  of  the  diagnosis.  Two  of  these  occurred  in  men  under  twenty- 
eight,  and  the  other  in  a  woman  twenty-one.  In  two  of  these  cases  all  the  cardiac  valves  were  healthy, 
except  the  pulmonic.  The  pulmonic  orifice  would  barely  admit  a  goose  quill.  Warbiirton  Begbie  men- 
tions a  case  (man:  aet.  18)  in  whom  reflux  and  stenosis  at  the  pulmonary  orifice  coexisted.  There  were 
four  valves,  and  these  were  incompetent.  All  the  other  valves  were  normal.  Congenital  stenosis  of  the 
infundibulum  of  the  right  ventricle  is  the  probable  result  of  foetal  myocarditis  or  syphilis. 


PULMONIC   REGURGITATION.  467 

ward,  and  by  this  it  could  be  distinguished  from  a  pulmonic  obstruction. 
Beside,  in  mitral  disease  the  pulse  is  very  different  from  the  pulse  of  pul- 
monary stenosis. 

Aortic  stenosis  can  hardly  be  mistaken  for  pulmonary  obstruction,  for  the 
arterial  pulsation,  the  peculiar  pulse,  aud  the  transmission  of  the  murmur 
into  the  arteries  of  the  neck  will  suffice  to  discriminate  between  them.  An 
aneurism  at  the  sitius  of  Valsalva  may  produce  a  murmur  in  the  pulmonary 
artery  by  the  pressure  which  is  exerted  upon  that  vessel.  It  would  be  im- 
possible to  distinguish  this  murmur  from  that  of  a  pulmonic  stenosis. 

The  diagnosis  of  pulmonary  obstruction  is  usually  reached  only  by  ex- 
clusion. 

PULMONIC    EEGUEGITATIOJSr. 

Many  doubt  the  occurrence  of  this  form  of  valvular  lesion.  There  are 
only  a  few  well  authenticated  cases,'  and  in  them  the  lesion  has  been  the 
result  of  injury  or  congenital  defect.  The  statement'  that  the  pulmonary 
valves  exhibit  a  cribriform  condition  nearly  as  often  as  the  aortic,  is  not 
sustained  by  post-mortem  examinations.  In  one  of  the  cases  to  which  I 
have  referred  as  an  example  of  pulmonary  stenosis,  the  valves  were  also  in- 
sufficient. In  Dr.  Begbie's  case,  where  there  were  four  flaps  to  the  valves 
(producing  obstruction),  marked  insufficiency  coexisted.  The  morUd  an- 
atomy^  etiology,  and  rational  symptoms  do  not  require  a  separate  considera- 
tion. The  anatomical  conditions  are  the  same  as  those  found  in  similar 
conditions  of  the  aortic  valves ;  and  the  etiology  and  rational  symptoms 
are  those  of  pulmonic  stenosis. 

Physical  Signs. — Theoretically  pulmonic  regurgitation  should  be  accompa- 
nied by  a  diastolic  murmur  having  its  maximum  intensity  over  the  pulmonic 
valves  ;  and  its  area  of  diffusion  should  be  downward  and  toward  the  xiphoid 
cartilage.  It  should  be  soft  and  blowing  in  character.  This  murmur  is 
rarely  heard  alone  ;  it  is  usually  associated  with  obstruction  at  the  same 
orifice,  or  with  some  murmur  whose  origin  is  on  the  left  side  of  the 
heart.  Niemeyer  states  that  dyspnoea,  hemorrhagic  infarction,  and  con- 
sumption of  the  lungs  have  followed  insufficiency  at  the  pulmonary  orifice. 
No  other  authority  mentions  such  symptoms,  while  the  assignment  of  val- 
vular disease  as  a  cause  of  phthisis  is  absurd.  With  a  pulmonic  regurgitant 
murmur  there  should  be,  on  palpation  and  percussion,  physical  evidences  of 
hypertrophy  and  dilatation  of  the  right  heart,  the  rationale  of  whose  pro- 
duction should  be  identical  with  that  which  was  considered  in  aortic  re- 
gurgitation.    I  have  never  heard  a  regurgitant  pulmonic  murmur. 

Differential  Diagnosis. — The  murmur  of  pulmonary  regurgitation  may  be 
mistaken  for  that  of  aortic  regurgitation.  The  points  in  connection  with 
their  differentiation  have  already  been  given.  The  prognosis  and  treat- 
ment are  the  same  as  those  of  the  former  lesion. 

Prognosis  in  Valvular  Disease  of  the  Heart. — The  duration  of  life  in  valvu- 
lar disease  of  the  heart  varies  greatly. 

1  Path.  Trans.,  vol.  xvi.,  p.  74.  "  Dis.  of  Heart.    Bellingham. 


468  DISEASES    OF   THE    HEAET. 

To  establish,  a  basis  of  comparison,  I  shall  give  a  resume  of  eighty-one 
cases,  in  all  of  which  the  diagnosis  of  valvular  disease  was  confirmed  by  a 
post-mortem  examination. '  In  fourteen  cases  of  different  valvular  diseases, 
each  of  which  was  complicated  by  cardiac  hypertrophy  and  dilatation,  fifty 
per  cent,  of  deaths  were  directly  due  to  the  valvular  lesion.  In  one  of 
these,  where  there  was  stenosis  at  both  the  mitral  and  tricuspid  orifices, 
death  was  sudden.  In  fifteen  cases  in  which  there  was  only  cardiac  hyper- 
trophy, eleven  deaths  occurred  from  the  heart-lesion,  five  of  which  were 
sudden  and  directly  due  to  the  valvular  lesion.  In  six  cases  in  which  dilata- 
tion alone  existed,  four  deaths  directly  resulted  from  the  heart-lesion,  and  two 
of  these  were  sudden.  In  not  one  of  fifteen  cases  of  aortic  disease  did  death 
occur  directly  from  the  heart-lesion.  Of  these  fifteen  cases,  sudden  death 
occurred  in  only  two.  In  twelve  cases  of  calcified  mitral  valve,  no  death  oc- 
curred directly  from  the  heart-lesion  ;  there  were  but  two  sudden  deaths, 
both  from  cerebral  apoplexy.  The  aortic  and  mitral  valves  were  diseased  in 
fourteen  cases  ;  two  deaths  were  due  to  the  heart-lesion,  and  there  were  but 
three  sudden  deaths  (uraemia,  apoplexy,  and  croupous  laryngitis).  The  aortic 
and  pulmonary  valves  were  involved  in  three  cases,  all  of  which  died  suddenly, 
and  none  directly  from  the  heart-lesion.  In  two  instances,  the  aortic,  mi- 
tral and  tricuspid  were  involved,  in  neither  of  which  sudden  death  occurred. 
Thus,  of  eighty-one  cases,  twenty-four  deaths  only  were  directly  due  to  the 
heart-lesion,  and  of  these  only  eight  were  sudden. 

From  the  above  cases  it  seems  evident  that  the  prognosis  is  not  bad  in 
valvular  disease,  except  when  hypertrophy  and  dilatation  coexist,  and  then 
many  complications  are  liable  to  occur.  In  1870,  I  had  a  patient  sixty 
years  old  with  extensive  aortic  reflux,  who  had  had  three  attacks  of  pneu- 
monia during  the  eight  years  he  was  under  my  observation.  There  was  only 
slight  cardiac  dilatation  in  this  case.* 

In  aortic  stenosis,  life  may  be  prolonged  many  years.  So  long  as  the 
left  ventricular  hypertrophy  compensates  for  the  stenosis,  the  prognosis  is 
good  ;  but  when  it  fails,  and  dilatation  begins,  cerebral  anaemia  soon  re- 
sults. If  violent  or  prolonged  efforts  are  followed  by  irregular  heart- 
action,  sudden  death  may  occur.  Hypertrophy  and  dilatation,  syncope, 
cerebral  anaemia,  vertigo,  muscular  debility,  a  very  pale  face,  and  an  irreg- 
ular pulse  render  the  prognosis  unfavorable.  Should  vegetations  be 
suspected,  there  is  danger  of  cerebral  embolism.  Complicating  (secondary) 
mitral  disease  renders  the  prognosis  unfavorable.  Death  results  from 
complications,  degenerations  of  the  heart,  and  pulmonary  cedema. 

Aortic  regurgitation  is  a  graver  form  of  disease  than  aortic  stenosis.  Its 
duration  is  indefinite,  as  it  may  give  rise  to  no  symptoms  until  it  is  far  ad- 
vanced. Twenty-one  days  and  five  years  are  the  extreme  limits  recorded. 
In  no  other  volvular  disea!>e  is  sudden  death  so  liahle  to  occur.  Refer- 
ence to  the  above  cases  shows  that  mitral  stenosis  ranks  nearly  equal  to  it 
in  this  respect.     The  shorter  and  more  gushing  the  murmur,  the  more  ex- 

1  Med.  Rec,  N.  Y.,  Apr.  1,  1870,  p.  66,  etc. 

*  Dr.  Walshe  states  that  the  oi-der  of  relative  gravity  of  valvular  lesion  is  :  Tricuspid  reflux,  Mitral 
reflux  and  stenosis,  Aortic  reflux,  Pulmonarj'  stenosis  and  Aortic  stenosis. 


PROGNOSIS    IN    CARDIAC   YALVL'LAR   DISEASE.  469 

tensive  the  regurgitation,  the  effects  of  which  must  always  be  carefully  esti- 
mated before  a  prognosis  can  be  given.  Aortic  regurgitation  is,  however, 
more  serious  in  the  young  than  in  adults,  because  in  children  the  changes 
are  less  atrophic  and  more  inflammatory.  In  middle  life  and  in  those 
who  are  subjected  to  great  physical  or  mental  strain,  the  prognosis  is  un- 
favorable ;  if  the  vessels  in  these  patients  show  evidences  of  degeneration, 
apoplexy  and  cerebral  thrombosis  are  liable  to  occur.  In  the  very  old,  I 
have  known  extreme  aortic  regurgitation  to  exist  a  long  time  and  cause 
little  inconvenience.  Cyanosis  and  dropsy  .and  signs  of  heart  failure,  dila- 
tation, or  degeneration  of  the  walls  of  the  heart,  render  the  prognosis  un- 
favorable ;  if  mitral  regurgitation  is  developed,  visceral  derangements 
occur  and  hasten  the  fatal  issue.  Sudden  valvular  incompetence  is  far 
more  dangerous  than  that  which  has  developed  slowly.  The  prognosis  is 
determined  more  by  the  condition  of  the  heart  walls  and  the  general  nutri- 
tion of  the  patient  than  by  any  other  elements.  When  aortic  regurgitation 
is  complicated  by  aortic  stenosis  and  mitral  regurgitation  with  marked 
derangement  of  the  general  circulation,  the  prognosis  is  bad.  Death  may 
result  from  embolism,  apoplexy,  dropsy,  pulmonary  oedema,  sudden  cardiac 
insufficiency,  or  from  visceral  complications.  When  the  radial  impulse  is 
felt  a  little  after  the  apex-beat,  it  is  always  important  to  determine  whether 
the  heart's  action  remains  regular  under  mental  excitement  or  violent 
physical  exertion  ;  if  it  does,  the  prognosis  is  good. 

Mitral  stenosis  admits  of  no  compensation.  If  extensive,  it  is  always  a 
grave  disease.  The  prognosis  is  estimated  by  the  severity  of  the  thoracic 
symptoms  ;  if  these  are  greatly  increased  by  physical  exertion,  the  prognosis 
is  bad,  for  pulmonary  congestion  and  oedema,  infarctions  and  diffused  pul- 
monary apoplexy  with  large  extravasations  are  liable  to  occur.  Statistics 
show  that  sudden  death  occurs  nearly  as  often  in  mitral  stenosis  as  in  aortic 
regurgitation.  Congenital  mitral  stenosis  is  not  dangerous,  nor  does  it  occa- 
sion inconvenience,  for  it  is  always  associated  with  hyperplasia  of  the  arterial 
system.     The  later  in  life  mitral  stenosis  occurs,  the  worse  the  prognosis. 

Mitral  regurgitation,  when  uncomplicated,  gives  rise  to  very  little  dis- 
turbance of  the  circulation,  because  it  is  generally  most  fully  compensated 
for,  and  the  changes  which  lead  to  it  are  of  slow  growth  and  their  tendency 
is  to  remain  stationary.  Patients  with  moderate  regurgitation  suffer  little, 
even  on  exercise.  As  long  as  right  ventricular  hypertrophy  compensates, 
there  is  no  dyspnoea.  As  regards  the  duration  of  life,  the  pi'ognosis  in 
mitral  reflux  is  good.  When,  however,  stenosis  and  regurgitation  coexist, 
sudden  pulmonary  complications  are  very  liable  to  occur,  and  the  prognosis 
is  bad.  When  signs  of  right  heart  failure  occur,  the  prognosis  is  bad. 
CEdema  of  the  extremities,  fluid  in  serous  cavities,  cyanosis,  dyspnoea,  and 
haemoptysis  are  indications  of  such  failure.  Death  may  result  from  gen- 
eral anasarca,  serous  effusions  into  the  pleurae,  peritoneum,  or  pericardium, 
pulmonary  cedema  and  congestion,  or  from  sudden  cardiac  insufficiency. 

Extensive  obstruction  or  regurgitation  at  the  pulmonic  orifice  would  lead 
to  serious  results,  but  we  have  no  statistics  upon  which  to  base  a  prog- 
nosis. 


470  DISEASES   OF  THE   HEAET. 

Tricuspid  stenosis  and  obstruction,  when  associated  with  mitral  dis- 
ease, are  very  grave  lesions,  but  not  so  bad  as  when  resulting  from  chronic 
bronchitis  or  pulmonary  emphysema.  When  Jugular  and  epigastric  pul- 
sation are  marked,  the  changes  in  the  viscera  already  referred  to  quickly 
ensue.  Walshe  says  :  "  Tricuspid  regurgitation  is  the  worst  of  all  valvular 
lesions."  Patients  with  tricuspid  regurgitation  are  in  constant  danger 
from  intercurrent  attacks  of  acute  pulmonary  hypersemia.  Tricuspid  dis- 
ease leads  more  rapidly  than  any  other  valvular  lesion  to  cyanosis  and 
dropsy. 

Treatment  of  Valvular  Diseases  of  the  Heart. — The  treatment  of  aortic 
valvular  disease  can  be  summed  up  in,  rest,  diet  and  regimen.  Rest  must 
be  mental  as  well  as  physical.  The  appetite,  emotions  and  passions  must 
be  under  perfect  control,  hence  a  sedentary  country  life  is  best.  Strain- 
ing, especially  when  the  hands  are  above  the  head,  is  to  be  avoided.  The 
nutrition  must  be  kept  as  perfect  as  possible  to  guard  against  cardiac  de- 
generative processes.  Sugar,  sweet  vegetables,  and  animal  fat  must  be 
sparingly  used.  The  food  should  consist  of  nitrogenized  material  taken 
in  quantities  that  do  not  interfere  with  the  heart's  action.  In  aortic  re- 
gurgitation, patients  while  sleeping  should  assume,  as  nearly  as  possible,  a 
horizontal  position,  as  they  thus  lower  the  height  of  the  distending  column 
of  blood,  and  relieve  both  the  cardiac  circulation  and  the  tendency  to  pul- 
monary congestion.  When,  defective  aortic  pressure  reacts  injuriously  on 
the  gastric  and  hepatic  secretions,  moderate  alcoholic  stimulation  may  be 
cautiously  employed.  The  bowels  should  be  daily  gently  moved.  That 
the  skin  may  be  active,  the  body  must  be  warmly  clothed.  Prolonged  ex- 
posure to  cold  is  to  be  avoided.  Warm  baths,  especially  warm  sea-baths, 
are  beneficial.  Medicine  is  not  to  be  given  until  the  hypertrophy  ceases 
to  compensate.  In  aortic  reflux  with  feeble  heart-power,  tr.  digitalis 
and  tr.  ferri  perchlor.  are  to  be  given  in  ten-drop  doses,  three  times  a  day. 
The  iron  is  especially  called  for  when  anaemia  is  present.  Digitalis  is 
given  as  a  cardiac  tonic,  hence  small  doses  only  are  required.  As  long  as  it 
increases  the  urinary  secretion  it  is  safe  to  continue  it.  When  vertigo  and 
syncope  are  prominent  symptoms,  quinine  and  strychnia  may  be  given 
with  the  digitalis.  Should  the  heart  act  with  violence  and  rapidity,  or 
if  there  is  evidence  of  high  arterial  tension,  aconite  is  serviceable. 

In  aortic  incompetence  small  doses  of  arsenic  have  a  stimulating  effect, 
when  given  with  digitalis  and  iron.  Iron  may  disturb  the  stomach  ;  arse- 
nic seldom  does.  Quassia  or  calumba  should  always  be  given  luith  iron. 
When  the  hepatic  or  gastric  vessels  are  engorged,  three  or  four  leeches 
over  the  epigastrium  or  liver,  followed  by  warm  anodyne  poultices,  will 
often  afford  relief.  Large  quantities  of  fluid  should  never  be  taken  into 
the  stomach  at  one  time.  Symptoms  of  angina  pectoris  with  dyspnoea  and 
local  pain  are  signs  of  aortitis,  which  demands  leeches  over  the  sternum 
and  small  doses  of  mercury.  The  treatment  of  dyspnoea,  dropsy,  etc.,  etc., 
will  be  considered  in  the  treatment  of  mitral  disease.  The  pain  of  aortic 
disease  may  be  so  severe  as  to  demand  an  anodyne  ;  opium  by  the  mouth 
cannot  be  given,  but  the   sulphate   or  hydrochlorate  of  morphia  can  be 


TBEATMENT   OF    CAKDIAC    VALVULAR   DISEASE.  471 

given  hypodermatically.  Nitrite  of  amyl  often  relieves  the  angina 
promptly.' 

The  first  thing  in  the  treatment  of  mitral  stenosis  is  to  have  the  patient 
fully  understand  his  exact  condition,  that  he  may  follow  your  advice  im- 
plicitly, for  the  treatment  is  for  the  most  part  in  his  own  hands.  As  to 
nutrition,  the  same  rules  hold  as  in  aortic  disease.  There  must  be  at  least 
one  gentle  daily  evacuation  of  the  bowels.  Straining  at  stool  is  to  be 
avoided.  The  use  of  alcohol,  strong  tea  or  coffee  or  tobacco  is  to  be  pro- 
hibited. If  anaemia  exists,  give  iron  one-half  hour  after  meals,  gr.  x — xx 
of  Vallette's  mass,  two  or  three  times  daily  for  a  long  period.  The  pro- 
longed use  of  the  voice  is  dangerous.  Small  doses  of  quinine  and  strych- 
nia alternating  with  the  iron  are  advantageous.  If  there  is  anorexia,  the 
vegetable  bitters  are  to  be  given.  The  triple  phoi^phates  of  iron,  quinine 
and  strychnine,  or  small  doses  of  dilute  sulphuric  acid  will  improve  these 
patients  when  they  show  signs  of  extreme  debility.  In  every  case  of  mitral 
disease  there  comes  a  time  when  pulmonary  hypergemia  shows  failure  of 
right  cardiac  compensation.  An  adjustment  of  the  heart  to  the  circula- 
tion is  now  effected  by  administering  digitalis,  which  should  only  be  given 
when  heart  failure  is  marked  and  is  accompanied  by  pulmonary  congestion. 
Half  an  ounce  of  the  infusion,  every  two  hours  for  twenty-four  or 
forty-eight  hours,  is  often  required  to  overcome  the  cardiac  failure.  The 
time  will  come  when  digitalis  ceases  to  sustain  the  heart,  hence  it  should 
be  used  sparingly  and  carefully — never  continuously.  When  the  pulse  is 
rapid,  feeble,  and  irregular,  more  time  and  greater  force  for  the  ejection  of 
blood  from  the  ventricle  are  demanded.  Digitalis  meets  both  indications. 
The  pulse  becomes  regular,  full,  and  forceful.  The  urine  becomes  abun- 
dant and  normal.  Pulmonary  engorgement  diminishes  and  commencing 
dropsy  slowly  disappears.  Hayden  advises  ]0  drops  of  chloroform,  15  drops 
of  tincture  of  digitalis,  and  15  drops  of  tincture  ferri  perchloridi,  in  one 
ounce  of  water  every  three  hours.  When  asystolism  is  present,  or  sup- 
pression of  urine  is  threatened,  digitalis  must  be  given  in  large  doses.  In 
most  cases  of  mitral  stenosis  digitalis  is  contraindicated.  The  dropsy  of 
advanced  mitral  reflux  may  be  promptly  relieved  by  pulvis  jalapm  co.  com- 
bined with  calomel  in  sufficient  quantity  to  produce  prompt  and  free  cathar- 
sis. Squills,  juniper,  broom,  and  cream  of  tartar  act  as  diuretics  in  such 
cases. 

In  mitral  regurgitation  a  compound  of  digitalis  and  nitrous  ether  acts 
well  as  a  diuretic.  Whenever  a  diuretic  is  given  in  heart  disease,  the  loins 
should  be  cupped  or  warm  poultices  applied  and  the  bowels  freely  purged. 
In  copious  hasmoptysis  in  cardiac  disease,  ergotin  in  full  doses  hypoder- 
mically  may  be  given.  The  haemoptysis  that  accompanies  pulmonary  apo- 
plexy of  heart  disease  may  relieve  the  dyspnoea  ;  hence  Drs.  Dickenson, 
Fagge  and  other  English  authorities  recommend  venesection  for  relief  of 
pulmonary  engorgement.  Precordial  pain  accompanying  valvular  disease 
may  be  relieved  by  the  application  of  leeches  over  the  precordial  space. 

I  Barlowe  and  Fagge  advise  senega  and  caibunate  of  ammonia  for  the  less  severe  effects  of  aortic  regu^ 
gitation,  which  they  regard  as  least  amenable  to  treatment  of  all  cardiac  diseases. 


472  DISEASES   OF  THE   HEAET. 

Hyoscyamus,  hydrochlorate  of  morphia,  nitrite  of  amyl,  chloroform,  and  a 
belladonna  plaster  over  the  precordiam  may  be  employed  for  the  same  pur- 
pose. Such  pain  is  the  cry  of  a  heart-muscle  for  higher  nutrition.  Bleed- 
ing favors  dropsy  by  thinning  the  blood  and  by  diminishing  the  heart- 
power  ;  it  should  never  be  practised  except  in  emergencies,^  When  digi- 
talis fails  to  regulate  the  circulatory  disturbances,  its  use  does  harm  ;  but 
in  all  cases  of  mitral  disease  where  this  drug  has  not  been  used,  it  is  safe  to 
say  that  its  administration  will  give  prompt  relief.  Morphia  is  the  best 
anodyne  and  hypnotic  to  be  used  in  mitral  disease. 

Hygiene,  diet,  and  exercise  are  to  be  the  same  in  pulmonary,  as  in 
mitral  disease,  further  treatment  is  solely  symptomatic. 

The  treatment  of  tricuspid  ohstruction  depends  on  the  gravity  and 
sequelae  of  the  accompanying  mitral  disease.  For  tricuspid  stenosis  never 
occurs  till  mitral  stenosis  is  excessive,  and  the  latter  condition  is  the  pre- 
dominant one.  The  general  treatment  is  the  same  as  in  aortic  and  mitral 
diseases.  The  patient  should  lead  a  perfectly  quiet  life  in  a  warm,  equa- 
ble climate.  When  this  lesion  occurs  with  mitral  disease,  digitalis  should 
not  be  omitted,  for  the  drug  promotes  ventricular  contraction,  and  thus 
relieves  the  tricuspid  pressure.  In  tricuspid  regurgitation  with  emphysema, 
this  drug  should  be  very  cautiously  given,  and  its  use  or  omission  must 
depend  upon  the  effects  produced  in  each  case.  If  cerebral  symptoms  are 
exaggerated  it  must  be  stopped.  Tonics  should  be  given  on  the  same  prin- 
ciples as  in  mitral  disease  and  the  same  drugs  used.  A  drastic  purge  or 
talking  a  few  ounces  of  blood  from  the  arm  temporarily  relieves  the  venous 
engorgement.  Dropsy  and  local  oedema  are  treated  as  in  mitral  disease. 
For  the  relief  of  the  gastric,  hepatic  and  intestinal  symptoms,  which  are 
often  the  most  troublesome  occurrences  in  tricuspid  regurgitation,  I  have 
found  one  or  two  purgative  doses  of  calomel  to  act  promptly  and  satisfac- 
torily— in  fact,  in  all  cases  of  heart  disease  in  which  there  is  evidence  of 
hepatic  hypersemia,  an  occasional  calomel  purge  will  be  followed  by  marked 
relief  and  improvement. 

CAEDIAC    HYPERTEOPHT. 

By  the  term  cardiac  hypertrophy  is  meant  thickening  of  the  walls  of  the 
heart  by  an  increase  in  their  muscular  tissue.  This  muscular  increase  may 
be  confined  to  one  portion  of  the  heart,  or  it  may  involve  the  walls  of  both 
auricles  and  ventricles.  There  are  three  recognized  forms  of  cardiac 
hypertrophy  : — 

I.  Simple  Hypertrophy. — In  this  form  there  is  an  increase  in  the  thick- 
ness of  the  cardiac  walls,  the  capacity  of  the  cavities  remaining  normal. 
Simple  hypertrophy  is  usually  confined  to  the  left  ventricle,  and  is  most 
frequently  met  with  in  connection  with  chronic  Bright's  disease  and  chronic 
alcoholismus. 

II.  Eccentric  Hypertrophy. — In  this  form  there  is  thickening  of  the  walls 
■of  the  heart,  with  increase  in  the  capacity  of  its  cavities.     It  is  most  com- 

1  Niemeyer  advises  arsenic  and  antimony  in  mitral  valvular  disease  ;  when  and  why  be  does  not  say. 


CAEDIAC   HYPERTROPHY.  473 

monly  met  in  connection  with,  or  occurs  as  the  result  of,  some  valvular 
lesion. 

III.  Concentric  Hiipertro])liy. — In  this  form  there  is  thickening  of  the 
walls  of  the  heart,  with  diminution  in  the  size  of  the  cavities.  Some  ob- 
servers deny  the  occurrence  of  this  form  of  hypertrophy,  and  claim  that  the 
diminution  in  the  capacity  of  the  cavities  is  only  apparent — that  it  is  the 
result  of  violent  ventricular  contraction  just  prior  to  death.  I  have  never 
seen  any  example  of  this  form  of  hypertrophy. 

Morbid  Anatomy. — The  anatomical  changes  in  cardiac  hypertrophy 
vary  according  to  its  seat,  and  sometimes  according  to  the  character 
of  the  hypertrophy.  In  eccentric  hypertrophy,  there  will  always  be  an 
increase  in  the  size  of  the  papillary  muscles,  and  the  septum  will  be 
thickened,  which  does  not  necessarily  occur  in  connection  with  simple 
hypertrophy.  The  ventricular  septum  is  far  less  liable  to  hypertrophy 
than  the  rest  of  the  ventricular  parieties.  It  is  often  difficult,  even  after 
death,  to  determine  the  existence  of  a  moderate  degree  of  cardiac  hyper- 
trophy, while  extensive  hypertrophy  is  very  readily  recognized. 

When  cardiac  hypertrophy  exists,  the  first  thing  noticed  is  a  change 
in  the  shape  of  the  organ,  and  this  change  will  correspond  to  the  seat  of 
the  hypertrophy.  If  the  hypertrophy  js  confined  to  the  left  ventricle,  either 
simple  or  eccentric,  the  heart  will  assume  a  more  than  usual  pyriform 
shape,  and  will  become  elongated — the  right  ventricle  seems  to  be  a  mere 
appendage  to  the  left.  On  the  other  hand,  hypertrophy  of  the  right  ven- 
tricle increases  the  horizontal  measurement  of  the  organ  and  gives  it  a  more 
oval  shape,  the  apex  not  being  as  pointed  as  in  health,  since  the  extremities 
of  both  ventricles  are  on  the  same  level.  If  all  the  cavities  of  the  heart 
are  increased  in  capacity,  and  their  walls  hypertrophied,  the  whole  heart 
will  be  increased  in  size,  but  the  change  will  be  most  marked  in  its  hor- 
izontal direction,  and  the  organ  will  assume  a  globular  shape.  Sometimes 
the  shape  of  the  organ  is  not  notably  changed  in  general  hypertrophy. 

Left  ventricular  hypertrophy  occurs  oftener  than  right,  and  hypertrophy 
of  the  riglit  auricle  much  oftener  than  that  of  the  left.  The  ventricles  are 
hypertrophied  oftener  than  the  auricles.  In  all  varieties  of  hypertrophy 
the  cardiac  walls  are  stiff,  so  that  when  the  cavities  are  opened  and  the 
blood  has  been  removed  from  them,  they  do  not  collapse.  The  substance 
of  an  hypertrophied  left  ventricle  can  generally  be  torn  with  ease,  while  an 
hypertrophied  right  ventricle  is  tough  and  leathery.  The  color  of  the 
muscular  tissue  is  redder  than  normal  ;  there  is  an  increase  in  the 
number  of  the  muscular  fibres,  which  differ  in  no  way  in  their  anatom- 
ical structure  from  those  of  normal  heart  muscle.  Occasionally  there 
is  an  increase  in  the  size  of  the  cardiac  muscular  fibres.^  There  may  be 
more  or  less  increase  of  connective-tissue  between  the  muscular  bundles  ; 
and  Dr.  Quain  stated  that  this  may  be  so  excessive  as  to  be  a  ''false  hyper- 
trophy."    Sometimes  there  are  accumulations  of  fusiform   involuntary 

•  Cornil  and  Ranvier  state  that  "it  is  not  yet  known  whether  hypertrophy  is  entirely  due  to  increase  in 
size  of  the  muscle-fibres,  or  to  a  new  formation  of  these  fihres.  The  phenomena  of  development  of  new 
tuuscle-fibres  have  never  been  observed,  so  that  the  former  hypothesis  seems  the  more  probable." 


474  DISEASES   OF  THE  HEAET. 

fibres  which  have  not  as  yet  developed  into  the  higher  state  of  striked 
fibres. 

There  is  no  limit  to  cardiac  hypertrophy.  The  heart  may  reach  such  a 
degree  of  enlargement  as  to  weigh  forty  ounces  more  than  in  its  normal 
state  ("cor  hovinum'-).  After  the  hypertrophy  reaches  a  certain  point 
there  is  dilatation,  preceding  and  accompanying  which  is  fatty  degen-. 
eration,  which  first  occurs  in  the  more  recently  formed  muscular  fibres. 
An  increase  in  the  number  or  size  of  the  muscular  fibres  of  the  heart  walls, 
causes  a  corresponding  increase  in  the  heart  power.  The  walls  of  the 
hypertrophied  heart  vary  in  thickness  according  to  the  cause  of  the  liyper- 
trophy.  The  walls  of  the  left  ventricle  may  become  an  inch  and  a  half,  or 
even  two  inches  thick,  while  those  of  the  right  ventricle  rarely  reach 
an  inch  in  thickness.  The  auricles  are  seldom  more  than  double  their 
normal  thickness.  The  columnas  carnese  of  the  right  ventricle  are  more 
liable  to  hypertrophy  than  the  walls.  Sometimes  the  walls  of  a  cavity  are 
thinned  at  one  point  while  they  are  hypertrophied  at  another.  The  heavier 
a  heart  becomes  the  deeper  does  it  lie  in  the  thoracic  cavity  ;  the  diaphragm 
is  pushed  down  and  the  heart  inclines  more  to  the  left  of  the  thorax. 

Etiology. — In  general  terms  cardiac  hypertrophy  is  caused  by  over- work ; 
for  some  reason  the  cardiac  walls  are  called  upon  to  perform  more  than 
their  normal  amount  of  labor,  and  an  increase  in  the  number  of  their  muscu- 
lar fibres  necessarily  follows.  Whenever  the  function  of  the  heart  is  per- 
manently or  repeatedly  overtaxed,  or  when  the  resistance  which  it  should 
normally  encounter  is  increased,  hypertrophy  of  its  walls  is  the  result.  The 
modes  by  which  it  is  directly  induced  are  as  follows  : — 

(1)  Dilatation  of  the  Cavities  of  the  Heart. — Under  certain  circumstances 
dilatation  of  one  or  all  of  the  cavities  of  the  heart  takes  place  during  its 
diastole  ;  the  capacity  of  the  cavities  is  consequently  increased,  and  they  re- 
ceive more  than  their  normal  quantity  of  blood.  A  certain  degree  of  force 
is  required  to  discharge  the  normal  quantity  of  blood  ;  if  there  is  more 
than  the  usual  amount,  an  abnormal  degree  of  force  is  required  to  expel 
it.  This  demand  for  increased  heart  power  is  supplied  by  an  increase  of  mus- 
cular fibres  in  the  heart  walls, — the  hypertrophy  is  developed  in  proportion 
to  the  increase  of  force  required.  This  is  the  cause  of  those  forms  of  car- 
diac hypertrophy  which  occur  in  connection  with  valvular  insufficiency. 
Under  these  circumstances  the  hypertrophy  is  always  eccentric,  and  is  not 
due  so  much  to  the  valvular  lesions  as  to  the  dilatation  of  the  heart  cavities 
which  occurs  as  a  result  of  these  lesions.  The  order  is,  first,  dilatation, 
then  hypertrophy  to  compensate  for  the  dilatation.  Dilatation  is  devel- 
oped during  cardiac  diastole  ;  hypertrophy  during  cardiac  systole. 

(2)  Mechanical  Obstruction. — Of  those  causes  which  originate  in  the 
heart,  aortic  stenosis  gives  rise  to  hypertrophy  of  the  left  ventricle ;  mitral 
stenosis  to  hypertrophy  of  the  left  auricle  ;  pulmonic  disease  to  hypertro- 
phy of  the  right  ventricle  ;  and  tricuspid  stenosis  to  hypertrophy  of  the 
right  auricle.  In  the  list  of  mechanical  causes  are  included  all  those  dis- 
eases of  the  arteries  which  diminish  their  elasticity.  The  walls  of  the  large 
arteries  may  lose  their  elasticity  from  atheromatous  degeneration,  or  tney 


CARDIAC   HYPERTROPHY.  475 

may  be  constricted  or  dilated,  and  thus  offer  obstruction  to  the  blood  cur- 
rent. An  aneurismal  tumor  may  have  developed  sufficiently  to  obstruct 
the  current  of  blood/  or  some  tumor  may  press  upon  and  diminish  the 
calibre  of  the  aorta  ;  under  such  circumstances  a  more  than  normal  amount 
of  work  wiil  be  imposed  upon  the  left  ventricle,  and  simple  cardiac  hyper- 
trophy will  be  developed  as  the  result.  Twisting  of  the  thorax  and  de- 
formities of  the  spine,  thorax,  etc.,  may  act  in  the  same  way.  Again,  ob- 
struction to  the  pulmonary  circulation  will  give  rise  to  hypertrophy  of  the 
walls  of  the  right  ventricle  ;  in  many  instances  dilatation  will  occur  prior 
to  the  hypertrophy,  but  in  quite  a  large  number  of  cases  direct  hypertrophy 
of  the  right  ventricular  walls  will  occur  as  the  result  of  obstruction  to  the 
pulmonary  circulation.  Such  obstruction  may  be  developed  in  connection 
with  pulmonary  emphysema,  fibroid  and  compressed  lung,  chronic  pleurisy, 
asthma,  hydrothorax,  and  other  chronic  diseases  which  interfere  with  the 
circulation  of  blood  through  the  lungs.  It  does  not  occur  in  the  early  stage 
of  pulmonary  phthisis,  for  the  pulmonary  circulation  is  not  obstructed  un- 
til the  advanced  stage  of  the  disease.  Hypertrophy  of  the  left  ventricle  may 
also  result  from  interference  with  the  general  capillary  circulation.  Exam- 
ples of  this  are  met  with  in  chronic  Bright's  disease. 

Simple  hypertrophy  of  the  cardiac  walls  is  one  of  the  most  constant 
attendants  of  the  cirrhotic  form  of  ividney  disease.  Gull  and  Sutton  regard 
this  as  secondary  to  arterio-capillary  fibrosis.'^  In  chronic  alcoholismus, 
rheumatic  hyperinosis,  or  any  other  condition  which  interferes  with  the 
systemic  capillary  circulation,  more  or  less  extensive,  simple  cardiac  hyper- 
trophy of  the  left  ventricle  is  developed. 

Anything  which  increases  for  any  length  of  time  the  rapidity  and  force 
of  the  heart's  contraction  may  produce  cardiac  hypertrophy.  Among  this 
class  of  causes  may  be  included  excessive  and  prolonged  muscular  exercise, 
especially  in  young  suljeds,  and  in  soldiers  who  are  on  the  march.  Emo- 
tional conditions  that  produce  cardiac  palpitation,  prolonged  mental  excite- 
ment, the  immoderate  use  of  strong  coffee  or  alcohol  are  causes  of  cardiac 
hypertrophy.  These  are  styled  ''nervous"  causes  (Quain)  ;  and  to  this 
class  probably  belong  those  cases  occurring  in  Grraves's  or  Basedow's  dis- 
eases. Pericarditis  is  not  infrequently  a  cause  of  cardiac  hypertrophy, 
either  by  inducing  softening  and  dilatation  of  the  ventricles,  or  by  the  ob- 
struction which  is  offered  to  the  heart's  action  by  the  adhesions  between  its 
two  surfaces.  The  heart  becomes  hypertrophied  in  pregnancy,  but  returns 
again  to  normal  after  delivery.  Sometimes  no  cause  can  be  found  for  car- 
diac hypertrophy. 

Symptoms. — The  valvular  lesions,  arterial  changes,  or  capillary  obstruc- 
tions which  are  associated  with  cardiac  hypertrophy  modify,  or  to  a  greater 
or  less  extent  obscure  the  phenomena  which  attend  the  hypertrophy.  Total 
eccentric  hypertrophy  usually  cannot  be  detected  except  by  a  physical  ex- 
ploration of  the  chest.     There  are,  however,  certain  subjective  symptoms 

'  But  this  is  rare  ;  Axel  Key  has  shown  that  aneurism  of  the  Morta  a!one.  1?  not  prodactive  of  left  ven- 
tricular hypertrophy,  since  it  does  not  lead  to  increase  in  the  arterial  tension. 

2  The  connection  between  chlorosis  and  cardiac  hypertrophy  has  recently  been  widely  discussed.  Lew- 
insky concludes  that  from  "  lessening  of  the  hiemoglobin  in  chlorosis  cardiac  hypertrophy  results." 


476  DISEASES    OF   THE   HEAET. 

which  are  important  and  which  will  aid  in  its  diagnosis.  The  direct  effect 
of  general  hypertrophy  of  the  heart  is  to  cause  an  abnormal  fulness  of  the 
arteries  and  a  lack  of  blood  in  the  veins.  The  pulse  is  full  and  strong,  and 
is  bounding  in  character ;  the  face  is  easily  flushed,  the  eyes  somewhat 
prominent  and  brilliant,  and  there  is  carotid  pulsation.  The  respiration  is 
not  usually  disturbed  until  the  heart  becomes  so  increased  in  size  as  to  give 
rise  to  pressure  upon  the  adjacent  lung-tissue  and  upon  the  diaphragm ; 
then  the  patient  will  have  a  sense  of  fulness  about  the  chest,  and  with  that 
sense  of  fulness  there  will  be  more  or  less  uneasiness  in  the  epigastrium, 
and  the  stomach  digestion  may  be  more  or  less  interfered  with.  If  dyspnoea 
is  present  it  is  due  to  the  pressure  of  the  enlarged  heart  rather  than  to  any 
change  in  the  lung-tissae.  In  eccentric  hypertrophy  with  dilatation,  more 
especially  when  the  right  cavities  are  affected,  pulmonary  oedema  and  con- 
gestion are  usually  present,  and  then  there  is  marked  dyspnoea. 

In  simple  hypertrophy  there  is  often  a  dry  irritating  cough  ;  and  in  young 
fleshy  females  it  has  a  wheezing  character.  In  right  heart  enlargements  the 
cough  is  often  distressing.  This  class  of  patients  when  excited  are  very  apt 
to  complain  of  cardiac  palpitation.  The  heart's  action  is  often  irregular 
and  intermittent.  In  almost  all  cases  there  is  some  cerebral  hyperaemia, 
consequently  it  will  be  found  that  in  those  who  are  the  subjects  of  eccen- 
tric cardiac  hypertrophy  alcoholic  stimulants,  nervous  excitement,  and 
active  physical  exercise  will  cause  headache,  vertigo,  ringing  in  the  ears  and 
bright  spots  or  flashes  before  the  eyes.  In  left  hypertrophy,  haemoptysis  is 
common  and  comes  on  suddenly.  Eupture  of  the  bronchial  arteries  may 
occur,  ^  Cerebral  apoplexy  may  at  any  time  occur,  when  the  arteries  are 
predisposed  to,  or  have  already  developed  small  aneurisms.  In  fact,  the 
majority  of  ce,rebral  apoplexies  which  occur  in  young  subjects  are  as- 
sociated with  cardiac  hypertrophy.  It  is  now  well  established  that  there 
is  a  close  connection  between  atheroma  of  the  arteries  and  cardiac  hyper- 
trophy. Some  observers  claim  that  the  cardiac  hypertrophy  is  secondary 
to  the  arterial  changes ;  but  it  is  a  fact  of  every-day  observation  that  hyper- 
trophy from  valvular  changes  will  give  rise  to  atheromatous  changes  in  the 
arteries  for  reasons  which  have  already  been  fully  considered  in  connection 
with  the  history  of  valvular  diseases.  The  steps  of  the  change  are,  first, 
cardiac  hypertrophy ;  second,  endarteritis ;  and,  lastly,  atheroma.  The 
general  syniptoms  considered  in  connection  with  its  physical  signs  render 
its  diagnosis  easy. 

Physical  Signs. — The  physical  signs  of  cardiac  hypertrophy  will  vary  with 
the  seat  and  extent  of  the  hypertrophy.  When  it  is  general,  upon  inspec- 
tion it  will  be  noticed  that  although  the  heart's  action  is  regular  there  is  an 
increased  area  of  impulse,  and  that  there  is  a  motion  with  each  cardiac 
pulsation  over  and  even  beyond  the  precordial  space.  In  children  there 
is  often  bulging  of  the  precordial  space. 

In  right  ventricular  hypertrophy,  inspection  may  reveal  a  rounded 
smoothness  of  the  epigastrium,  with,  perhaps,  some  bulging  of  the  ensi- 

1  Niemeyer  states  that  epistaxis  is  not  infrequent.  When  the  right  heart  is  hypertrophied  melsena  or 
haematemesis  may  be  produced  from  obstructed  liepatic  circulation. 


CARDIAC    HYPERTROPHY. 


477 


Fig.  104. 


Diagram  illustrating  the  Physical  Signs  ia  Hypertrophy 
of  the  Left  Ventricle. 

A.  Bight  ventricle  ;  B.  Left  ventncle  ;  C.  Bight  au- 
ricle ;  B.  Left  auricle ;  E.  Aorta ;  F.  Pulmonary 
artery ;  ff,  H.  Dotted  lines  showing  limit  of  hyper- 
trophy  of  the  venti'icle. 


form  and  lower  left  costal  carti- 
lages. The  apex-beat  may  be  dif- 
fused, extending  toward  the  ensi- 
form  cartilage. 

On  palpation  the  cardiac  area  is 
abnormally  increased,  and  the  im- 
pulse has  a  heaving,  lifting  char- 
acter. The  shock  of  an  hyper- 
trophied  heart  may  be  perceptible 
over  the  whole  precordial  space, 
and  in  cases  of  extensive  hyper- 
trophy the  head  of  the  listener  is 
often  lifted  by  the  shock.  When 
the  right  ventricle  is  the  seat  of 
the  hypertrophy,  it  may  cause  a 
strong  epigastric  impulse.  When 
the  left  ventricle  is  the  seat  of  the 
hypertrophy  the  apex-beat  is  felt 
farther  to  the  left  than  normal, 
sometimes  three  inches  below,  and 
three  or  four  inches  to  the  left  of 
the  normal  position. 

On  percussion,    in   general   cardiac  hypertrophy,    the  normal   area   of 

cardiac  dulness,  both  deep-seated 
and  superficial,  will  be  increased 
to  the  right,  left  and  downward. 
The  dulness  is  increased  upward 
only  when  the  auricles  are  not  only 
hypertrophied  but  also  dilated.  If 
the  hypertrophy  is  confined  to  the 
right  ventricle  the  area  of  dulness 
may  extend  considerably  to  the 
right  of  the  sternum,  sometimes 
reaching  an  inch  or  more  beyond 
the  right  sternal  edge,  and  extends 
lower  down  than  normal.  While  if 
the  hypertrophy  is  confined  to  the 
left  side  of  the  heart,  the  area  of 
dulness  may  extend  considerably 
beyond  the  left  nipple.  The  area 
of  superficial  dulness  will  also  be 
increased.  In  eccentric  hypertrophy 
of  the  left  ventricle,  the  superficial 
area  of  dulness  will  be  increased  to  the  left ;  when  the  same  condi- 
tion of  hypertrophy  is  present  in  the  right  ventricle,  the  superficial  area 
of  dulness  will  be  increased  to  the  right  and  downward. 

On  auscultation,  the  first  sound  of  the  heart,  if  not  accompanied  by  a 


Fig.  105. 
Diagram  Illustrating    the  Physical    Signs  in  Hyper- 
trophy of  the  Right  Venticle. 
A,  A.  Limit  of  hypertrophy. 


478  DISEASES    OF   THE   HEART. 

murmur,  is  dull,  muffled,  and  prolonged,  and  in  some  cases  greatly  in- 
creased in  intensity.  The  post-systolic  silence  is  shortened.  If  the  hyper- 
trophy is  confined  to  the  left  ventricle,  the  second  sound  heard  over  the 
aortic  orifice  is  increased  in  intensity ;  if  the  right  ventricle  is  hyper- 
trophied  the  second  sound  over  the  pulmonic  orifice  will  be  increased  in 
intensity.  In  hypertrophy  of  the  right  ventricle  the  first  sound  is  more 
distinct  and  more  superficial  than  normal,  and  the  second  sound  is  not 
infrequently  reduplicated.  In  extensive  hypertrophy  both  sounds  of  the 
heart  often  have  a  metallic  ring.  There  is  a  diminution  or  an  entire  ab- 
sence of  the  respiratory  murmur  over  the  normal  precordial  region.  When 
extensive  pulmonary  emphysema  exists,  although  the  heart  may  be  very 
much  increased  in  size,  the  increase  in  the  volume  of  the  lungs  will  prevent 
appreciation  of  the  increased  force  in  the  apex-beat,  and  the  heart-sounds 
will  be  diminished  rather  than  increased  in  intensity.  It  may,  however, 
be  assumed  that  when  extensive  pulmonary  emphysema  is  present  and  is 
attended  by  venous  pulsation  in  the  neck,  there  is  hypertrophy  and  dilata- 
tion of  the  right  ventricle. 

Differential  Diagnosis. — Cardiac  hypertrophy  may  be  confounded  with 
cardiac  dilatation,  thoracic  aneurism,  mediastinal  tumors,  consolidation 
of  lung-tissue  surrounding  the  heart,  and  displacement  of  the  heart.  Under 
certain  circumstances  pleuritic  effusion  may  be  confounded  with  cardiac 
hypertrophy.  The  differential  diagnosis  of  the  first  four  conditions  can 
be  better  considered  in  connection  with  cardiac  dilatation. 

Displacement  of  the  (normal)  heart  may  be  distinguished  from  hyper- 
trophy by  there  being  no  increase  in  the  area  of  dulness,  no  change  in 
character  or  intensity  of  heart-sounds,  and  no  '*  heaving  "  impulse.  Be- 
sides, certain  subjective  symptoms,  especially  those  of  cerebral  hypergemia, 
are  marked  in  cardiac  hypertrophy  and  absent  in  displacement. 

Prognosis. — Cardiac  hypertrophy  admits  of  a  more  favorable  prognosis 
than  any  other  cardiac  affection.  In  almost  all  instances  it  is  compensa- 
tory ;  the  urgent  symptoms  of  some  other  cardiac  affection  are  relieved  by 
it  and  life  is  prolonged.  Simple  cardiac  hypertrophy,  unless  the  result  of 
aortic  stenosis,  may  exist  for  years  without  the  occurrence  of  any  danger- 
ous or  very  troublesome  symptoms.  Slight  hypertrophy  of  the  left  ventri- 
cle is  very  common  in  those  who  have  led  an  active  life,  and  have  been 
compelled  to  perform  active  and  prolonged  physical  labor  ;  the  hyper- 
trophy is  no  more  than  is  required  to  maintain  an  equilibrium  in  the  cir- 
culation, and  in  no  way  interferes  with  duration  of  life.  In  the  young  and 
in  athletes,  if  the  cause  be  removed,  the  prognosis  is  very  favorable.  The 
patient  should  not  be  made  aware  of  the  presence  of  such  hypertrophy,  for 
although  there  is  no  danger  attending  it,  a  knowledge  of  the  fact  may 
greatly  alarm  him.  When  there  is  not  only  hypertrophy  but  also  degen- 
eration of  the  hypertrophied  walls,  the  result  of  imperfect  nutrition,  the 
prognosis  is  very  unfavorable. 

The  prognosis  in  hypertrophy  of  the  right  ventricle  is  not  as  favorable  as 
in  hypertrophy  of  the  left,  because  it  must  inevitably  be  accompanied  by 
considerable  pulmonary  obstruction,  and  consequently  is  rapidly  progres- 


CARDIAC   HYPEETROPHY.  479 

sive.  In  Bright's  disease,  or  when  there  is  disease  of  the  arterial  coats,  the 
prognosis  is  unfavorable.  The  prognosis  in  any  case  of  cardiac  hyper- 
trophy depends  upon  the  cause  of  the  hypertrophy,  and  upon  the  kind  of 
valvular  or  other  cardiac  lesion  coexisting. 

Treatment. — Althougii  cardiac  hypertrophy  cannot  be  removed,  still, 
much  can  be  done  to  arrest  its  development  by  removing  the  causes  which 
produce  it,  or  by  rendering  them  inoperative.  Patients  with  cardiac  hy- 
pertrophy must  especially  avoid  alcoholic  stimulants,  immoderate  eating, 
active  and  prolonged  physical  exercise  and  mental  excitement.  All  those 
conditions  which  interfere  with  the  general  circulation  must,  if  possible, 
be  removed.  This  embraces  interference  with  the  abdominal  circulation, 
as  well  as  with  the  pulmonary  and  systemic.  Straining  at  stool  and  con- 
stipation should  be  avoided  by  daily  keeping  the  bowels  freely  moved.  This 
condition  of  the  bowels  should  be  maintained  chiefly  by  habits  of  life  and 
regulation  of  diet,  cathartics  being  resorted  to  only  in  exceptional  cases. 
As  little  liquid  as  possible  should  be  taken  into  the  stomach.  Any  symp- 
toms of  cerebral  hyperaemia  must  be  immediately  relieved  by  those  means 
which  diminish  the  force  of  the  heart's  action.  When  the  pulse  is  full  and 
strong  and  there  are  evidences  of  cerebral  hyperaemia,  it  has  been  the  prac- 
tice of  some  to  bleed,  but  this  treatment  is  contraindicated,  for  the  pres- 
ence of  anaemia  greatly  aggravates  the  dangers  arising  from  cardiac  hyper- 
trophy, since  it  increases  irritability  and  excitability  of  the  heart.  The 
symptoms  must  be  very  urgent  to  warrant  venesection. 

Of  all  the  remedial  agents  which  diminish  the  force  of  the  heart's  action, 
I  have  found  aconite  the  best.  When  given  in  full  doses  it  is  more  reliable 
than  any  other  means.  From  two  to  three  drops  of  Fleming's  tincture  of 
the  root  may  be  administered  every  three  or  four  hours.  No  drug  that  I 
have  used  so  fully  and  promptly  relieves  the  vertigo  and  other  painful  sen- 
sations that  attend  cardiac  hypertrophy.  Hydrocyanic  acid,  belladonna, 
and  conium  are  used,  but  are  inferior  to  aconite.  Whenever  the  dilatation 
of  the  cavities  exceeds  the  hypertrophy  of  the  cardiac  walls,  aconite  does 
harm. 

Digitalis  is  contraindicated,  unless  there  is  evidence  of  heart  insuffi- 
ciency. When  digitalis  is  administered  in  chronic  Bright's  disease,  although 
hypertrophy  of  the  left  ventricle  is  one  of  its  constant  attendants,  its  ad- 
ministration is  for  the  relief  of  the  kidneys,  which,  when  relieved,  give 
secondary  relief  to  the  hypertrophied  heart.  Besides,  in  many  cases  of 
Bright's  disease,  the  heart,  although  hypertrophied,  is  not  able  to  overcome 
the  obstruction  to  the  circulation  in  the  small  arteries  and  capillaries,  and 
the  tonic  effect  of  the  digitalis  raises  the  heart-power  to  the  point  where  the 
obstruction  is  overcome  and  the  equilibrium  of  the  circulation  established. 
Acetate  of  lead  and  veratrum  viride  axe  much  thought  of  by  many  Ameri- 
can authorities.  For  painful  palpitation,  wild  cherry  bark  is  the  best  drug. 
Morphine  is  seldom  of  service. 


480  DISEASES    OF   THE   HEAET. 


CAEDIAC    DILATATIOlSr. 

By  the  term  cardiac  dilatation  is  understood  a  condition  of  the  heart  in 
which  there  is  an  increase  in  the  capacity  of  its  cavities,  with  diminution 
of  its  contractile  power.     There  are  three  forms  : — 

I.  Simple  Cardiac  Dilatation,  in  which  the  capacity  of  the  heart-cavities 
is  increased  without  any  marked  change  in  the  cardiac  walls.  Such  a  con- 
dition is  apt  to  occur  during  convalescence  from  any  disease  in  which  there 
has  been  great  impairment  of  nutrition,  such  as  typhoid  fever. 

II.  Hypertrophic  Cardiac  Dilatation. — In  this  form  there  is  increase  in 
the  capacity  of  the  heart-cavities  and  increase  in  the  thickness  of  the  heart- 
walls  ;  but  the  contractile  power  of  the  heart  may  be  diminished  as  the  re- 
sult of  a  degeneration  following  eccentric  hypertrophy,  or  independent  of 
any  hypertrophy  of  the  cardiac  walls. 

III.  Atrophic  Cardiac  Dilatation. — In  this  form  the  capacity  of  the  heart- 
cavities  is  markedly  increased,  and  the  cardiac  walls  are  thinner  than  nor- 
mal. Sometimes  the  ventricular  walls  are  not  more  than  two  or 
three  lines  thick,  and  the  auricular  walls  may  become  so  thinned  that 
they  will  present  the  appearance  of  a  simple  membrane.  Under  these 
circumstances  the  contractile  power  of  the  heart  is.  almost  lost.  Anatom- 
ically, as  well  as  clinically,  the  significance  of  cardiac  dilatation  is  in  pro- 
portion to  the  excess  of  the  capacity  of  the  cavities  over  the  thickness  of 
the  cardiac  walls.  A  cardiac  cavity  may  be  very  much  increased  in  capac- 
ity, but  so  long  as  there  is  an  increase  in  the  muscular  power  of  its  walls 
sufficient  to  meet  the  demand  for  the  increased  work  they  are  called  upon 
to  perform,  there  will  be  little  or  no  disturbance  of  the  general  circulation. 
Eccentric  hypertrophy  and  hypertrophic  dilatation  approach  each  other 
very  closely,  and  it  is  often  very  difficult  to  draw  the  line  between  them. 

Morbid  Anatomy. — One  or  all  of  the  heart  cavities  may  be  the  seat  of 
dilatation.  The  shape  of  the  heart  is  changed  according  to  the  cavity 
which  is  the  seat  of  the  dilatation.  If  the  dilatation  is  confined  to  the 
right  ventricle,  the  heart  will  be  increased  in  breadth  and  the  apex  may 
appear  bifid  ;  while  if  the  dilatation  afPects  mainly,  or  only,  the  left  ven- 
tricle the  heart  will  be  elongated.  Dilatation  occurs  most  frequently  in 
the  auricles,  and  thinning  of  the  cardiac  walls  is  most  commonly  met 
with  here  ;  next  the  right  ventricle  and  last  of  all  the  left  ventricle  is  the 
seat  of  dilatation.  When  all  the  ■  cavities  are  dilated  the  entire  organ  is 
increased  in  size  and  assumes  a  globular  shape.  "When  the  ventricles  are 
excessively  dilated,  the  trabeculge  are  sometimes  reduced  to  the  condition 
of  fleshy  tendinous  cords.  When  the  walls  of  the  left  ventricle  are  very 
much  thinned  they  collapse  when  the  ventricle  is  cut  into.  It  is  a  question 
whether  dilatation  ever  exists  without  some  hypertrophy..  The  hypertro- 
phy is  apt  to  be  overlooked,  for  the  walls  of  the  dilated  cavities  seem  to 
be  of  normal  thickness. 

The  structural  changes  which  take  place  in  the  muscular  tissue  of  the 
walls  of  the  dilated  cavities  vary  with  the  morbid  process  which  precedes 


CAEDIAC    DILATATION".  481 

and  attends  the  dilatation.  When  it  results  from  pericarditis  or  myocar- 
ditis there  are  serous  infiltration  and  granular  degeneration  of  the  muscu- 
lar fibres  ;  when  it  is  the  result  of  fatty  metamorphosis  the  muscular  fibres 
undergo  fatty  degeneration.  In  hypertrophic  dilatation  it  is  often  impossi- 
ble even  by  a  microscoj)ic  examination  to  determine  the  exact  changes 
which  the  muscular  fibres  undergo  ;  the  abnormal  state  of  the  muscular 
fibres  can  only  be  determined  by  the  other  evidences  of  feeble  heart  power. 

A  heart  distended  with  blood  and  relaxed  by  putrefaction  may,  on  first 
view,  be  mistaken  for  a  dilated  heart.  The  distinctive  marks  of  a  heart 
softened  by  the  putrefaction  processes  are  its  extreme  softness,  its  satura- 
tion with  the  coloring  matter  of  the  blood,  and  the  evidences  of  decom- 
position in  other  parts  of  the  hody. 

Etiology. — The  causes  of  cardiac  dilatation  are  numerous.  One  class  of 
causes  may  be  included  under  the  head  of  changes  in  the  muscular  tissue 
of  the  cardiac  walls. 

I.  Changes  in  the  muscular  tissue  which  accompany  pericarditis  and 
endocarditis. 

II.  Fatty  degeneration  of  the  muscular  fibres. 

III.  Cardiac  dilatation  which  occurs  with  certain  forms  of  protracted  dis- 
ease, such  as  typhoid  fever,  when  the  most  careful  microscopical  examina- 
tion will  fail  to  detect  any  uniform  change  in  the  muscular  fibre,  except, 
perhaps,  a  general  atrophy  of  all  the  tissues. 

All  the  causes  of  cardiac  hypertrophy  may  become  the  causes  of  dilata- 
tion in  a  heart  which  has  a  feeble  resistant  power,  either  inherent  or  ac- 
quired.    This  group  of  causes  may  be  classed  under  three  heads. 

I.  Internal  pressure  during  a  cardiac  diastole. — The  wall  of  a  heart 
may  become  weakened  hy  the  changes  which  occur  in  certain  prolonged 
diseases,  or  it  may  become  the  seat  of  serous  infiltration  or  some  form  of 
degeneration  ;  then,  an  abnormal  pressure  within  its  cavities  during  its 
diastole  will  cause  the  cai'diac  walls  to  yield  beyond  their  normal  limits. 
Such  distention  is  certain  to  be  followed  by  permanent  dilatation  of  its 
cavities.  Most  of  the  valvular  lesions  may  be  the  direct  cause  of  such 
internal  pressure  during  the  cardiac  diastole,  after  the  manner  already  de- 
scribed in  connection  with  the  etiology  of  cardiac  hypertrophy.  Gener- 
ally, when  the  cardiac  cavities  become  distended  beyond  their  normal  lim- 
its, and  thus  temporarily  lose  their  contractile  power,  rapid  hypertrophy  of 
the  cardiac  walls  is  developed  which  compensates  for,  and  to  a  certain  ex- 
tent overcomes,  the  dilatation.  But,  if  the  cardiac  walls  are  enfeebled 
by  any  degenerative  changes,  such  compensatory  hypertrophy  does  not  take 
place.  Any  valvular  lesion  which  will  permit  a  double  current  of  blood 
to  flow  into  a  cardiac  cavity  during  its  diastole,  the  heart  walls  having  be- 
come enfeebled  by  degenerative  changes,  will  give  rise  to  dilatation. 

II.  Wien  the  muscular  tissue  of  a  heart  is  the  seat  of  primary  fatty  de- 
generation, after  a  time  dilatation  of  the  cavities  takes  place,  the  normal 
blood  pressure  being  sufficient  to  produce  the  dilatation.  In  the  same  man- 
ner a  heart  will  become  dilated  when  its  walls  are  the  seat  of  myocarditis. 
That  form  of  cardiac  dilatation  which  follows  rheumatic  fever,  pyaemia, 

•J  I 


482  DISEASES   OF   THE   HEART. 

erysipelas,  typhus  and  typhoid  fevers,  or  chlorosis,  usually  disappears 
when  the  attenuated  muscular  fibres  of  the  heart,  with  the  general  muscu- 
lar system,  regain  their  normal  condition  ;  but  the  dilatation  which  results 
from  fatty  or  fibroid  degeneration  of  the  muscular  walls  of  the  heart  or  from 
new  growths  steadily  increases.'  These  fibroid  changes  usually  accom- 
pany chronic  alcoholismus. 

III.  Another  cause  of  cardiac  dilatation,  which  has  already  been  referred 
to  in  connection  with  the  history  of  valvular  diseases,  is  degeneration  of  the 
muscular  substance  of  the  heart,  which  is  the  seat  of  eccentric  hypertrophy  j 
the  manner  of  its  development  has  been  already  described.  The  dilatation 
does  not  occur  in  this  class  of  cases  until  long  after  the  development  of  the 
valvular  diseases  which  give  rise  to  hypertrophy.  Usually  the  hypertrophy 
becomes  very  extensive  before  the  degenerative  dilatation  commences,  but 
when  it  once  begins  it  progresses  very  rapidly,  and  the  failure  of  heart 
power  is  attended  by  very  distressing  symptoms.  The  power  which  ob- 
struction to  the  pulmonary  circulation  has  to  produce  dilatation  of  the 
right  ventricle,  has  been  considered  in  connection  with  valvular  diseases  of 
the  heart.  When  these  obstructions  exist,  eccentric  hypertrophy,  rather 
than  dilatation,  is  generally  developed. 

Symptoms. — The  symptoms  that  attend  the  development  of  cardiac  dila- 
tation will  depend  upon  the  character  and  seat  of  the  dilatation.  In  simple 
cardiac  dilatation  the  heart  walls  are  of  normal  power,  but  the  capacity  of 
the  cavities  is  increased,  and  the  amount  of  blood  to  be  expelled  with  each 
cardiac  pulsation  is  greater  than  normal  ;  consequently  there  is  labored 
action  of  the  heart  (often  so  great  as  to  be  mistaken  for  the  action  of  an 
hypertrophied  heart),  yet  the  force  of  the  heart's  action  does  not  increase, 
and  therefore  we  have  a  feebleness  of  the  radial  pulse.  The  rhythm  of 
the  heart's  action  will  not  be  disturbed.  In  that  form  termed  atrophic 
dilatation  there  is  a  very  different  state  of  affairs.  The  heart  cavities  are 
not  only  dilated,  but  the  walls  of  the  cavities  are  thinner  than  normal ;  the 
heart  power  is  insufficient  for  the  expulsion  of  the  blood  from  its  cavities,  and 
as  a  result  there  is  a  labored  action,  and  the  heart,  on  account  of  the  increased 
amount  of  labor,  staggers  in  its  action,  the  arteries  are  imperfectly  filled 
with  blood,  the  veins  become  over-distended,  the  rhythm  of  the  heart's 
action  is  disturbed,  and  the  radial  pulse  becomes  markedly  feeble  and  inter- 
mitting. These  latter  points  are  of  special  importance  as  affecting  the 
question  of  prognosis,  for  if  a  patient  has  all  the  symptoms  of  cardiac 
dilatation  without  an  irregular  and  intermitting  pulse,  the  prognosis  is  com- 
paratively good.  The  same  disturbance  of  the  circulation  occurs  in  that 
form  of  dilatation  which  is  developed  from  the  degeneration  of  eccentric 
hjrpertrophy. 

The  first  and  perhaps  the  most  constant  symptom  which  is  common  to 
all  varieties  of  cardiac  dilatation,  is  cardiac  palpitation.  At  times  this 
palpitation  is  very  distressing.     There  is  almost  constantly  a  sense  of  pain- 

i  Eecently  not  a  f ew  cases  of  idiopathic  cardiac  dilatation  have  been  recorded.  Extreme  but  passing 
debility,  the  occurrence  of  the  menopause,  and  too  hard  physical  work  for  the  years  of  strength — these 
have  induced  marked  dilatation,  which  in  most  cases  was  recovered  from.  (Med.  Times  and  Gaz.,  AprU 
^7,  1880.) 


CAEDIAC   DILATATION.  483 

ful  pulsation  in  the  region  of  tne  heart.  The  patient  complains  of  weight, 
oppression,  or  uneasiness  in  the  cardiac  region,  with  a  sense  of  fluttering 
and  a  tendency  to  sighing  respiration.  Very  soon  after  the  palpitation  has 
manifested  itself,  the  patient  will  begin  to  suffer  from  dyspnoea  on  slight 
exertion;  when  he  is  perfectly  quiet  he  suffers  very  little.  As  the  irreg- 
ularity of  the  heart's  action  and  the  palpitation  increase,  the  patient's 
countenance  assumes  a  pale,  languid,  anxious  expression,  with  more  or  less 
lividity  of  the  lips.  The  extremities  are  habitually  cold.  On  excitement, 
or  active  physical  exertion,  the  entire  face  and  neck  become  livid  ;  the 
pulse,  which  is  usually  regular,  for  a  time  becomes  irregular  and  inter- 
mittent. In  this  condition  patients  often  live  some  time  in  comparative 
comfort;  but  they  are  conscious  not  only  of  a  loss  of  physical,  but  also  of 
mental  power,  and  they  are  troubled  with  dyspeptic  symptoms  and  a  sense 
of  fulness  about  the  epigastrium.  Vomiting  is  not  infrequently  a  trouble- 
some symptom. 

As  the  cardiac  dilatation  reaches  a  point  at  which  there  is  constant  car- 
diac insufficiency,  the  patient  suffers  constant  dyspnoea,  which  becomes 
severe  on  slight  exertion  ;  the  cardiac  palpitation  is  always  present,  and 
often  accompanied  by  attacks  of  syncope.  The  countenance  assumes  a  still 
more  anxious  expression,  and  the  lips  are  always  livid ;  the  pulse  is 
constantly  irregular  and  intermitting.  With  these  symptoms  there  will 
be  scantiness  of  urine,  which  will  contain  albumen  and  perhaps  blood  ;  the 
feet  and  ankles  become  oedematous,  the  oedema  generally  extending  up- 
ward until  the  patient  is  in  a  state  of  general  anasarca.  The  breathing 
becomes  very  difficult,  so  much  so  that  the  patient  is  unable  to  lie  down, 
but  is  obliged  to  sit  with  his  head  inclined  forward  and  resting  on  some 
firm  support ;  he  is  unable  to  utter  more  than  a  single  word  at  a  time.  The 
respirations  may  be  thirty  or  forty  per  minute,  and  panting  and  noisy  in 
character.  Cough  and  expectoration  are  not  uncommon;  hsemoptysis may 
occur,  and  in  some  cases  pulmonary  infarctions  form.  Petechial  extravasa- 
tions not  infrequently  occur,  especially  in  dilatation  of  the  right  heart. 
The  extremities  become  cold  and  blue ;  the  mind  wanders,  the  skin  as- 
sumes a  yellow  tinge,  and  the  patient  dies  from  general  anasarca  with  pul- 
monary oedema  or  from  urinary  suppression.  During  the  advanced  stage 
of  this  affection  violent  paroxysms  of  dyspnoea  sometimes  occur,  in  some 
cases  of  which  it  seems  as  though  the  patient  must  die,  yet  they  are  rarely 
immediately  fatal,  but  the  patient  passes  from  them  into  a  state  of  coma 
and,  later,  dies  unconscious.  There  is  always  danger  from  sudden  syncope, 
which  may  prove  immediately  fatal. 

Although  the  general  symptoms  vary  greatly  in  different  cases,  the 
physical  signs  are  very  distinctive. 

Physical  Signs. — Upon  inspection  it  will  be  noticed  that  the  area  of  the 
cardiac  impulse  is  increased  ;  but  it  is  so  indistinct  that  it  will  be  difficult  to 
determine  (by  inspection)  the  exact  point  where  the  apex  of  the  heart  strikes 
the  walls  of  the  chest.  This  is  especially  the  case  if  the  chest  walls  are  cov- 
ered with  adipose  tissue,  or  are  at  all  oedematous.  Epigastric  pulsation  oc- 
curs in  dilatation  of  the  right  ventricle.     In  persons  with  thin  chest- walls. 


484  DISEASES   OF   THE    HEAET. 

there  will  sometimes  be  noticed  an  undulating  motion  over  the  whole  of  the 
precordial  space.  Successive  beats  strike  the  chest-wall  at  different  points, 
and  cause  the  undulatory  motion. 

Upon  palpation,  dilatation  can  readily  be  distinguished  from  hypertro- 
phy by  the  feebleness  of  the  cardiac  impulse.  Although  it  can  sometimes 
be  felt  as  far  to  the  left  as  the  axillary  line,  yet  there  is  an  absence  of  the 
lifting,  forcible  impulse  which  attends  cardiac  hypertrophy.  It  is  often 
difficult  to  determine  the  exact  point  of  its  maximum  intensity,  but  it  will 
be  accompanied  by  an  undulating  motion,  wanting  in  power.  Sometimes 
a  purring  thrill  may  be  obtained. 

Percussion  shows  a  greatly  increased  area  of  lateral  dulness.  The  area 
will  be  increased  to  the  right  if  the  right  side  of  the  heart  is  dilated,  and 
it  may  extend  to  the  right  nipple.  If  the  left  side  of  the  heart  is  the  seat 
of  the  dilatation,  the  area  of  dulness  will  be  increased  to  the  left,  and  it 
may  extend  well  into  the  axillary  space.  In  general  dilatation  the  shape 
of  the  increased  precordial  area  will  be  oval.  This  point  is  of  importance 
in  the  differential  diagnosis  between  cardiac  dilatation  and  pericardial  effu- 
sion. The  area  of  the  superficial  cardiac  dulness  is  not  increased  in  the  same 
proportion  as  the  deep-seated,  as  is  the  case  in  cardiac  hypertrophy.  Di- 
lated auricles  are  recognized  by  an  upward  increase  in  the  area  of  dulness, 
even  to  the  first  rib.  When  the  Jugular  veins  are  permanently  dilated  and 
knotted,  the  existence  of  dilatation  of  the  right  auricle  will  not  be  difficult 
to  determine. 

Auscultation. — The  sounds  of  a  dilated  heart  are  short,  abrupt,  and  fee-, 
ble  ;  the  second  sound  is  often  inaudible  at  the  apex,  and  the  two  sounds  are 
of  very  nearly  equal  duration  and  character,  so  that  it  is  very  often  difficult 
to  distinguish  them.  Eeduplication  of  the  first  sound  sometimes  occurs. 
A  systolic  murmur  generally  accompanies  dilatation  ;  many  authorities  re- 
gard its  production  as  possible  without  attendant  valvular  lesion,  from 
tardy  and  incomplete  contraction  of  the  ventricle.  Whenever  a  cardiac 
murmur  has  existed  prior  to  the  development  of  the  dilatation,  the  rhythm 
of  the  murmur  is  lost  as  the  dilatation  develops,  and  it  becomes  simply  a 
confused  murmuring  sound.  This  condition  has  been  denominated  asys- 
tolism.  It  is  a  condition  in  which  it  is  impossible  to  determine  whether 
the  murmur  is  synchronous  with  the  first  or  second  heart-sound  ;  pauses  or 
intermissions  occur  at  irregular  intervals,  which  are  of  more  frequent  oc- 
currence during  exercise  than  when  the  patient  is  quiet.  When  the  asys- 
tolic  condition  is  present,  the  prognosis  is  very  unfavorable,  independent  of 
the  general  condition  of  the  patient ;  under  such  conditions  the  patient  is 
liable  to  die  suddenly.  Asystolism  is  generally  accompanied  by  a  diffused 
cardiac  impulse,  which  is  peculiar,  and  readily  appreciated  by  the  ear  as 
it  rests  over  the  precordial  space.  The  respiratory  murmur  is  diminished 
in  intensity  over  the  whole  of  the  upper  portion  of  the  left  lung. 

Differential  Diagnosis. — The  diagnosis  of  dilatation  of  the  heart  rests 
mainly  on  the  following  conditions  : — feeble  heart  action,  undulating  im- 
pulse, indistinctness  of  apex-beat,  lateral  increase  in  the  area  of  percussion 
dulness,  very  nearly  square  in  its  outline  ;  short,  abrupt  and  feeble  heart 


CARDIAC   DILATATION".  485 

sounds  that  strikingly  resemble  each  other,  and  a  feeble,  irregular  and  in- 
termitting pulse,  accompanied  by  the  general  symptoms  of  systemic  and 
pulmonary  obstruction  and  congestion. 

The  differential  diagnosis  between  cardiac  hypertrophy  and  cardiac  dila- 
tation is  never  difficult.  The  heart  sounds  are  intensified  in  hypertrophy 
and  feeble  in  dilatation.  In  both  cases  there  is  an  increased  area  of  apex- 
beat,  but  in  hypertrophy  it  is  distinct  and  forcible,  in  dilatation  it  is  feeble, 
diffused  and  indistinct.  The  fact  that  an  individual  has  had  cardiac  hyper- 
trophy with  all  its  attendant  symptoms,  but  now  has  a  tired  expression  of 
countenance,  livid  lips,  and  loss  of  physical  vigor,  daily  becoming  more  and 
more  marked,  and  accompanied,  it  may  be,  by  oedema  of  the  feet,  shows  that 
cardiac  hypertrophy  is  giving  place  to  cardiac  dilatation.  The  pulse  is  full, 
strong  and  bounding  in  hypertrophy,  and  weak  and  feeble  in  dilatation. 
The  first  sound  is  dull,  muffled,  prolonged,  and  intensified  in  hypertrophy  ; 
while  it  is  indistinct  and  resembles  the  second  sound  in  dilatation.  The 
face  is  flushed  in  hypertrophy  ;  pale,  livid  and  anxious  in  dilatation.  The 
presence  of  distended,  irregular,  turgid  jugular  veins  tells  very  positively  of 
dilatation  of  the  right  auricle ;  and  pulsation  in  the  jugulars,  with  feeble 
heart  action  and  increase  in  the  area  of  cardiac  dulness  to  the  right,  indi- 
cates dilatation  of  the  right  ventricle  associated  with  tricuspid  regurgitation. 
At  the  same  time  there  will  be  hepatic,  renal,  and  cerebral  disturbance. 

The  differential  diagnosis  between  enlargement  of  the  heart  (whether  from 
dilatation  of  its  cavities  or  hypertrophy  of  its  walls)  and  thoracic  tumors  is 
sometimes  difficult.  One  very  reliable  differential  sign  is  the  direction  of 
the  increased  area  of  percussion  dulness  ;  thoracic  aneurisms  and  medias- 
tinal tumors  always  enlarge  upward  and  to  the  right  or  left,  while  in  car- 
diac enlargement  the  area  of  dulness  is  increased  laterally  and  downward. 
In  aneurism  there  is  a  dilating  impulse,  vibratory  thrill,  dysphagia,  pain 
in  the  dorsal  spine  and  the  peculiar  aneurismal  "  bruit." 

Consolidation  of  lung-tissue  in  the  region  of  the  heart  may  give  rise  to 
some  of  the  signs  of  cardiac  enlargement,  but  the  other  attending  physical 
signs  of  pulmonary  consolidation  will  distinguish  between  the  dulness  on 
percussion  thus  produced  and  the  increased  area  of  dulness  due  to  cardiac 
enlargements.  The  character  of  the  first  sound  of  the  heart,  the  pulse,  the 
shape  of  the  dulness  and  the  presence  or  absence  of  pulmonary  or  bronchial 
symptoms  will  aid  in  the  diagnosis. 

Prognosis. — The  prognosis  in  cardiac  dilatation  is  always  bad,  and  the 
danger  to  life  is  increased  in  proportion  to  the  excess  of  the  capacity  of  the 
cavities  over  the  thickness  of  their  walls.  The  greater  the  increase  in 
the  capacity  of  the  cavities,  and  the  greater  the  diminution  in  thickness  of 
the  cardiac  walls,  the  greater  will  be  the  danger  to  life.  Feebleness  of 
the  general  muscular  system  and  impoverishment  of  the  blood  increase 
the  danger.  The  presence  of  disease  of  the  kidney,  or  other  disease  of  the 
heart  renders  the  prognosis  in  dilatation  very  grave.  If  patients  have  been 
subject  to  paroxysms  of  dyspnoea  and  attacks  of  syncope,  the  prognosis  is 
especially  bad,  for  then  there  is  danger  of  sudden  death.  Whenever  dropsy 
exists,  the  prognosis  is  immediately  unfavorable  ;  under  such  conditions  few 


486  DISEASES    OF   THE    HEAUT. 

patients,  even  with  the  best  of  care,  live  more  than  eighteen  months;  the 
majority  die  within  a  year.  In  those  cases  in  which  the  pulse  is  regular 
or  only  becomes  irregular  after  violent  physical  exertion,  the  prognosis  is 
comparatively  good ;  much  can  be  done  to  relieve  symptoms  and  prolong  life. 
When  general  anasarca  exists  and  the  patient  is  no  longer  able  to  assume  the 
recumbent  posture,  relief  may  be  given,  but  it  will  only  be  temporary. 

Treatment.  — Cardicic  dilatation  is  incurable.  Even  the  good  effects  of 
palliative  measures  are  temporary.  There  are,  however,  two  important 
things  to  be  accomplished.  First,  the  nutrition  of  the  body  must  be  main- 
tained at  its  highest  point.  Second,  all  irregular  or  violent  action  of  the 
heart  must  be  prevented. 

To  accomplish  the  first  result,  the  diet  must  be  most  nutritious  and  taken 
in  small  quantities  and  at  short  inteiYals.  An  exclusive  milk  diet  will  often 
be  found  most  advantageous  ;  stimulants  must  only  be  taken  in  small  quan- 
tities and  with  the  food.  When  symptoms  of  angemia  are  present,  iron  may 
be  administered  with  the  food  ;  as  a  rule  it  is  always  safe  to  daily  administer 
iron  to  a  patient  with  dilated  heart.  Strychnia  and  arsenic  are  recom- 
mended with  iron.  The  greatest  amount  of  fresh  air  and  the  best  hygienic 
surroundings  should  be  secured. 

To  accomplish  the  second  result,  this  class  of  patients  must  be  placed 
under  strict  rules  in  regard  to  exercise.  They  should  never  allow  them- 
selves to  be  placed  in  such  circumstances  as  to  render  sudden  and  violent 
exertion  necessary,  for  a  single  violent  physical  strain  may  jeopardize  life. 
Flannel  should  be  worn  next  the  skin.  A  dry,  bracing  air  generally  best 
agrees  with  this  class  of  patients.  As  regards  the  medicinal  agents  to  be 
employed,  each  case  must  be  studied  by  itself.  All  discharges  that  are  ex- 
hausting must  be  arrested.  If  hypergemia  of  the  liver  and  of  other  abdom- 
inal viscera  exists,  it  must  be  relieved  by  the  occasional  administration  of 
an  aloetic  or  mercurial  purge  ;  excessive  purgation  is  not  admissible,  but  a 
daily  movement  of  the  bowels  without  exhausting  is  important.  When 
there  is  loss  of  appetite  and  impaired  digestion,  vegetable  tonics  and  mineral 
acids  are  indicated. 

Those  remedial  agents  which  have  a  direct  effect  upon  the  heart  itself  are 
important.  The  most  serviceable  of  this  class  of  remedies  is  digitalis.  It 
can  always  be  administered  in  full  doses,  or  at  least  in  sufficiently  large 
doses  to  regulate  the  heart's  action.  Often  when  the  feet  become  cedema- 
tous  and  the  patient  cyanotic  it  has  a  wonderful  effect,  entirely  removing 
for  a  time  all  unpleasant  symptoms.  When  the  heart's  action  becomes 
regular,  the  digitalis  may  be  given  in  smaller  doses,  but  the  small  doses 
must  be  continued  for  a  long  time.  If,  after  a  time,  the  heart's  action 
cannot  be  controlled  by  the  digitalis,  belladonna  or  opium  may  be  combined 
with  it  ;  the  effect  of  the  combination  is  to  tranquillize  the  excited  heart, 
but  they  should  only  be  resorted  to  when  the  digitalis  has  been  thoroughly 
tested  and  has  failed.  In  the  use  of  digitalis  the  same  restriction  is  to  be 
observed  which  was  described  in  connection  with  the  treatment  of  other 
cardiac  diseases — that  is,  it  should  never  be  used  indiscriminately.  It  is 
always  desirable  to  postpone  its  use  as  long  as  possible      Should  the  heart 


MYOCARDITIS. 


487 


become  nervously  excited  during  the  administration  of  the  digitalis,  as  it 
often  does,  the  various  antispasmodic  remedies  may  be  employed.  Should 
cough  be  j)ersistent  morphine  may  be  given.  Paroxysms  of  dyspnoea  may 
be  temporarily  relieved  by  lobelia,  hydrocyanic  acid,  cannabis  indica,  ether, 
and  dry  cujoping  along  the  spine. 

During  the  slow  progress  of  a  chronic  case  of  cardiac  dilatation,  a  great 
variety  of  measures  may  be  indicated  and  afford  temporary  relief;  still,  our 
chief  reliance  will  always  be  upon  digitalis  and  iron,  combined  with  the 
most  nutritious  diet  and  absolute  rest.  Ammonia  and  the  diffusible  stim- 
ulants are  rarely  of  service. 


JVIYOCARDITIS. 

{Carditis.) 

Myocarditis,  or  carditis,  is  an  inflammation  of  the  muscular  structure  of 
the  heart ;  it  may  be  acute  or  chronic.  The  chronic  form  is  attended  by 
fibroid  changes,  general  or  local.  It  is  met  with  most  frequently  in  con- 
nection with  peri-  or  endocarditis. 

Morbid  Anatomy. — The  diseased  process  consists  in  changes  which  take 
place  either  in  the  primitive  bundles  of  muscular  fibre  or  in  the  connective- 
tissue.  Both  are  usually  involved,  but  when  the  muscular  structure  alone 
is  attacked,  it  is  called  parencliymatous  myocarditis.  When  the  change 
primarily  affects  the  connective-tissue  it  is  called  interstitial  myocarditis.^ 
Although  these  two  varieties  may  not  be  determined  during  life,  they  are 
very  readily  recognized  after  death. 
As  a  rule,  the  layers  of  myocardium 
just  beneath  the  peri-  and  endocardium 
are  primarily  and  chiefly  affected.  The 
change  may  have  its  seat  in  any  portion 
of  the  muscular  tissue  of  the  heart ; 
the  portion  most  frequently  affected  is 
the  left  ventricle.  The  first,  change 
noticed  is  one  in  color ;  at  first,  the 
muscle  is  a  dark  red,  later  it  assumes 
a  grayish,  mottled,  opaque,  buff  color, 
and  finally  it  changes  to  a  dark  green. 

The  microscopical  appearances  will 
vary  with  the  stage  of  the  inflamma- 
tion. At  first  the  primitive  bundles 
are  large,  opaque,  and  swollen  from 
infiltration  of  serum  ;  their  stride  be- 
come indistinct,  and  there  is  nuclear 
proliferation.  Later  the  fibrillae  rupt- 
ure and  break  down  into  a  finely 
granular  detritus ;  then  the  muscular 
fibre  is  replaced  by  connective-tissue,  or  the  degenerative  process  goes  on 


Fig.  106. 
Section  of  Acute  Mj'ocarditis. 
A.  Longitudinal  section  showing  granular  muscle- 
fibres,  obliteration  of  strice,  and  prominence  of 
nvcki. 
At  B  the  section  includes  some  fasicidl  cut  ob- 
liquely and  transversely.    The  connective-tissve 
inJUtration  may  be  noted  at  C,  C.     x  500. 


'  Cornil  and.  Ranvier  deny  the  existence  of  Virchow'B  parenchymatous  myocarditis,  p.  200. 


488  DISEASES  OF  THE  HEART. 

until  there  is  a  breaking  down  of  tissue  and  the  formation  of  abscesses. 
When  a  large  amount  of  the  muscular  tissue  of  the  ventricular  wall  is 
replaced  by  new  connective-tissue  formations,  the  power  of  resistance  of 
the  ventricular  wall  is  diminished,  so  that  during  the  ventricular  diastole 
the  new  connective-tissue  is  liable  to  become  gradually  and  slowly  stretched, 
and  finally  it  gives  rise  to  aneurism  of  the  heart.  This  is  the  manner  in 
which  aneurisms  of  the  heart  are  most  commonly  formed.  Calcareous 
matter  may  also  be  deposited  in  the  newly  formed  connective-tissue,  and 
then  calcareous  developments  will  take  place  in  the  walls  of  the  aneurism. 

When  the  inflammatory  process  terminates  in  the  formation  of  an.  abscess 
the  molecular  degeneration  replaces  more  and  more  the  muscular  fibres, 
until  finally  there  are  formed  swollen  yellow-white  masses  (abscesses)  sur- 
rounded by  red  ecchymotic  and  boggy  embryonic  tissue,  which  gives,  on 
section,  a  small  quantity  of  various  colored  puriform  material  consisting  of 
pus  and  muscular  debris.  Sometimes  the  whole  cardiac  tissue  is  infiltrated 
with  pus.  This  form  is  not  met  with  except  in  pyaemia  and  low  forms  of 
fever.  Abscesses  from  acute  local  myocarditis  are  small ;  they  may  burst  ex- 
ternally into  the  pericardium  or  one  of  the  heart  cavities.  As  a  result  of 
this  gradual  destruction  of  muscular  tissue,  rupture  of  the  heart  may  take 
place  with  or  without  abscesses,  and  at  the  post-mortem  the  pericardium 
will  be  distended  with  blood.  Pycemic  abscesses  are  very  small  and  multi- 
ple, they  may  project  from  either  surface  of  the  heart,  and  the  surround- 
ing muscular  tissue  may  be  either  fatty  or  granular ;  bacteria  are  often 
present.  There  may  be  emboli  in  the  coronary  arteries  that  serve  as  foci 
for  the  pygemic  abscesses. 

Etiology. — The  causes  of  myocarditis,  endocarditis,  and  pericarditis  are 
almost  identical.  Rheumatism,  the  most  frequent  cause  of  pericardial  and  • 
endocardial  inflammation,  is  a  frequent  cause  of  myocarditis.  It  is  main- 
tained by  some  that  endocarditis  and  pericarditis  never  occur  unless  they 
are  associated  with  some  myocarditis  ;  but  in  most  cases,  the  myocarditis  is 
so  slight  that  it  little  affects  the  diagnosis  or  prognosis.  Myocarditis  may 
be  the  result  of  embolism  or  degeneration  of  the  coronary  arteries.  It  oc- 
curs in  connection  with  all  septic  dieases,  such  as  pyaemia,  septicaemia, 
typhus,  typhoid  fevers,  and  acute  ulcerative  endocarditis.  When  it  occurs 
with  pygemia  it  generally  terminates  in  abscess  ;  when  it  occurs  with 
rheumatism,  it  usually  terminates  in  connective-tissue  formation,  especially 
at  the  apex  of  the  left  ventricle. 

Eheumatic  myocarditis  may  be  independent  of  either  peri-  or  endo-car- 
ditis.  It  most  frequently  occurs  in  males  before  the  twenty-fifth  year. 
Sometimes  no  cause  can  be  discovered.  Occasionally  it  has  its  starting- 
point  in  syphilitic  connective-tissue  changes.  Prolonged  high  temperature 
and  exposure  to  cold  are  mentioned  as  possible  exciting  causes. 

Symptoms. — There  are  no  distinctive  symptoms  of  myocarditis.  In  a 
large  majority  of  instances  it  is  impossible  to  positively  determine  its  ex- 
istence during  life.  A  rapid,  feeble,  compressible,  and  irregular  pulse, 
•coming  on  suddenly  in  the  course  of  an  acute  endocarditis  or  pericarditis, 
is  its  most  reliable  symptom.     Eestlessness  and  urgent  dyspnoea  are  com- 


MYOCAEDITIS.  489 

mon.  The  face  is  anxious  and  cyanotic,  there  is  great  restlessness,  anxi- 
ety, and  sometimes  delirium.  Tlie  principal  symptoms  which  should  lead 
one  to  suspect  its  existence,  are  attacks  of  cardiac  palpitation,  a  feeble,  ir- 
regular, intermitting  pulse,  syncope  on  slight  exertion,  and  all  the  phe- 
nomena of  heart  failure  ;  if  these  come  on  suddenly  in  one  who  is  suffer- 
ing from  some  severe  septic  disease  there  is  reason  to  suspect  myocarditis. 

There  are  no  physical  signs  except  those  common  to  all  conditions  of 
heart  failure,  though  at  first  the  heart  action  is  violent.  The  heart  sounds 
are  at  first  short  and  sharp,  and  then  feeble.  If,  however,  the  myocarditis 
has  terminated  in  connective-tissue  formations,  and  aneurism  of  the  ven- 
tricular wall  has  occurred  it  may  be  recognized  by  a  change  in  the  shape 
of  the  heart. 

The  area  of  precordial  dulness  will  be  increased  upward  and  toward  the 
left  shoulder,  rather  more  than  when  there  is  cardiac  hypertrophy  or  dila- 
tation. The  diagnosis  of  myocarditis  can  only  be  conjectural.  When  ab- 
scess of  the  heart  occurs  as  a  termination  of  myocarditis,  it  will  probably 
go  unrecognized  until  the  post-mortem.  But  the  sudden  occurrence  of  a 
murmur  indicative  of  rupture  of  a  portion  of  the  wall  or  of  a  valve,  along 
with  restlessness,  delirium,  and  rigors,  may  cause  one  to  suspect  it. 

Differential  Diagnosis. — The  existence  or  non-existence  of  a  murmur 
alone  enables  us  to  distinguish  endo-  and  peri-  from  myo-carditis.  In  chil- 
dren it  may  be  mistaken  for  acute  meningitis. 

Prognosis. — General  myocarditis  must  of  necessity  prove  fatal  ;  circum- 
scribed myocarditis  may  be  recovered  from.  The  present  state  of  our  clin- 
ical knowledge  of  the  disease  admits  only  of  a  speculative  prognosis,  based 
rather  on  our  knowledge  of  its  pathological  lesions  than  on  any  symptoms 
to  which  these  changes  may  give  rise.  Extensive  connective-tissue  for- 
mations, frequently  found  in  the  cardiac  walls,  give  evidence  that  circum- 
scribed myocarditis  is  frequently  recovered  from.  But  the  extent  and  stage 
at  which  recovery  is  possible  and  the  symptoms  which  indicate  fatal  termi- 
nation are  still  undetermined.  It  lasts  from  a  few  hours  to  a  few  days, 
death  occurring  from  asthenia,  heart  failure,  rupture,  aneurism,  hasmo- 
pericardium,  embolism,  and  secondary  septicaemia. 

Treatment. — If  myocarditis  is  suspected  in  the  course  of  an  endocarditis 
or  pericarditis,  the  plan  of  treatment  will  not  be  materially  changed.  It  is 
essentially  the  same  as  that  already  indicated  for  the  management  of  those 
affections.  Great  care  should  be  exercised  not  to  overtax  the  heart.  This 
class  of  patients  should  never  be  allowed  to  go  up-stairs  or  take  active  ex- 
ercise until  some  time  after  convalescence.  "Warmth  to  the  extremities  is 
of  service,  as  it  tends  to  equalize  the  circulation,  and  thus  relieve  and  pre- 
vent cardiac  strain.  It  is  probable  that  many  cases  of  fatty  heart  are  the 
sequelae  of  myocarditis. 

Palpitation  is  an  indication  for  the  moderate  use  of  alcoholic  stimulants. 
Digitalis  and  ammonia  should  be  very  cautiously  given.  Not  infrequently 
septic  and  fever  patients,  after  violent  physical  exertion  during  convales- 
cence, die  suddenly  ;  death  under  such  circumstances  may  be  the  result  of 
overtaxing  a  heart  weakened  by  myocarditis.     Besides  absolute  rest  and 


490  DISEASES    OF   THE    HEAKT. 

sustaining  measures,  all  tliat  can  be  done  for  these  patients  is  to  relieve 
unpleasant  symptoms. 

FIBEOID    DISEASE    OF    THE    HEART. 

{Chronic  Myocarditis. ) 

As  has  been  stated,  acute  inflammation  of  the  myocardium  ends  in  ab- 
scess or  in  connective- tissue  formation.  When  fibroid  tissue  replaces  part 
of  the  muscular  structure  of  the  heart,  we  have  a  fibroid  heart,  or  what 
some  call  '"  connective-tissue  hypertrophy,"  a  condition  analogous  to  what 
Gull  and  Sutton  call  arterio-capillary  fibrosis. 

Morbid  Anatomy, — The  walls  of  the  ventricle  are  oftenest  involved ; 
there  may  be  distinct  patches  of  fibroid  tissue  or  there  may  be  patches  just 
under  the  endo-  or  peri-cardium,  radiating  from  which  are  bands  of  fibrous. 
tissue  which  insinuate  themselves  into  the  deeper  muscular  structure. 
A  ''  fibroid  patch  "  is  most  frequently  found  near  the  apex  of  the  left  ven- 
tricle. When  it  is  a  continuation  of  endo-  or  pericarditis  the  new  tissue 
blends  imperceptibly  from  the  lining  or  covering  membranes  into  the  mus- 
cular structure  of  the  heart.  The  tissue  is  dense,  firm,  inelastic,  and 
gray-white  in  color.  Sometimes  it  has  a  glistening  blue  or  even  green  ap- 
pearance ;  the  form  of  the  masses  is  variable :  sometimes  they  are  little 
spherical  projections  into  some  one  of  the  cardiac  cavities,  and,  again,  they 
bulge  out  into  the  pericardial  sac.  They  may  be  dots,  streaks,  bundles, 
or  islands.  The  hard  tissue  interferes  materially  with  the  movements  of 
the  heart.  Aneurism,  dilatation,  and  annular  constriction  within  one  of 
tlie  cavities  not  infrequently  result  from  interstitial  myocarditis.  The 
aneurismal  dilatations  sometimes  contain  thrombi. 

In  "  connective-tissue  "  hypertrophy  the  heart  is  enlarged,  the  weight  in- 
creased, and  the  walls  are  firm,  tough,  and  leathery.  The  color  varies  from 
a  pale  pink  to  a  deep  purple.  Gummy  tumors  are  not  infrequently  found 
along  with  fibroid  (syphilitic)  patches.  Under  the  microscope  the  muscu- 
lar tissue  is  seen  atrophied,  granular,  or  fatty ;  in  some  places  it  has  entirely 
disappeared.  The  apices  of  the  papillary  muscles  are  not  infrequently  in- 
volved in  the  same  process. 

Etiology. — All  the  causes  of  acute  myocarditis  are  causes  of  chronic  myo- 
carditis. Rheumatism  and  syphilis  are  its  most  frequent  causes.  In  the 
latter  case  the  fibroid  mass  is  called  a  *' syphilitic  patch,"  but  histologically 
it  is  identical  with  non-specific  developments.  Arterial  fibrosis  and  cir- 
rhotic kidney  seem  to  be  associated  with  its  development.  It  occurs  oftenest 
in  males  who  are  past  middle  life.  In  many  instances  no  cause  can  be  made 
out.     It  has  been  regarded  by  some  as  part  of  a  "  senile  "  change. ' 

Symptoms. — In  limited  or  in  slight  general  fibrosis  there  are  no  symptoms. 
Slight  precordial  pain,  palpitation  on  exertion  or  excitement,  dyspnoea  on 
active  exercise,  small  and  sometimes  irregular  pulse,  and  later  dropsy  and 
visceral  complications  are  frequent  accompaniments  of  fibroid  disease  of  the 

1  Long  continued  congestion  of  the  heart,  Jenner  states,  may  lead  to  its  induration. 


FATTY    DEGENERATION    OF   THE    HEART.  491 

heart.'  Should  fibrosis  of  the  columnse  carnese  induce  insufficiency  on  ac- 
count of  shortening  of  the  papillary  muscles,  then  there  will  be  a  systolic 
murmur.  But  a  murmur  is  usually  evidence  of  the  non-existence  of  fibro- 
sis. The  heart  sounds  may  be  sharp  and  short,  resembling  the  sounds 
''tick  tack."  The  patients  emaciate  and  are  very  feeble.  In  connective- 
tissue  hypertrophy,  the  phj^sical  signs  are  in  nowise  different  from  those 
of  ordinary  hypertrophy." 

Differential  Diagnosis. — The  subjective  symptoms  of  chronic  endocardi- 
tis simulate /a^^2/  degeneration  of  the  heart.  The  etiology  will  aid  in  estab- 
lishing a  diagnosis,  which  can  never  be  positive. 

Prognosis.— The  disease  is  not  immediately  fatal,  though  it  is  incurable 
and  sooner  or  later  causes  death.  Its  course  is  chronic,  but  sudden  death 
is  possible  at  any  moment,  and  a  very  common  ending.  Dropsy  and  con- 
gestion and  oedema  of  the  lungs  are  common  complications. 

Treatment. — To  relieve  symptoms  and  aid  nutrition,  is  all  that  can  be 
done  unless  syphilis  be  a  cause,  and  then  anti-syphilitics  often  cause  marked 
improvement.  They  should  be  administered  tentatively  in  all  cases  and 
the  results  carefully  watched.  Digitalis  is  of  doubtful  efficacy  ;  a  restricted 
diet  is  an  imj)ortant  part  of  the  treatment. 

FATTY    DEGENEEATION    OF    THE   HEART. 

This  is  a  common  form  of  cardiac  degeneration.  It  may  he  circum- 
scribed or  diffused.  When  circumscribed  it  has  a  local  cause.  There  are 
two  distinct  morbid  processes  connected  with  fatty  degeneration  of  the 
heart. 

I.  Fatty  degeneration  of  the  primitive  muscular  fihre,  termed  "  Quain's 
fatty  degeneration." 

II.  Fatty  accumulation  on  the  surface 
and  in  the  substance  of  the  heart  so  as 
to  interfere  with  its  functions. 

Morbid  Anatomy. — In  true  fatty  de- 
generation the  first  change  noticed  is 
that  the  primitive  muscular  fibres  lose 
their  nuclei,  their  stri^  disappear,  and 
they  become  completely  granular.  This 
granular  material  at  first  presents  the 
appearance  of  albuminous  matter  ;  soon, 
however,  the  sarcous  substance  gives 
place  to  fat  granules  and  to  oil  globules, 

which  are  arranged  in  rows,   and   event-      Teased  Fibres  from  the  Heart  in  Fatty  De- 

nally    entirely     obliterate     the    muscle  ^^   ^  ^,    ^      generation. 

•J  •'  The  fatty  change  is  seen,  m   varying  degrees 

fibres.        The    dearenerated    fibres    are   of        from  the  granular  condition  A,  to  the  com- 

°  T   /^i  All  plete  obliteration  of  the  muscle  fihres  l)y  fat 

the  same  size  as  the  normal  fibres.     All       globules,  b.    x  4oo. 

I  Ruble,  who  has  made  a  careful  Btudj'  of  this  disease  (and  considers  it  as  fur  more  frequent  nnd  less 
often  diagnostieated  than  acute  myocarditis)  regards  the  irregularity  and  variability  of  the  pulse,  occurring 
at  any  moment  during  the  day,  as  being  most  characteristic. 

*  Hyde  Salter's  case  was  marked  by  epistaxis  and  haamoptysis. 


492  DISEASES    OF   THE   HEAET. 

the  fibres  are  not  inyolved.  The  muscular  tissue  assumes  a  yellow,  buff,  oi 
dirty  brown  color,  and  loses  its  power  of  resistance,  sometimes  tearing  like 
paper  and  readily  breaking  down  under  pressure.  The  heart  in  most 
instances  is  dilated  ;  it  may  be  hypertrophied.  When  a  fatty  heart  is 
hyjoertrophied  it  is  friable,  not  flabby.  The  coronary  arteries  may  be 
atheromatous,  calcified,  obliterated,  or  normal;  when  the  degeneration 
occurs  secondarily  to  muscular  hypertrophy,  the  coronary  circulation  is 
more  or  less  obstructed  and  the  fatty  changes  are  local.  Its  most  frequent 
seat  is  in  the  left  ventricle,  and  is  most  marked  in  the  columnse  carnese  and 
in  the  inner  wall  of  the  heart. 

In  fatty  infiltration  there  is  simply  an  increase  of  fat  in  the  areolar 
tissue  of  the  heart ;  this  fat  does  not  interfere  with  the  function  of  the  mus- 
cular fibres  except  by  its  pressure.'  If  the  fatty  accumulation  is  extensive, 
it  may  cause  atrophy  of  the  muscular  fibres.  Fatty  degeneration  may 
cause  death  by  so  weakening  the  walls  of  the  heart  that  rupture  will  take 
place,  or  by  so  weakening  the  contractile  power  of  the  heart  as  to  render 
it  incapable  of  performing  its  function.^  Fatty  infiltration  may  diminish 
the  heart-power,  but  it  rarely,  if  ever,  either  directly 
or  indirectly  causes  death. 

Etiology. — All  the  causes  of  fatty  degeneration  of  the 
muscular  fibres  of  the  heart  are  as  yet  undetermined. 
It  is  evident,  however,  that  anything  which  interferes 
with  the  nutrition  of  the  heart  tends  to  fatty  degenera- 
tion of  its  walls  ;  it  is  essentially  a  disease  of  middle  and 
advanced  life ;  it  comes  on  with  senile  decay.^  It  is 
often  a  prominent  sign  of  the  marasmus  which  comes 
FigHos  ^^  ^^  Bright's  disease,  chronic  alcoholismus  (especially 

Fatty  Infiltration.        when  Combined  with  syphilis),  gout,  phthisis,  cancer, 
■^^roOT*%/r^ie«VTftrf  ^^^-j  when  developed  in  this  connection  it  never  reaches 
teamed  and  showing  tj^e  g,  point  where  it  seriously  interferes  with  the  action  of 

infiltration  of  fat,  B,         ^  .  -^ 

in  the  areolar  tissue  the  heart.     In  Quitc  a  large  proportion  of  cases,  fatty 

With,     CttvOwlV    of     1/16  o        X  L  7  ,1 

heart  fibres,  A.  'x  400.  degeneration  of  the  heart  is  the  result  of  mal-nutri- 
tion  from  some  interference  with  the  supply  of  blood  through  the  coronary 
arteries.  Such  interference  may  arise  from  atheroma  or  calcification  of  the 
coronary  vessels,  embolic  obstruction,  external  compression  from  pericar- 
dial thickenings,  or  impairment  of  the  aortic  recoil ;  it  is  met  with  in  con- 
nection with  phosphorus  poisoning,  changes  in  the  heart  in  specific 
fevers,  acute  yellow  atrophy,  etc.  The  same  degenerative  tendency  which 
manifests  itself  in  other  tissues  of  the  body,  due  to  constitutional  condi- 
tions, either  hereditary  or  acquired,  predisposes  to  it. 

Fatty  infiltration  of  the  heart  occurs  as  a  part  of  general  obesity,  which 
so  frequently  develops  after  persons  have  passed  middle  life.  It  is  quite 
frequently  met  with  in  connection  with  chronic  alcoholismus.  Sedentary 
habits  increase  the  liability  to  its  development. 

1  Normally  there  is  more  or  less  fat  in  the  auriculo-ventricular  grooves. 

^  One-half  the  cases  of  true  fatty  degeneration  end  in  rupture  of  the  heart.  Partial  rupture  called 
"cardiac  apoplexy  "  is  common;  aneurism  is  not  uncommon,  and  the  weakened  columnse  carnese  per- 
mit of  valvular  insufficiency. 

'  Hence  the  French  call  it  "  senile  cardiac  softening." 


FATTY    DEGEKERATION    OF   THE    HEAET.  493 

Symptoms. — Moderate  fatty  degeneration  of  the  heart  will  go  unrecog- 
nized. ;  sudden  death  has  occurred  from  this  cause  when  there  was  no  sus- 
picion of  its  existence.  As  a  rule,  the  progress  of  the  disease  is  very  gradual 
and  insidious,  and  most  of  the  symptoms  which  attend  its  dfvelopment  are 
due  to  heart-insufficiency.  Persons  who  are  subjects  of  fatty  heart  cannot 
under  goactive  physical  exertion  for  any  length  of  time,  without  complete 
exhaustion  ;  their  skin  is  of  a  pale,  "  pasty"  yellow  color,  at  times  more  or 
less  livid.  Their  extremities  are  cold  and  oedema  is  not  uncommon,  espe- 
cially in  old  age  ;  digestion  is  feeble  ;  they  persj^ire  profusely  on  slight  ex- 
ertion ;  they  suffer  from  paroxysms  of  dyspnoea  after  physical  exercise. 
"  Uneasy  "  feelings  and  pain  about  the  heart,  and  sudden  suffocating  palpita- 
tion of  the  heart  are  not  infrequent.  During  these  paroxysms  the  liver 
enlarges,  the  respiration  is  feeble  and  irregular,  often  sighing  in  its  charac- 
ter ;  "  Cheyne-Stokes'  breathing  "  is  present  in  some  cases,  and  is  regarded 
as  an  important  symptom.  The  cardiac  insufficiency  is  progressive.  The 
tissues  become  flabby ;  there  are  evidences  of  arterial  degeneration ;  the 
arcus  senilis  is  often  present.  The  temper  is  irritable  ;  there  is  habit- 
ual depression  of  spirits,  disturbance  of  vision,  failure  of  memory,  giddi- 
ness and  vertigo  ;  sudden  cerebral  ansemia  may  occur  during  excitement, 
inducing  syncope  or  epileptiform  attacks.  Frequent  attacks  of  fainting  in 
one  who  has  the  symptoms  of  fatty  heart  are  always  alarming.  The  pulse 
is  peculiar  :  it  is  always  feeble,  although  it  apparently  varies  in  force  ;  it 
may  be  perfectly  regular  in  rhythm  while  the  patient  is  quiet,  yet  on  slight 
exertion  it  becomes  greatly  accelerated  and  irregular  both  in  force  and 
rhythm.  It  may  be  very  rapid  for  some  minutes,  then  suddenly  it  becomes 
irregular,  not  beating  more  than  thirty  or  forty  times  in  a  minute  ; — this 
is  very  characteristic. 

In  an  advanced  stage  of  the  disease,  in  addition  to  cerebral  symptoms  al- 
ready referred  to,  patients  sometimes  get  into  a  condition  which  bears  a 
stiking  resemblance  to  a  state  of  anaesthesia.  Attacks  of  angina  pectoris 
sometimes  occur  in  connection  with  fatty  heart.  Fatty  infiltration  of  the 
heart  gives  rise  to  no  functional  disturbance  of  the  organ,  and  is  not  at- 
tended by  any  unpleasant  or  dangerous  phenomena.  Should  atrophy  of 
the  muscular  substance  of  the  heart,  from  pressure  of  the  fatty  accumula- 
tion, occur  (which  seldom  happens),  the  attending  symptoms  and  results 
differ  in  no  respect  from  those  already  detailed  as  attendants  of  fatty  de- 
generation of  its  muscular  fibres. 

Physical  Signs. — The  physical  signs  of  fatty  heart  are  few  and  not  diag- 
nostic. 

On  inspection,  the  apex-beat  will  be  indistinct. 

On  palpation,  no  impulse  will  be  detected  over  the  precordial  space,  or  it 
will  only  be  perceptible  when  the  body  is  bent  forward.  If  the  fatty  meta- 
morphosis has  occurred  in  an  hypertrophied  heart,  there  will  be  an  undu- 
lating motion  similar  to  that  which  accompanies  excessive  cardiac  dilata- 
tion. 

On  perc  ^ssion,  the  area  of  precordial  dulness,  both  superficial  and  deep, 

is  normal. 


494  DISEASES    OF   THE    HEAET. 

Upon  auscultation,  the  muscular  element  of  the  first  sound  will  be  indis- 
tinct or  absent.  The  valvular  element  is  "  toneless/'  and  is  followed  by  an 
unusually  long  period  of  silence. 

Differential  Diagnosis. — Fatty  heart  may  be  confounded  with  other  cardiac 
degenerations.  The  differential  diagnosis  between  cardiac  dilatation  and 
fatty  heart  is  always  difficult.  In  both  there  may  be  a  feeble,  irregular  pulse, 
vertigo,  ringing  in  the  ears,  and  attacks  of  syncope.  A  dilated  heart  occu- 
pies an  abnormal  space  in  the  thoracic  cavity,  and  consequently  gives  rise  to 
an  abnormal  area  of  cardiac  dulness ;  the  area  of  a  fatty  heart  does  not  ex- 
ceed the  normal  area.  The  muscular  element  of  the  first  sound  may  be 
feeble  in  dilatation,  but  it  is  never  absent,  as  in  fatty  heart. '  Cerebral  symp- 
toms, and  Cheyne-Stokes'  breathing  are  marked  symptoms  in  fatty  heart  and 
absent  in  dilatation.  If  fatty  degeneration  accompanies  cardiac  dilatation, 
there  will  be  a  greater  disturbance  of  the  heart's  action  than  in  fatty  degen- 
eration ivitliout  dilatation. 

Prognosis. — The  prognosis  is  always  unfavorable  ;  its  tendency  is  steadily 
to  advance.'  Individuals  with  fatty  heart  may  live  for  years,  but  when  the 
disease  reaches  an  advanced  stage,  life  is  very  uncertain  ;  a  fatal  termina- 
tion may  occur  suddenly  from  syncope/  from  rupture  of  the  heart,  coma, 
or  as  the  result  of  cerebral  anaemia  ;  it  may  also  terminate  slowly  by  asthenia, 
which  is  usually  attended  by  dropsy. 

Treatment. — There  is  no  plan  of  treatment  that  can  restore  the  degener- 
ated muscular  fibres.  The  principal  thing  is,  to  improve  or  rather  increase 
the  tissue-making  power  of  the  blood  ;  to  this  end,  iron,  cod-liver  oil, 
and  strychnine  may  be  given  in  connection  with  a  good  nutritious  diet,  fresh 
air,  and  light  physical  exercise.  If  alcoholic  stimulants  have  been  used 
habitually,  or  to  excess,  they  must  be  stopped.  All  active  or  violent  physi- 
cal exercise  and  excitement  must  be  avoided  ;  the  life  of  the  patient  must  be 
that  of  an  invalid.  By  avoiding  everything  that  may  stimulate  the  heart's 
action,  and  by  strict  observance  of  all  the  laws  of  hygiene,  life  may  be  pro- 
longed.    Digitalis  does  harm. 

In  fatty  infiltration  the  only  treatment  which  seems  to  be  of  any  service 
is  to  restrict  the  diet  to  animal  food  and  place  the  patient  under  a  system- 
atic physical  training  so  as  to  diminish  or  remove  fatty  accumulations  in 
other  parts  of  the  body.  All  the  exci^eting  organs  must  be  kept  active  so  as 
to  relieve  the  heart  as  much  as  possible.  Quain  says  that  galvanism  applied 
from  the  back  of  the  neck  to  the  precordium,  by  the  interrupted  current, 
has  been  found  useful. 

AMYLOID    DEGEKEEATION. 

Amyloid  or  waxy  degeneration  of  the  heart  is  rare. 

Morbid  Anatomy. — This  form  of  cardiac  degeneration  is  never  met  with 
except  in  connection  with  similar  changes  in  other  organs  of  the  body,  and  is 
due  to  a  constitutional  cause  ;  it  consists  in  the  formation  of  a  shining 


1  Rindfleisch  states  that  "  new  fibrillse  can  be  formed  from  cell-elements  remaining  within  the  ?arco 
Jemma." 

2  Quain  says  death  is  sudden  in  fatty  heart  in  the  proportion  of  five  to  one  to  any  other  mode  of  death. 


PIGMKNTAIIY    DBGENERATIOlSr   OF   THE    HEART.  495 

homogeneous  substance  in  the  primitive  muscular  fibres,  which  gives  the 
reaction  of  amyloid  material.  It  is  most  frequently  found  in  the  walls  of 
the  right  ventricle,  causing  its  cut  surface  to  present  the  characteristic 
appearance  of  waxy  metamorphosis.  The  primary  changes  take  place  in 
the  connective-tissue  surrounding  the  muscle-bundles  ;  it  is  often  associated 
with  syphilitic  gummata. 

Etiology.— Waxy  degeneration  of  the  walls  of  the  heart  is  due  to  those 
causes  which  produce  similar  degeneration  in  the  other  organs  and  tissues 
of  the  body  ;  among  these  causes  syphilis  stands  first. 

Symptoms. — There  are  no  special  symptoms  attending  it,  except  those 
which  are  indicative  of  cardiac  failure.  Its  existence  can  only  be  suspected, 
never  positively  determined.  If  the  signs  of  cardiac  failure,  with  waxy  de- 
generation of  other  organs,  as  the  spleen  and  liver,  are  present  in  an  indi- 
vidual who  has  never  been  the  subject  of  rheumatism  or  any  valvular  dis- 
ease, but  who  has  a  syphilitic  history,  there  is  good  reason  to  suspect  waxy 
degeneration  of  the  heart. 

Treatment. — There  are  no  special  indications  different  from  the  treatment 
of  waxy  degenerations  in  other  organs. 

PAEENCHYMATOUS    DEGENERATIOlSr    OF   THE   HEAET. 

Parenchymatous  or  granular  degeneration,  or  "cloudy  swelling,"  is  that 
variety  usually  met  with  in  acute  (specific)  diseases  attended  by  high  tem- 
perature. 

Morbid  Anatomy. — The  whole  heart  is  soft,  flabby,  friable,  and  of  a  dirty 
red-yellow,  clouded  appearance.  It  may  be  slightly  enlarged.  The  peri- 
cardium is  dull,  clouded,  ecchymotic  and  somewhat  oedematous.  Under 
the  microscope  the  muscle-fibres  are  swollen,  some  of  them  rupture,  and 
they  all  have  a  granular  appearance,  which  disappears  on  the  addition  of 
acetic  acid.     The  striations  are  very  indistinct. 

Etiology. — Parenchymatous  degeneration  of  the  heart  is  caused  by  ex- 
tensive blood  poisoning  and  high  temperature  combined. 

Symptoms. — Its  symptoms  are  obscured  by  those  that  attend  the  causa- 
tive disease.  The  heart  impulse  is  feeble,  the  apex-beat  is  indistinct.  The 
first  sound  gradually  disappears  and  the  second  sound  becomes  indistinct. 
Violent  palpitations  are  often  present. 

The  Diagnosis  is  made  by  the  character  of  the  pulse  and  the  indistinct 
apex-beat,  common  in  the  course  of  any  acute  febrile  disease. 

The  Prognosis  depends  on  the  conditions  under  which  it  occurs.  If  in 
the  course  of  any  acute  specific  fever,  signs  of  heart-failure  come  on,  the 
prognosis  is  very  bad . 

Its  Treatment  consists  in  the  prompt  and  judicious  administration  of 
stimulants. 

PIGMENTARY    DEGElSTERATIOlSr    OF   THE   HEAET. 

Pigment  granules  are  found  in  the  cardiac  muscle-fibres  in  nearly  every 
case  of  chronic  valvular  disease.     In  atrophy  of  the  heart  pigmentation  is 


496  DISEASES   OF  THE   HEART. 

especially  marked,  and  the  particles  lie  near  the  axis  of  the  fibres.  Pig'- 
mentation  also  occui's  in  cases  of  long-standing  jaundice.  In  melanosis  we 
find  a  pigmentary  infiltration  of  the  heart  differing  from  the  above  by  the 
black  color  of  the  granules, 'by  their  seat  being  in  the  connective-tissue 
and  in  the  muscular-tissue  at  the  same  time,  and  by  their  localization  in 
points  and  circumscribed  spots. 

This  condition  has  no  clinical  importance. 


ATEOPHT  OF  THE  HEAET. 

Atrophy  is  a  diminution  in  the  size  and  weight  of  the  heart.  When 
the  term  eccentric  atrophy  is  used  a  condition  of  simple  dilatation  is  indi- 
cated. Atrophy  may  be  confined  to  the  walls  of  one  cavity,  or  it  may  in- 
volve the  walls  of  all  the  cavities  of  the  heart. 

Morbid  Anatomy. — Some  writers  describe  atrophy  of  the  heart  under  the 
head  of  simple,  concentric,  and  eccentric  ;  but  these  terms  are  hardly  nec- 
essary, as  all  cases  of  true  cardiac  atrophy  are  concentric  ;  that  is,  are  ac- 
companied by  diminution  in  the  capacity  of  its  cavities.  In  some  cases, 
wasting  of  the  cardiac  muscles  is  attended  by  inter-muscular  connective- 
tissue  increase  ;  in  such  cases  there  will  be  no  decrease  in  the  size  of  the 
heart,  but  a  marked  diminution  in  its  contractile  power.  There  may  be  a 
decrease  in  size  and  number  of  the  muscular  fibres.  The  pericardium  is 
puckered  and  opaque.  The  coronary  vessels  are  tortuous  and  prominent. 
When  fatty  or  fibroid  changes  have  induced  by  (pressure)  atrophy  of  the 
heart-muscles,  the  term  "yellow  atrophy  "has  been  given  to  it.  Senile 
("brown")  atrophy  is  due  to  extensive  pigmentation.  There  may  be  no 
histological  change  in  the  muscular  fibres,  or  they  may  undergo  fatty  de- 
generation. 

Etiology. — Any  chronic  exhausting  disease,  as  phthisis,  syphilis,  can- 
cer, or  any  disease  that  is  accompanied  by  wasting  of  the  general  muscular 
system,  may  produce  atrophy  of  the  heart.  It  is  frequently  met  with  in  the 
very  aged.  Atrophy  of  the  heart  may  result  from  the  pressure  of  extensive 
chronic  pericardial  effusion.  Mediastinal  growths  may  also  cause  it,  by 
their  pressure.  Fibrous  thickening  of  the  pericardium,  causing  constric- 
tion of  the  coronary  arteries,  as  well  as  atheroma  and  thrombosis  of  these 
vessels,  may  cause  partial  or  complete  cardiac  atrophy.  Abnormally  small 
hearts  are  not  infrequently  congenital,  and  are  associated  with  imperfect 
vascular  and  sexual  development. 

Symptoms. — Cardiac  atrophy  is  usually  attended  by  no  special  symptoms, 
as  it  is  rarely  met  with  except  in  connection  with  wasting  of  the  muscles  of 
the  general  system.  It  is  difficult  to  decide  whether  the  symptoms  indi- 
cating enfeebled  circulation  depend  upon  loss  of  heart-power  or  upon  gen- 
eral muscular  feebleness.  The  existence  of  that  form  of  cardiac  atrophy 
which  is  met  with  in  the  aged  cannot  be  positively  determined  during 
life.  That  form  which  results  from  local  interference  with  the  nutrition 
of  the  heart  is  attended  by  symptoms  similar  to  those  of  fatty  heart.     In 


CARDIAC   THROMBOSIS.  497 

both  forms,  the  heart's  impulse  is  feeble  and  its  sounds  indistinct,  and  the 
apex-beat  is  to  the  right  of  and  above  its  normal  position. 

Prognosis. — The  prognosis  depends  upon  the  cause  and  extent  of  the 
atrophy.  In  extensive  atrophy  attended  by  fatty  degeneration,  and  in 
atrophy  depending  upon  the  pressure  of  a  pericardial  effusion,  the  progno- 
sis is  unfavorable  ;  the  atrophy  of  old  age  is  not  attended  by  any  special 
danger  to  life. 

Treatment. — All  that  can  be  done  in  this  disease  is  to  avoid  excessive 
physical  exertion  and  mental  excitement.  The  food  must  be  nutritious 
and  wine  may  be  indulged  in  rather  freely.  Iron,  which  is  so  serviceable 
in  other  cardiac  affections  attended  by  enfeebled  nutrition  and  failure  of 
heart-power,  will  be  found  of  service  in  this  condition. 

EUPTUEE    OF    THE   HEAET. 

Eupture  of  the  heart  rarely  if  ever  occurs,  unless  preceded  by  degenerative 
changes  in  the  heart  walls.  The  seat  of  the  rupture  is  usually  in  the  left 
ventricle,  and  it  may  be  single  or  multiple.  The  fissure  generally  runs  par- 
allel to  the  fasciculi  of  the  heart  fibres — it  may  be  partial  at  first,  and 
complete  some  time  after.  Complete  rupture  may  vary  in  size  from  two 
inches  to  an  opening  only  large  enough  to  admit  a  probe  ;  ecchymoses  are 
usually  found  around  the  rent ;  fluid  blood  and  large  coagula  distend  the 
pericardium  ;  the  rupture  usually  takes  place  from  within  outward,  and 
occurs  or  commences  during  the  cardiac  systole. 

Etiology. — Rupture  of  the  heart  may  follow  atrophy,  cardiac  aneurism, 
abscess,  hemorrhagic  softening,  fatty  and  other  degenerations  of  the  cardiac 
walls  ;  its  immediate  cause  is  usually  some  violent  physical  effort  or  mental 
excitement.  If  it  occurs  during  sleep,  or  when  the  individual  is  quiet, 
there  is  reason  to  believe  that  it  commenced  some' time  before  it  became 
complete,  and  that  this  apparently  sudden  rupture  is  only  its  com- 
pletion. It  is  rare  before  forty  and  occurs  usually  after  the  sixtieth 
year. 

Symptoms. — If  the  rupture  is  complete  the  patient's  hand  is  suddenly  car- 
ried to  the  chest,  a  few  convulsive  twitches  occur,  and  unconsciousness  and 
death  immediately  follow.  If  the  rupture  is  partial,  the  symptoms  are 
those  of  collapse  : — rapid,  feeble  pulse,  restlessness,  faintness,  pallor,  cold 
skin,  vomiting,  dyspnoea,  and  perhaps  convulsions  ;  death  may  not  occur 
for  several  hours.  Eupture  of  the  heart  sometimes  occurs  in  connection, 
with  a  paroxysm  of  precordial  pain  resembling  angina  pectoris. 

Prognosis. — Death  is  certain  ;  nothing  can  avert  it.  In  seventy-five  per 
cent,  it  is  sudden. 

Treatment. — Necessarily  this  can  only  be  palliative.  Stimulants  and  nar- 
cotics may  be  given  to  afford  temporary  relief, 

CAEDIAC   THROMBOSIS 

At  nearly  every  autopsy  there  will  be  found  a  dark  red  clot  of  blood  in 
the  right  heart,  or  in  the  auricles.     This  clot  will  be  most  firm  in  those 
33 


498  DISEASES    OF   THE   HEART. 

wlio  die  of  chronic  disease  ;  it  will  be  more  or  less  adherent  to  the  cardiac 
walls  and  the  trabeculae  and  may  extend  like  a  cord  into  the  vessels.  In 
phthisis  they  are  usually  very  firm  ;  in  anaemia  they  are  jelly-like  and  pale  ; 
in  leukgemia  they  are  soft,  creamy  and  puriform.  In  the  exanthemata  they 
ar9  yery  soft,  and  when  an  acute  disease  runs  a  very  short  sharp  course 
there  is  often  no  clot.  At  one  time  these  clots  are  entirely  composed  ot 
fibrin,  and  are  of  a  pale  straw-color  ;  at  another  time  they  contain  red 
globules,  and  are  of  a  dark  red  color.  The  coagulum  is  not  infrequently 
whitish  at  its  upper  portion,  and  deep  red  at  its  lower,  according  to  the 
position  of  the  body.  These  clots  are  formed  during  the  last  hours  of  life, 
and  immediately  after  death.  They  have  no  pathological  significance. 
They  are  often  called  passive  coagula. 

Morbid  Anatomy. — In  true  cardiac  thrombosis  coagula  are  formed  in  the 
heart-cavities,  either  a  short  time  before  death,  or  they  may  have  existed 
for  years.  They  vary  in  size  from  a  pin's  head  to  a  walnut,  and  may  fill 
the  greater  part  of  one  of  the  heart-cavities.  If  they  are  of  small  size  and 
firmly  adherent  to  the  valves  or  chordae  tendinese,  they  are  called  vegetations. 
If  they  are  of  large  size,  they  are  called  thrombi,  and  form  in  any  of  the 
heart-cavities  ;  they  are  more  or  less  firmly  adherent  to  the  endocardium. 
Their  projecting  portion  is  smooth  and  globular.  In  those  diseased  con- 
ditions which  interfere  with  the  free  circulation  of  the  blood  through  the 
heart,  thrombi  usually  form  in  such  portions  of  the  heart-cavities  as 
are  farthest  removed  from  the  active  blood-currents.  The  constitution  of 
these  thrombi  varies;  sometimes  they  are  firm,  dry  and  of  a  whitish  color, 
composed  of  exsanguinated  fibrin  ;  at  other  times  they  have  a  globular 
outline,  are  firmly  attached  to  the  endocardium,  and  have  the  constitution 
of  cysts. 

Cardiac  thrombi  may  remain  permanently  attached  to  the  endocardium, 
or  they  mav  become  separated  from  it  in  masses  of  considerable  size,  or  in 
minute  particles,  giving  rise  either  to  embolism  or  septic  infection  ;  they 
may  be  detached,  and,  as  '^  fibrinous  balls,"  lie  free  in  the  auricular 
.cavities.  ^ 

Etiology. — All  cardiac  thrombi  originate  in  coagulation  of  the  blood.  In 
;some  instances  the  coagulation  is  rapid  and  the  coagula  are  of  large  size  ; 
in  others,  the  coagulation  is  slow,  and  the  coagula  are  of  small  size.  The 
conditions  which  favor  these  coagulations  are,  first,  obstruction  to  the  pas- 
sage of  blood  through  the  heart  ;  second,  abnormal  changes  in  the  compo- 
sition of  the  blood  ;  and  third,  inflammatory  changes  in  the  interior  of  the 
heart.  Obstruction  to  the  passage  of  blood  through  the  heart  may  be  due 
to  valvular  lesions,  cardiac  dilatation,  or  feebleness  of  the  contractile  power 
of  the  heart,  inherent,  or  from  degenerations.  The  thrombi  in  the  latter 
case  are  called  marantic  tJirombi.  The  condition  of  the  blood  which 
favors  its  coagulation,  is  that  which  we  find  in  acute  inflammation, 
rheumatism,   Bright's  disease,   and  certain  acute  infectious  diseases,   as 


1  According  to  the  theory  of  Schmidt,  the  formation  of  true  or  cardiac  thrombi  is  due  to  condensation 
of  the  fibrogenic  substance  of  the  blood  in  contact  with  an  inflamed  wall.  Hence  results  a  slow  coagula- 
tion and  one  that  does  not  include  the  red  corpuscles. 


CAEDIAC   THKOMBOSIS.  4-99 

hemorrhagic  variola  and  puerperal  fever.  Phosphorus  poisoning  causes  it. 
Coagulation  in  endocarditis  is  due  to  the  roughening  of  the  endocardial 
surface  produced  by  the  inflammation. 

Symptoms.— The  symptoms  of  cardiac  thrombosis  in  its  gravest  form  are 
urgent.  At  the  moment  of  coagulation,  the  heart's  action  becomes  fre- 
quent and  irregular,  the  pulse  is  small,  weak,  and  irregular  in  force  and 
rhythm.  Partial  syncope,  with  restlessness  and  jactitation  are  combined 
with  symptoms  of  more  or  less  complete  pulmonary  obstruction.  Dyspncea 
is  intense,  there  is  active  delirium,  convulsions,  and  finally  a  fatal  coma. 
Pulmonary  congestion,  infarction  and  cedema  occur.  Life  is  rarely  pro- 
longed beyond  the  third  day. 

In  less  grave  forms,  the  symptoms  are  not  so  urgent.  The  dyspniea  is 
slight,  the  cyanosis  is  not  extreme,  the  jugular  veins  are  but  slightly  dis- 
tended, the  respiration  is  somewhat  hurried,  and  the  pulse  is  increased  in 
frequency,  is  intermittent  and  irregular  ;  the  symptoms  are  those  of  ad- 
vanced heart  disease.  Where  the  coagula  are  of  small  size,  and  the  coagu- 
lation takes  place  slowly,  there  will  be  few,  if  any,  subjective  symptoms  to 
indicate  their  presence,  and  life  may  not  be  seriously  endangered ;  these 
latter  cases,  however,  are  rather  cases  of  vegetations  forming  on  the  valves 
and  chordae  tendinese,  than  true  cardiac  thrombosis.  The  dislodgment  of 
a  large  piece  of  a  thrombus  en  masse  may  block  up  a  valvular  orifice  com- 
pletely, and  thus  cause  sudden  death.  Arterial  embolism  results  from 
breaking  off  of  small  pieces,  and  there  may  be  subsequent  well-marked 
pygemic  symptoms. 

Physical  Signs. — Inspection  and  palpation  show  irregularity  in  the  cardiac 
impulse.  The  area  of  cardiac  percussioti  dulness  is  increased  to  the  right 
of  the  sterniTm. 

On  auscultation,  there  is  marked  irregularity  in  the  heart-sounds. 
New  murmurs  are  developed,  or,  if  murmurs  existed  prior  to  the  occurrence 
of  the  thrombosis,  they  are  increased  in  intensity.  The  most  common 
murmur  is  that  indicative  of  obstruction  at  the  right  auriculo-ventricular 
or  at  the  pulmonic  orifice,  having  its  maximum  intensity  at  the  xiphoid 
cartilage  and  being  conveyed  to  the  left  of  the  sternum.  Occasionally 
there  will  be  a  murmur  indicating  obstruction  in  the  left  ventricle.  If  the 
coagula  are  of  small  size,  the  murmurs  are  similar  to  those  which  accom- 
pany endocarditis. 

Differential  Diagnosis. — The  symptoms  of  sudden  shock  to  the  heart,  and 
the  systemic  effects  of  sudden  intra-cardiac  obstruction,  taken  in  connection 
with  the  sudden  development  of  a  loud  cardiac  murmur  evidently  origi- 
nating on  the  right  side  of  the  heart  are  sufficient  to  lead  one  to  suspect 
the  existence  of  cardiac  thrombosis.  The  only  condition  which  is  liable  to 
be  mistaken  for  it  is  the  rupturing  of  a  valve,  or  of  one  of  the  cTiordoR 
tendinecB  from  ulcerative  endocarditis.  I  know  of  no  means  by  which  a 
differential  diagnosis  can  be  made  between  them  until  some  time  after  the 
occurrence. 

Prognosis. — It  is  unfavorable  in  all  cases  of  extensive  cardiac  throm- 
bosis.    If  the  coagula  are  small,  it  is  possible  for  them  to  disappear  after  a 


500  DISEASES   OF  THE  HEAET. 

time,  or  to  become  changed  into  vegetations ;  but  large  cardiac  thrombi 
destroy  life,  sometimes  in  twelve  hours,  and  at  other  times  life  may  be  pro- 
longed for  two  or  three  days. 

Treatment. — Theoretically,  the  alkaline  carbonates  have  the  power  of  ar- 
resting or  preventing  the  formation  of  cardiac  thrombi,  hence  some  give  ses- 
quicarbonate  of  ammonia  in  endocarditis  and  pneumonia,  to  prevent  the 
formation  of  heart-clots,  which  they  believe  to  be  very  frequently  the  cause 
of  sudden  death  in  these  diseases.  There  is  no  positive  evidence  in  favor 
of,  or  against  this  theory.  Bleeding,  and  every  agent  which  has  a  tendency 
to  enfeeble  the  heart-power  must  be  avoided.  Absolute  quiet  must  be  in- 
sisted upon  and  digitalis  and  opium  may  be  administered  in  small  doses. 
Alcoholic  stimulants  must  be  given  with  great  care,  and  only  to  prevent 
collapse.  Formerly  many  described  cardiac  thrombosis  as  ''polypi"  and 
polypoid  growths  in  the  heart. 

ANEUBISM    OF   THE    HEAET. 

Aneurisms  of  the  heart  may  be  fusiform,  sacculated,  or  globular,  and 
they  are  usually  situated  in  the  wall  of  the  left  ventricle  near  its  apex.* 
They  may  be  single  or  multiple,  and  if  multiple,  open  separately  or  in  com- 
mon. Sometimes  cardiac  aneurism  looks  like  an  elongated  sac  winding 
around  the  aorta. 

Morbid  Anatomy. — In  most  instances,  cardiac  aneurisms  form  slowly, 
and  are  the  result  of  inflammatory  processes  in  the  endocardium  and  myo- 
cardium. These  processes  (as  I  have  already  stated)  may  convert  a  small 
or  large  portion  of  the  muscular  wall  of  the  ventricle  into  fibrous  tissue. 
The  portion  so  charged  yields  to  the  internal  blood  pressure,  and  a  cir- 
cumscribed pouch  or  sac  is  formed  which  communicates  with  the  heart- 
cavity  by  an  opening  which  may  be  very  narrow,  or  may  be  the  largest 
part  of  the  sac.  The  neck  is  hard,  often  cartilaginous,  and  may  be  smooth 
or  jagged.  As  these  pouches  increase  in  size,  their  walls  become  thinner 
and  sometimes  rupture  ;  they  may  undergo  calcification.  The  wall  consists 
mainly  of  fibrous  tissue  with  endocardium  internally  and  pericardium  ex- 
ternally.^ Adherent  pericardium  usually  strengthens  the  sac,  which  varies 
in  thickness  from  that  of  a  sheet  of  paper  to  a  quarter  of  an  inch.  These 
sacs  may  be  partially  or  completely  filled  with  fibrin,  fluid  blood,  or  blood- 
clots.  Aneurisms  of  the  inter- ventricular  septum,  and  at  the  base,  usually 
result  from  the  extension  of  a  "  valvular  aneurism."  The  heart  is  usually 
enlarged. 

Etiology. — Among  the  causes  of  aneurism  of  the  heart  may  be  included 
endocardial,  pericardial,  and  myocardial  inflammations,  the  different  forms 
of  degeneration,  fibroid  changes,  and  tuberculous  and  syphilitic  new 
growths.  Eare  before  twenty,  it  seems  to  become  more  frequent  as  age 
advances.     Males  suffer  twice  as  frequently  as  females. 

Symptoms. — The  symptoms  of  this  affection  are  obscure.     There  is  noth- 

1  In  Quain's  56  cases,  52  were  in  the  left  ventricle. 
a  The  cells  are  flat  and  arranged  parallel  to  the  surface  of  the  aneurism  on  account  of  pressure. 


NEW   FOEMATIONS   IN   THE   HEAET.  501 

ing  in  its  clinical  history  which  distinguishes  it  from  other  diseases  of  the 
ventricular  walls.  In  some  instances  every  known  symptom  of  cardiac  dis- 
ease is  present. 

The pliysical signs  are  equally  unsatisfactory  and  unintelligible.'  The 
physical  signs  of  chronic  pericarditis,  endocarditis,  hypertrophy,  and  dila- 
tation are  sometimes  all  present.  In  twenty  per  cent,  of  cases  murmurs 
exist  that  replace  the  heart  sounds. 

Prognosis. — Sudden  death  may  occur  from  rupture  of  the  heart  into  the 
pericardium,  or  the  patient  may  be  worn  out  by  the  attendants  of  cardiac 
dilatation. 

Treatment. ^It  has  no  special  treatment.  Those  means  advised  for  the 
relief  of  cardiac  dilatation  will  be  found  most  serviceable. 

NEW  EOKMATIONS  UST    THE    HEART. 

Morbid  growths,  or  new  formations  in  the  walls  of  the  heart  have  no 
clinical  importance,  and  I  shall  only  enumerate  them. 

Cancer  of  the  heart,  as  a  primary  affection,  is  exceedingly  rare  ;  while 
cancerous  nodules  in  the  walls  or  on  the  surface  of  the  heart,  in  connec- 
tion with  general  cancerous  infection,  occasionally  occur.  It  is  apt  to  be 
associated  with  cancer  of  the  lungs,  or  mediastinum.  Under  these  circum- 
stances, the  disease  usually  manifests  itself  in  the  form  of  small  circum- 
scribed medullary  or  melanotic  tumors,  which  are  developed  either  in  the 
heart  walls  or  under  the  pericardium  or  endocardium.  The  surfaces  of  the 
heart  rather  than  the  substance  of  the  myocardium  are  affected,  and  the 
right  heart  suffers  oftener  than  the  left,  although  the  cancer  nodules  are 
nearly  always  multiple.  Encephaloid  is  the  form  most  frequently  met  with, 
and  epithelioma  is  the  rarest.  When  cancer  of  the  heart  is  the  result  of 
extension  of  cancer  from  the  neighboring  parts,  large  portions  of  the  heart 
may  become  transformed  into  cancerous  tissue.  Its  existence  cannot  be 
recognized  during  life  ;  it  is  of  interest  only  pathologically.  In  a  few  cases 
local  pain,  anginal  symptoms,  murmurs  and  symptoms  generally  indica- 
tive of  heart  disease  have  led  to  suspicion  of  cancer  of  the  heart  when  evi- 
dences of  cancer  existed  elsewhere. 

Tubercle  is  found  in  the  heart  only  in  connection  with  acute  general  tu- 
berculosis ;  then  it  develops  in  the  connective-tissue.  Its  existence  cannot 
be  recognized  during  life.  Both  gray  miliary  and  yellow  cheesy  masses  are 
found  at  the  post-mortem.    They  are  usually  situated  near  the  pericardium. 

Fibroma,  lymphoma,  lipoma,  sarcoma,  and  myoma  are  rare  forms  of  cir- 
cumscribed tumors  found  in  the  cardiac  walls,  or  under  the  endocardium 
or  pericardium.     Their  existence  cannot  be  determined  during  life. 

Parasites. — The  heart  may  be  the  seat  of  parasites.  The  echinococcus, 
the  cysticercus,  and  entozoa  have  all  been  found  in  the  heart-walls,  and 
have  been  known  to  lead  to  their  rupture,  causing  death.  Three  and  one- 
half  per  cent,  of  the  cases  of  hydatid  disease  occur  in  the  heart.  ^     They 

'  Extensive  dulness  down  and  to  the  left  nccompanied  by  a  feeble  impulse  may  cause  one  to  suspect  it 
2  C'obbold  states  that  hydatid  cysts  in  the  heart  are  commonly  multiple. 


502  DISEASES    OF    THE    HEART. 

project  into  the  pericardium  or  into  the  heart-cavities  as  cystic  tumors.  The 
sac  may  rupture  in  either  direction,  giving  rise  to  embolism  or  to  pericar- 
ditis, usually  with  haemopericardium. 

True  cysts,  containing  serum  or  grumous  fluid,  are  very  rarely  found 
in  the  heart-walls.  All  of  these  developments  have  the  effect  of  depress- 
ing or  interfering  with  the  heart's  action,  hut  their  diagnosis  in  most  cases 
cannot  be  made. 

TUBERCULOSIS  OF    THE   PEEICARDIUM. 

Tuberculosis  of  the  pericardium  is  only  met  with  in  connection  with 
acute  general  miliary  tuberculosis.  Unless  the  tubercular  development 
takes  place  only  a  short  time  previous  to  death,  it  will  give  rise  to  pericar- 
ditis. Its  presence  may  be  suspected  from  the  existence  of  the  pericarditis 
in  connection  with  the  symptoms  of  general  tuberculosis.  In  these  cases 
tubercles  may  develop  in  the  layer  of  fibrinous  exudation  or  be  in  the  vis- 
ceral membrane  itself.  Hemorrhage  is  common  when  the  neoplasm  is  ac- 
companied by  pericarditis. 

CANCEK    OF    THE   PEEICARDIUM. 

The  pericardium  may  be  the  seat  of  cancer,  but  the  cancerous  develop- 
ment is  nearly  always  secondary  to  cancerous  developments  in  other  parts 
of  the  body.  It  may  comport  itself  (as  to  pseudo-membrane  and  exuda- 
tion) precisely  like  tubercle  in  the  pericardium.  More  frequent  than  either 
is  the  formation  of  tuberculous  or  cancerous  masses  in  the  lung  or  medi- 
astinum, which  by  pressure  and  nearness  to  the  pericardium  excite  fatal 
pericarditis,  by  some  called  cancerous  or  tuberculous  pericarditis. 

CARDIAC    NEUROSES. 

The  two  prominent  neuroses  of  the  heart  are  nervous  palpitation  and. 
angina  pectoris.     Both  are  functional  disorders. 

Nervous  Cardiac  Palpitation. — As  has  already  been  stated,  cardiac  pal- 
pitation is  a  very  common  symptom  of  organic  disease  of  the  heart.  A 
purely  nervous  cardiac  palpitation  may  occur  independently  of  organic 
heart  disease.  It  comes  on  suddenly,  and  is  generally  intermittent.  Indeed, 
all  cardiac  neuroses  have  a  paroxysmal  character. 

Morbid  Anatomy. — There  are  no  known  anatomical  changes  either  in  the 
heart,  or  in  its  nerve-supply,  which  can  be  regarded  as  the  constant  causes 
or  concomitants  of  cardiac  palpitation. 

Etiology. — The  direct  cause  of  this  affection  is  over-stimulation  of  the 
cardiac  muscle,  or  the  excitability  from  functional  derangement  of  the  vagus 
or  cardiac  ganglia,  which  is  either  induced  by  director  reflex  causes.  Violent 
physical  exercise,  or  indulgence  in  intoxicating  liquors  will  accelerate  the 
circulation  and  give  rise  to  a  form  of  cardiac  palpitation,  which  ceases  as 
soon  as  the  cause  is  removed.  Blows  on  the  epigastrium  cause  it.  Adults 
with  contracted  chests,  and  young  persons  about  the  time  of  puberty,  whose 


CARDIAC    NEUROSES.  503 

growth  has  been  raj)id,  often  complain  of  palpitation.  In  these  cases  it 
seems  to  be  caused  by  the  narrowness  of  the  chest,  which  interferes  with  the 
free  play  of  the  heart.  Palpitation  is  a  very  frequent  symptom  in  states  of 
debility  or  anaemia.  Under  this  head  are  included  sexual  excesses,  chlo- 
rosis, enervating  habits,  diabetes,  and  all  acute  infectious  diseases  that  are 
attended  by  extensive  nutritive  disturbances,  as  typhoid  fever,  scurvy, 
etc. 

Cardiac  palpitation  is  of  frequent  occurrence  in  persons  with  what  is 
called  a  nervous  temperament,  induced  by  late  hours,  the  habitual  use  of 
strong  tea  and  coffee,  the  inordinate  use  of  tobacco,  derangements  of  the 
digestive  organs,  sudden  shock  or  fright,  chorea,  etc.  The  excessive  habit- 
ual use  of  aconite  and  digitalis  is  known  to  have  caused  it.  Cardiac  palpi- 
tation is  frequently  met  with  in  those  with  a  gouty  diathesis  and  chronic 
diease  of  the  liver,  accompanied  by  dyspeptic  symptoms  which  are  attended 
by  flatulence.  It  is  more  common  in  women  than  in  men,  and  often  seems 
distinctly  allied  to  hysteria. 

Symptoms. — In  a  perfectly  healthy  subject  with  a  well-formed  chest,  the 
cardiac  impulse  is  so  slight  that  the  motion  is  not  perceptible,  unless  the 
hand  be  applied  to  the  precordial  space.  Whenever  a  person  becomes 
sensible  of  the  beating  of  his  own  heart,  he  may  be  said  to  have  cardiac 
palpitation  ;  by  the  term  is  understood  an  unnaturally  strong  cardiac  im- 
pulse accompanied  by  an  unnaturally  rapid  action  of  the  heart,  which  may 
be  irregular  or  intermitting.  Sometimes  there  is  a  loss  of  three  or  four 
beats  which  causes  a  sense  of  oppression  or  even  of  impending  death.  It 
may  be  accompanied  by  a  choking,  paroxysmal,  "  fluttering  "  sensation. 
In  some  cases  the  impulse  communicates  a  quick  shock  to  the  chest  walls  ; 
in  other  cases  the  impulse  is  prolonged  and  heaving  in  character,  and  in 
others  is  weaker  and  almost  imperceptible.  The  heart-sounds  may  be  so 
increased  in  intensity  as  to  be  audible  to  the  patient  when  he  lies  on  his 
left  side.  There  may  be  precordial  pain,  but  usually  it  only  amounts  to 
precordial  "anxiety."  The  carotids  throb  ;  the  heart  may  beat  from  thirty 
to  one  hundred  beats  in  a  minute  ;  the  impulse  and  sounds  increase  and 
diminish  at  the  same  time  ;  the  fits  of  palj)itation  may  come  on  suddenly, 
and  be  of  short  duration,  or  they  may  come  on  gradually,  and  be  protracted 
and  severe.  Murmurs  are  usually  due  to  the  accompanying  ansemia.  Re- 
duplication of  the  second  sound  is  quite  characteristic.  Sometimes  there 
is  extreme  dyspnoea  and  headache,  vertigo  and  ringing  in  the  ears,  and 
photophobia.  The  mind  may  be  bewildered  and  the  jjatient  may  stagger, 
yet  no  paralysis  or  vertigo  exists.  The  respirations  are  irregular  or  op- 
pressed, with  dyspnoea  and  a  short,  dry  cough. 

DifiFerentialDiagnosis. — To  distinguish  between  cardiac  palpitation  inde- 
pendent of  organic  disease  of  the  heart,  and  cardiac  palpitation  depending 
upon  organic  cardiac  disease,  is  of  the  greatest  importance.  Cardiac  pal- 
pitation independent  of  cardiac  disease  comes  on  suddenly,  and  is  not  con- 
stant, whereas  organic  cardiac  palpitation  comes  on  slowly  and  is  constant. 
In  functional  palpitation,  all  the  physical  signs  of  organic  cardiac  disease 
are  absent.     Persons  free  from  organic  heart  disease  complain  more  fre- 


504  DISEASES   OF   THE    HEAET. 

quently  of  palpitation  than  those  who  are  the  subjects  of  organic  disease  ; 
palpitation  of  organic  heart  disease  is  increased  by  exercise. 

Prognosis. — In  cardiac  palpitation  independent  of  organic  heart  disease, 
the  prognosis  is  always  good  ;  although  it  may  cause  the  patient  great  un- 
easiness, it  neyer  destroys  life. 

Treatment. — In  each  case  of  cardiac  palpitation  it  is  important  to  find  out 
and,  if  possible,  remove  its  cause.  Ansemic  subjects  should  take  iron  in 
large  doses  for  a  long  period.  In  hysterical  palpitation  all  uterine  derange- 
ments must  be  relieved.  If  the  excessive  use  of  alcoholic  stimulants,  to- 
bacco, strong  tea  or  coffee,  causes  it,  they  must  be  stopped.  Occurring  in  a 
gouty  subject,  those  means  which  have  been  found  to  relieve  gouty  mani- 
festations must  be  employed.  Those  in  whom  no  special  cause  can  be 
found,  should  be  directed  to  sponge  the  surface  of  the  body  night  and 
morning  in  cold  water,  exercise  moderately  in  the  open  air,  and  live  on  a 
nutritious  diet. 

During  the  attacks,  relief  will  usually  be  obtained  by  the  administration 
of  some  of  the  more  reliable  nervines  and  diffusible  stimulants.  Narcotics 
generally  do  harm.  Digitalis  should  never  be  given  in  purely  nervous  car- 
diac palpitation.  Ether,  ammonia,  chloral  hydrate,  and  tlie  bromides  are 
occasionally  useful ;  sometimes  camphor,  assafcBtida,  musk  and  valerian  are 
serviceable  as  anti-spasmodics.  A  very  important  element  in  the  successful 
management  of  an  attack  of  nervous  cardiac  palpitation,  is  the  positive 
assurance  of  the  medical  attendant  that  there  is  ho  danger  attending  the 
paroxysm,  and  that  there  is  no  disease  of  the  heart. 

ANGINA   PECTOEIS. 

Angina  pectoris  is  a  neurosis  of  the  heart  due  to  organic  changes  in  its 
structure  or  to  diseases  involving  its  nerve  supply ;  strictly  speaking,  it  is  a 
symptom  or  a  collection  of  symptoms  of  organic  cardiac  disease.  It  has  no 
special  morbid  anatomy. 

Etiology. — There  is  no  form  of  cardiac  or  aortic  disease  with  which  angina 
pectoris  has  not  been  found  associated,  and  there  is  no  form  with  which  it 
is  invariably  or  even  generally  present.  Inherited,  nervous  or  ^^  neuralgic  " 
tendencies  predispose  to  it ;  eighty  per  cent,  of  cases  occur  after  the  fortieth 
year.  Gout,  albuminuria,  diabetes,  and  certain  hepatic  diseases  are  often 
associated  with  it.  Trousseau  dwells  on  the  relationship  between  angina 
pectoris  and  epilepsy.  There  are,  however,  two  forms  of  heart  disease  with 
which  it  is  especially  liable  to  occur  : — obstruction  to  the  coronary  circula- 
tion, and  fatty  degeneration  of  the  heart. 

The  other  diseased  states  with  which  it  is  liable  to  occur  are,  insufficiency 
of  the  aortic  valves,  with  a  rigid  dilated  state  of  the  ascending  portion  of 
the  arch  of  the  aorta,  combined  with  dilatation  of  the  left  ventricle.  When 
these  conditions  exist,  angina  pectoris  will  not  occur  unless  the  heart's 
action  is  suddenly  disturbed,  or  its  movements  impeded  by  some  mechanical 
cause. 

Symptoms. — The  symptoms  which  attend  an  attack  of  angina  pectoris  are 


AISTGIKA   PECTORIS.  505 

quite  characteristic.  The  ])atient  is  suddenly  seized  with  an  intense  ago- 
nizing pain  in  the  precordial  region  (usually  commencing  on  a  level  with  the 
xiphoid  cartilage)  extending  tlirough  the  back  and  along  the  left  arm 
This  pain  is  of  a  stabbing  or  lancinating  character  and  produces  a  sensa- 
tion of  impending  suffocation — a  feeling  as  though  death  was  near  at 
hand.  There  may  be  true  laryngeal  pain.  At  the  commencement  of 
this  pain  the  countenance  becomes  deadly  pale  and  is  expressive  of  ex- 
treme anxiety  and  suffering  ;  the  surface  is  covered  with  a  cold  perspira- 
tion, the  pulse  falters,  and  may  be  almost  imperceptible,  the  respiration  is 
short  and  hurried,  the  face  livid,  and  the  patient  is  unable  to  lie  down  or 
even  to  move,  for  the  least  motion  aggravates  his  sufferings.  His  conscious- 
ness is  undisturbed,  and  his  spinal  as  well  as  his  cerebral  functions  are  un- 
affected, but  there  may  be  slight  wandering  as  the  attack  passes  off.  Not 
infrequently  the  rhythm  of  the  heart's  action  is  undisturbed  and  the  patient 
does  not  even  experience  palpitation.  Sometimes  the  action  of  the  heart  is 
so  much  deranged  that  syncope  or  even  sudden  death  occurs.  The  pulse 
may  be  slow  and  feeble  or  markedly  irregular.  Usually  after  the  paroxysm 
has  continued  for  a  few  moments,  or  at  the  longest  an  hour,  it  gradually 
subsides.     The  attack  may  come  on  during  sleep. 

At  first,  there  are  long  intervals  between  these  attacks,  but  after  a  time 
they  become  frequent.  Between  the  attacks  the  general  health  may  be  un- 
impaired. 

DifFerential  Diagnosis. — Angina  pectoris  may  be  confounded  with  spas- 
modic asthma,  hysteria,  intercostal  neuralgia,  myalgia,  and  the  first  stage 
of  acute  pleurisy. 

Although  the  phenomena  attending  a  paroxysm  of  angina  pectoris  may 
bear  a  striking  resemblance  to  those  of  spasmodic  asthma,  a  physical  ex- 
amination of  the  chest  will  detect  the  presence  or  absence  of  the 
characteristic  physical  signs  of  the  asthma,  and  thus  lead  to  a  correct 
diagnosis. 

The  intermitting  and  irregular  character  of  the  pulse  in  angina  pectoris 
will  distinguish  it  from  an  hysterical  paroxysm. 

In  intercostal  neuralgia,  the  duration  of  the  attack,  the  points  of  tender- 
ness, the  direction  of  the  pain,  and  the  absence  of  cardiac  disturbance,  will 
distinguish  it  from  angina  pectoris. 

Myalgia  and  acute  pleurisy  may  simulate  angina  pectoris.  In  each, 
acute  pain  and  catching  breath  are  present ;  but  the  condition  of  the  circu- 
lation, taken  in  connection  with  the  locality  of  the  pain  and  the  physical 
signs  of  pleurisy,  will  generally  decide  the  question. 

Prognosis. — The  prognosis  in  angina  pectoris  is  necessarily  unfavorable. 
Sometimes  the  first  attack  proves  fatal  ;  in  more  instances  the  second  or 
third,  while  in  many  more,  perhaps  in  the  majority  of  instances,  the 
patient  at  irregular  intervals  experiences  a  succession  of  attacks,  each 
paroxysm  being  more  severe  than  the  previous  one,  until  finally,  after  a 
period  extending  from  one  to  six  or  eight  years,  an  attack  occurs  in  which 
the  heart's  action  is  arrested  and  death  ensues.  The  later  attacks  are  excited 
by  trivial  causes,  or  apparently  come  on  spontaneously.     The  tendency  of 


506  DISEASES  OF  THE  HEART. 

angina  pectoris  associated  with  organic  disease  of  the  heart  is  to  grow 
steadily  worse,  and  terminate  in  death  within  a  year. 

Treatment. — During  an  attack,  means  should  be  employed  to  alleyiate  or 
arrest  the  paroxysm  ;  during  the  interval  the  exciting  cause  should  be  re- 
moved or  its  predisposing  power  diminished.  It  is  doubtful  whether  there 
are  any  remedial  agents  that  have  the  power  to  arrest  or  very  greatly  relieve 
a  paroxysm.  Diffusible  stimulants,. sedatives,  and  anti-spasmodics  have  all 
been  employed,  but  so  far  as  my  experience  goes  they  have  no  power  to 
alleviate  or  arrest  the  paroxysm.  Kest,  and  the  free  administration  of 
digitalis,  are  of  the  greatest  service.  Chloroform  should  not  be  used.  An 
emetic  for  an  overloaded  stomach,  or  hot  foot  baths,  etc.,  when  cold  causes 
a  paroxysm,  are  often  advantageous.  Quain  and  many  others  advocate  the 
nitrite  of  amyl,  tti,  v — vi,  inhaled  from  the  handkerchief  ;  nitro-glycerine 
(1-1 00  TTl  a  dose)  is  very  useful,  and  hypodermatics  of  morphine  may  be 
given  in  conjunction  with  it. 

During  the  interval  all  violent  emotions  and  all  active  physical  exercise 
must  be  avoided.  Indigestion,  or  flatulence,  when  present,  should  be 
relieved  by  careful  attention  to  the  diet.  The  only  medicinal  remedies 
whicl^  I  have  found  of  service  in  delaying  and  I'endering  less  severe 
the  paroxysm  of  angina  pectoris  are  iron,  strychnine,  and  arsenic ;  these 
should  be  administered  daily  in  small  doses.  Phosphorus  and  zinc  are 
useful  in  "nervous  temperaments."  When  angina  pectoris  is  associated 
with  fatty  heart,  the  rules  given  for  the  management  of  the  latter  disease 
should  be  observed.  Quain  states  that  a  continuous  current,  the  +  pole 
on  the  sternum  and  the  —  pole  on  the  lower  vertebrae,  has  often  produced 
marked  amelioration  of  anginal  paroxysms.  Trousseau  strongly  advises 
belladonna  given  continuously  in  small  doses,  on  the  ground  of  the  analogy 
of  the  affection  to  epilepsy. 

HYDEOPERICAEDIFM. 

{Dropsy  of  the  Pericardium.') 

Hydropericardium  is  a  sero-albuminous  effusion  into  the  pericardial 
sac,  non-inflammatory  in  character,  and  when  absorbed  leaves  no  trace 
behind  it.  It  is  often  very  abundant  and  a  source  of  great  discomfort  to 
the  patient,  but  rarely  directly  causes  death.  The  effect  of  such  fluid 
effusions  is  to  embarrass  the  action  of  the  heart,  while  the  heart-fibre  be- 
comes pale  and  is  easily  torn,  the  result  of  the  serous  infiltration.  Six, 
seven,  or  more  ounces  of  fluid  are  usually  found,  of  a  yellow,  green,  red, 
or  red-brown  color.  Thirty-three  per  cent,  of  albumen  is  usually  present, 
and  a  small  amount  of  fibrinous  matter  that  coagulates  on  exposure  to  the 
air. 

Etiology. — l^on-inflammatory  effusions  into  the  pericardium  occur  most 
frequently  in  connection  with  renal  and  cardiac  diseases.  In  that  form  of 
renal  disease  which  complicates  scarlatina,  it  is  especially  liable  to  occur, 
and  under  such  circumstances  it  is  passive  in  character  and  is  soon  reab- 
sorbed on  the  restoration  of  the  renal  function.  When  it  occurs  in  chronic 


PNEUMOPERICARDIUM.  507 

forms  of  Bright's  disease,  it  is  more  serious  and  obstinate.  When  it  ac- 
companies chronic  cardiac  disease  it  is  the  result  of  tha  general  venous 
congestion,  and  its  pressure  greatly  embarrasses  the  already  enfeebled 
heart.  It  may  result  from  any  disease  where  there  is,  from  physical  causes, 
a  tendency  to  serous  transudation  into  the  cavities  of  the  body. 

Symptoms. — The  symptoms  and  the  physical  signs  "N^mh  attend  such 
effusions  do  not  materially  differ  from  those  already  detailed  as  marking 
the  stage  of  fluid  effusion  in  pericarditis,  except  that  there  is  entire  ab- 
sence of  any  febrile  disturbance.  There  is  no  friction  sound  present  at 
any  time  during  the  progress  of  the  effusion.  It  is  an  early  symptom 
when  due  to  heart  or  lung  disease  ;  and  occurs  late  when  due  to  splenic, 
hepatic,  or  renal  disease.  It  occurs  very  late  in  the  tuberculous  and  can- 
cerous cachexiae. 

Prognosis.  — In  chronic  Bright's  disease  and  in  advanced  cardiac  disease, 
it  is  usually  the  precursor,  although  it  can  scarcely  be  called  the  cause  of 
death.  In  other  conditions  the  prognosis  will  depend  upon  the  circum- 
stances which  attend  its  development. 

Treatment. — In  the  treatment  we  must  be  guided  by  the  peculiarities  of 
each  case.  All  the  measures  recommended  for  the  treatment  of  hydro- 
thorax  may  be  employed  in  the  treatment  of  hydropericardium.  To  find 
out  and  remove  its  cause  is  of  the  greatest  importance  ;  in  other  words, 
treat  the  diseased  condition  which  gives  rise  to,  or  permits  the  effusion. 
Only  in  scarlatinal  albuminuria  is  the  accumulation  so  sudden  that  para- 
centesis may  be  demanded. 

PNEUMOPERICAEDroM. 

Pneumopericardium,  or  air  in  the  pericardial  sac,  is  the  result  either  of 
a  perforating  wound  of  the  thorax,  or  the  perforation  of  the  pericardial 
sac  by  an  ulcerative  process  and  the  admission  of  air  from  some  organ 
naturally  containing  it — stomach,  intestine,  lung,  or  oesophagus  ;  or  to  the 
putrefaction  of  an  exudation. 

The  diagnosis  of  this  accident  rests  on  the  tympanitic  percussion  sound 
over  the  pericardial  space,  and  the  tinkling,  splashing,  or  metallic  sound 
heard  directly  over  the  heart.  With  the  exception  of  those  cases  which 
are  of  traumatic  origin,  this  accident  rapidly  proves  fatal ;  80  per  cent, 
die  in  non-traumatic  and  50  per  cent,  in  traumatic  cases.  Its  treatment  is 
altogether  symptomatic. 

H  iEMOPERIC  ARDroM. 

Hsemopericardium,'  or  blood  in  the  pericardial  sac,  may  be  of  trau- 
matic origin,  or  may  result  from  rupture  of  the  heart,  or,  far  more  fre- 
quently, the  pericardium  becomes  distended  with  blood  from  the  rupture 
of  one  of  those  small  aortic  aneurisms  which  develop  on  that  portion  of 
the  aorta  included  within  the  pericardial  sac.     Unless  of  traumatic  origin, 

1  nifimoperioardium  is  non-inflammatory.  Blood  may  fill  tlie  sac  when  inflammation  exists  ;  then  the 
name  hemorrlia;^ic  pericarditis  is  api)lied, 


508  DISEASES   OF  THE  HEART. 

it  rapidly  proves  fatal,  and  will  be  found  at  the  autopsy  of  many  cases  of 
sudden  death.  When  of  traumatic  origin,  the  effused  blood  is  not  often 
absorbed. 

SYPHILITIC    DISEASE    OF    THE    HEART. 

There  may  be  two  manifestations  of  syphilis  in  the  heart,— the  fibroid 
vatch  and  the  gummy  tumor  or  gumma. 

Morbid  Anatomy. — Pale,  yellow,  gummy  masses  are  found,  usually  inti- 
mately blended  with  the  cardiac  substance,  but  often  projecting  as  nodules 
from  its  surface.  At  first  they  are  elastic,  firm,  homogeneous,  often  very 
hard  ;  later  they  soften  and  become  cheesy.  They  may  become  fluid  and 
open  inward  and  give  rise  to  cardiac  aneurism.  As  a  rule  the  cheesy  prod- 
ucts are  absorbed  and  a  puckered,  fibrous  scar  remains  at  their  site.  Some- 
times the  gummata — which  are  nearly  always  multiple — appear  as  "  infil- 
trations "  or  "deposits."  They  may  occur  in  miy  portion  of  the  heart. 
When  the  outer  zone  of  a  gumma  undergoes  development  into  fibroid  tissue, 
the  caseous  portion  remains  as  a  compact  mass.  Bruce  regards  this  as  an 
intermediate  form  between  the  fibroid  patch  and  the  true  gumma  or 
••syphiloma."  The  myocardial  vessels  are  not  infrequently  the  seat  of 
(syphilitic)  endarteritis  obliterans,  giving  rise  to  infarctions  in  the  wall  of 
the  heart ;  and  the  pericardium  is  commonly  found  adherent. 

Etiology. — Fibroid  patches  and  gummata  arise  both  from  congenital  and 
acquired  syphilis. 

Symptoms. — Symptoms  of  cerebral  or  visceral  syphilis  may  and  often  do 
mask  those  of  the  cardiac  affection.  Should  the  puckered  fibroid  tissue  nar- 
row or  distort  any  part  of  the  heart,  or  involve  the  valves  to  such  an  extent 
as  to  cause  obstruction  or  allow  of  regurgitation,  then  a  murmur — differing 
in  no  respect  from  other  murmurs — will  be  the  chief  symptom.  Syncope, 
infrequent  pulse,  palpitation,  dyspncea,  choking,  and  many  other  symptoms 
of  heart  disease  have  occurred  in  the  few  recorded  cases  of  syphilis  of  the 
heart. 

The  diagnosis  rests  mainly  on  the  exclusion  of  all  other  forms  of  heart 
disease,  and  the  evidences  of  syphilis,  hereditary  or  acquired,  in  the  indi- 
vidaal 

The  prognosis  would  be  more  favorable  than,  probably,  with  any  other 
similar  condition,  on  account  of  its  amenability  to  treatment,  which,  of 
course,  is  purely  anti-syphilitic. 

Basedow's  disease. 

{Exophthalmic  Goitre,) 

Basedow's  or  Graves'  disease  is  an  affection  in  which  there  is  enlargement 
and  hyperemia  of  the  thyroid  body,  protrusion  of  the  eyeballs,  cardiac  pal- 
pitation and  anaemia.     It  is  closely  allied  to  functional  cardiac  diseases. 

Morbid  Anatomy.— It  is  attended  by  no  constant  morbid  lesions.  The 
enlargement  of  the  thyroid  body  is  due  to  a  dilatation  of  its  vessels.  The 
protrusion  of  the  eyeball  is  caused  by  dilatation  of  the  vessels  behind  the 


BASEDOW'S    DISEASE.  509 

globe  ;  both  of  these  changes  appear  simultaneously  with  derangement  of 
the  circulation,  and  cardiac  palpitation.  There  are  many  circumstances 
which  render  it  probable  that  the  enlargement  of  the  vessels  is  due  to  some 
vasa-motor  disturbance  which  allows  of  their  passive  dilatation  in  the  neck, 
the  thyroid  body,  and  the  orbit ;  at  the  same  time  it  causes  an  excited 
action  of  the  heart.  The  thyroid  body  may  be  filled  with  cysts  or  be  the 
seat  of  hyperplasia.  Atheroma  of  the  ophthalmic  arteries  has  been 
found. 

Etiology. — It  rarely  occurs  in  males.  It  is  met  with  in  women  between 
twenty  and  thirty  years  of  age.  A  "  neuropathic  tendency "  is  usually 
strongly  marked.  Menstrual  derangements  attended  by  violent  mental 
emotions  of  various  kinds  often  precede  its  development. 

Symptoms. — This  disease  may  come  on  suddenly  or  slowly  ;  if  it  develops 
slowly,  the  patient  will  at  times  for  a  long  period  complain  of  severe  attacks 
of  cardiac  palpitation,  and  pulsation  in  the  arteries,  gradually  these  attacks 
of  palpitation  will  become  more  frequent  and  severe,  the  eyes  will  become 
slightly  prominent  and  staring,  and  after  a  time  they  may  become  so  promi- 
nent that  the  lids  will  not  cover  them.  Occasionally  the  insertion  of  the 
recti  muscles  can  be  seen.  The  protrusion  is  often  greatly  increased  under 
excitement.  The  attacks  of  cardiac  palpitation  grow  more  severe,  the  thyroid 
gland  visibly  enlarges,  and  the  eyes  become  lustrous  and  projecting.'  On 
casting  the  eye  down,  the  eyelids  follow  but  slowly; — this  gives  a  peculiar 
look  to  the  patient.  Vision  is  not  usually  disturbed,  but  there  may  be 
slight  loss  of  co-ordination.  In  proportion  as  the  eyes  bulge  the  eye- 
lashes and  eyebrows  fall  out.  Diplopia,  traceable  to  paresis  of  the  right 
trochlearis  has  been  noted.  Profuse  lachrymation  is  not  uncommon. 
Exophthalmus  is  often  more  marked  on  one  side  than  the  other,  and  is 
then  apt  to  be  attended  by  enlargement  of  the  thyroid  body  on  the  opposite 
side. 

The  thyroid  gland  usually  enlarges  slowly ;  the  patient's  attention  is  first 
attracted  to  it  on  account  of  a  continued  pulsation  of  the  lower  part  of  the 
neck.  It  is  usually  unequally  enlarged,  is  soft,  elastic,  and  at  first  pul- 
sates, due  to  the  dilatation  of  the  vessels  in  the  gland  ;  after  a  time  there 
is  increase  of  tissue,  and  blowing  sounds  are  audible  over  the  enlargement. 
There  may  be  a  change  in  the  pitch  of  the  voice,  perhaps  from  pressure  of 
the  enlarged  gland  on  the  recurrent  laryngeal  nerve.  Sometimes  the  voice 
is  hoarse  or  entirely  lost.  There  is  always  danger  from  pressure  of  the  en- 
larged thyroid  gland  upon  the  trachea.  The  cardiac  palpitations  are  rapid 
and  irregular,  the  pulse-rate  varying  from  one  hundred  to  one  hundred  and 
forty  per  minute.  The  heart-sounds  are  loud,  and  a  soft,  systolic  bellows- 
murmur  may  be  heard  at  the  base  and  in  the  large  arteries.  There  may 
be  a  distinct  thrill.  The  carotids  may  be  dilated.  The  circulation  is  rapid, 
the  veins  filling  rapidly,  and  the  pulsation  of  the  small  arteries  is  felt  by 
the  patient.  Mental  emotion  and  violent  physical  exertion  bring  on  attacks 
of  palpitation,  which  may  be  so  violent  as  to  produce  a  visible  enlarge- 

J  Eulenberg  regards  increased  development  of  fat  in' the  cellular  tissue  of  the  orbit,  as,  in  part,  the 
c^use  of  the  bulging  cf  the  eyeballs. 


510  DISEASES    OF   THE   HEART. 

ment  of  the  precordia  with  every  heat.  Stimulation  of  the  accelerator 
nerves  of  the  heart  probably  causes  the  palpitation.' 

Debility,  anaemia,  indigestion,  anorexia,  and  diarrhoea  may  be  present 
during  the  whole  course  of  the  disease.  Insomnia,  amenorrhoea,  and  hys- 
terical symptoms  are  very  frequently  observed  in  nervous  females.  In  a 
few  instances  the  temperature  is  often  elevated  to  103°  F.,  and  followed  by 
profuse  sweats. 

LifFerential  Diagnosis. — When  the  three  classical  symptoms  are  present  in 
a  female,  viz.,  bulging  of  the  eyeballs,  cardiac  palpitation,  and  enlargement 
of  the  thyroid,  a  mistake  in  the  diagnosis  will  scarcely  occur.  Von  Graefe 
makes  a  diagnosis  on  the  "  want  of  harmony  between  the  movement  of  the 
eye  and  its  lid." 

Cystic  goitre  is  not  accompanied  by  exophthalmus,  nor  by  paroxysmal 
enlargements.  The  thyroid  in  Basedow's  is  far  more  elastic  than  in  cystic 
goitre. 

The  lustrous  appearance  of  the  eye  suffices  to  diagnosticate  it  from  prom- 
inence due  to  heart  disease  {e.  g.,  hypertrophy),  which  latter  would  give  evi- 
dence of  organic  changes. 

Local  orbital  or  cranial  causes  of  exophthalmus  are  excluded  by  the 
absence  of  squint  and  other  cerebral  symptoms. 

Prognosis. — This  must  always  be  guarded.  It  may  increase  for  months, 
remain  stationary  for  a  year  or  two,  and  then  gradually  decline  but  not 
wholly  disappear.  In  some  instances  its  course  has  been  acute  and  rapid. 
Recovery  occurs  in  from  four  to  five  per  cent,  of  cases.  G-reat  im- 
provement has  occurred  in  from  thirty  to  forty-five  per  cent,  of  cases. 
It  does  not  directly  cause  death,  but  intercurrent  affections  are  gen- 
erally ill-borne  and  fatal.  Any  heart-disease  (organic),  great  anaemia,  or 
evidence  of  the  ' '  neuropathic  disposition, "  renders  the  prognosis  unfavora- 
ble. Pregnancy  is  said  to  have  a  favorable  influence.^  Death  may  occur 
from  valvular  disease  of  the  heart,  pulmonary  tuberculosis,  gangrene  of  the 
extremities,  pulmonary  apoplexy,  or  oedema. 

Treatment. — The  first  remedies  proposed  in  the  treatment  of  this  affection 
were  quinine  and  iron,  and  their  use  is  still  followed  by  the  best  results. 
Traube  gives  them  alternately,  five  grains  of  quinine  one  day,  and  ten  grains 
of  iron,  in  the  form  of  Vallett's  mass,  the  following  day.  Arsenic  does 
harm.  Iodine  is  condemned  by  some  and  recommended  by  others.  It  has 
been  claimed  that  belladonna,  hydrocyanic  acid,  and  ergot  tranquillize  the 
heart.  Galvanization  of  the  cervical  sympathetic  diminishes  the  exoph- 
thalmus and  lowers  the  pulse-rate  : — it  is  to-day  the  favorite  plan  of  treat- 
ment with  many.  Hydropathic  treatment  is  highly  praised  by  some  French 
authorities.  My  own  experience  has  shown  that  a  prolonged  residence  in 
a  high  elevation  (Colorado)  seems  to  arrest  its  progress,  and  in  one  instance 
led  to  apparent  recovery. 

1  Friedrich'g  ingenious  theory  is  that,  the  vaso-motor  nerves  being  paralyzed,  dilatation  of  the  coronary 
artery  follows,  and  hence  there  is  increased  excitement  in  the  ganglia  of  the  heart. 

2  Trousseau  and  Corlies. 


CHRONIC    ENDARTERITIS,  511 

DISEASES  OF  THE  BLOOD-VESSELS. 

Under  this  head  will  be  considered  the  following  diseases  of  the  arteries 
and  veins. 

DISEASES  OF  THE  ARTERIES. 

I.  Acute  Endarteritis.  V.   Syphilis  of  Arteries. 

IL   Chronic   Endarteritis,  or  "Ather-  VL  Atrophy,  Hypertropay 

oma.'"  Dilatation,  Narrowing. 

III.  Periarteritis. 

IV.  Degenerations :   Fatty,  Waxy,  and  Calcareous. 

DISEASES  OF  THE  VEINS. 

I.  Acute  and  Chronic  Phlebitis.  II.  Dilatation  of  the  Veins. 

Emtolism  and  Thrombosis. 

ACUTE   EISTDAETERITIS. 

Acute  endarteritis  is  an  inflammation  of  the  tunica  intima,  which  is 
formed  of  endothelium  lying  on  longitudinally  arranged  elastic  tissue.  As 
an  isolated  lesion  it  is  rare. 

Morbid  Anatomy. — Along  some  vessel,  chiefly  the  aorta,  numerous  ele- 
vated round  patches  are  seen  projecting  from  the  internal  layer.  They  are 
red,  opalescent,  soft,  and  elastic  {"  gelatinous  patches  of  the  aorta  ").  The 
elevated  patches  are  made  up  of  embryonic  cells  arranged  in  parallel  lines. 
These  patches  may  undergo  ulceration.  Fibrin  may  form  on  their  surface 
and  inclose  either  the  white  blood  corpuscles  or  the  proliferated  and  free 
elements  of  the  diseased  surface.  Pus  formations  and  gangrene  may  result. 
The  middle  coat  is  not  extensively  involved,  but  a  periarteritis  nearly  al- 
ways occurs.  The  whole  vessel  becomes  friable.  Emboli  form,  and  coagu- 
lation may  result  in  arterial  thrombosis. 

Etiology. — Wounds,  emboli,  extension  of  inflammation  from  without,  and 
irritation  from  a  hard  vegetation  may  cause  it.  Acute  aortitis  is  usually  of 
rheumatic  origin.  A  purulent  aortitis  is  described  by  some  as  occurring  in 
septic  conditions. 

Symptoms. — There  are  no  special  symptoms  by  which  it  can  be  distin- 
guished. When  coagula  are  formed  thrombi  result,  and  then  the  symptoms 
will  be  those  of  thrombosis  complicated  by  pyaemia. 

CHEOlSriC    ENDAETEEITIS. 

A  theroma,  or  endarteritis  deformans,  is  a  common  disease. 

Morbid  Anatomy.— It  is  an  inflammation  of  the  internal  coat,  with  thick- 
ening in  patches,  the  thickening  being  due  to  multiplication  of  the  cellu- 
lar elements  ;— granular  fatty  degeneration  of  these  elements  and  of  the 
middle  coat  follows,  and  a  yellow  atheromatous  focus  is  produced,  separated 


512 


DISEASES    OF    THE    BLOOD-VESSELS. 


from  the  blood  current  by  a  thin  tense  pellicle.  As  the  atheromatous 
changes  take  place,  the  centre  of  the  patch  contains  a  putty-like  mass 
of  cholesterin  crystals,  fat  granules,  and  crystals  of  fatty  acid.      When 

there  is  little  or  no  fatty 
change  in  the  patches,  the 
process  is  called  "sclero- 
sis," and  they  are  then 
stained  dark  brown.  When 
these  processes  progress 
slowly,  calcareous  granules 
infiltrate  the  tunica  intima, 
and,  later,  form  thin,  fria- 
ble calcareous  plates  just 
underneath  an  internal  pel- 
licle. The  vessels  above 
the  heart  in  the  thorax  are 
most  frequently  affected  ; 
they  become  enlarged,  ir- 
regular, and  friable.  When 
the  stiffened  internal  coat 
breaks,  chinks  are  formed 
^'«-  ^0^-  which  fill  with  blood  and 

M     .^  ^Chronic  Endarteritis  :Atherom^^^  later  bccome  melanotic.  In 

Magnified  View  of  a  Small  Artery,  partly  diagrammatic.  •  t  ti 

A.  Endotheliu7nofariery,ceUsturnedinward.—B.  Intima  thrmvn  ^"^^    aorta  the   middle    COat 
into  folds  by  C,  the  elastic  lamina. — D.  Muscular  coat  {tunica  often    disannears     COnnCCt- 

ive-tissue  taking  its  place  ; 
destruction  of  the  middle 
coat  is  the  only  cause  of 
spontaneous  aneurism  of 
the  aorta.  The  external  coat  finally  assumes  the  histological  characters  of 
the  altered  internal  coat.  After  the  aorta,  the  cerebral,  coronary,  and 
splenic  vessels  and  those  of  the  lower  extremity  may  become  involved.  In 
the  small  vessels,  narrowing  and  stenosis  are  the  results  of  chronic  arteritis. 
Cardiac  hypertrophy  is  a  common  result  of  the  rigidity  and  inelasticity  of 
the  aorta  and  its  branches. 

Etiology. — Atheroma  or  arterial  sclerosis  is  a  disease  of  advanced  life. 
Men  are  far  oftener  affected  than  women.  It  is  predisposed  to  by  gout, 
rheumatism,  syphilis,  Bright's  disease,  lead  poisoning,  and  especially  by 
alcoholismus.  Over-strain  of  the  vessel  is  often  its  immediate  cause.  It 
is  said  sometimes  to  be  an  extension  from  the  endocardium  into  the 
aorta. 

Symptoms. — Nearly  all  its  symptoms  are  the  mechanical  results  of  rigidity 
of  the  artery.  The  left  ventricle  is  hypertrophied.  The  peripheral  arteries 
are  enlarged,  lengthened,  and  tortuous,  and  an  irregular  outline  is  readily 
felt  along  their  course.  The  pulse  is  feeble,  sometimes  imperceptible ; 
the  sphygmograph  shows  a  short  up-stroke  and  a  flat  summit  (pulsus  tar- 
dus).    The  extremities  are  cold  and  parts  may  become  gangrenous  (senile 


media).— E.  Adventitia. 

F.  Swollen  and  proliferating  intima. 

G.  Irregular  spaces  containing  calcareous,  granular,  and  fatty  mat 
ter. 

H.  Elastic  lamina,  limiting  the  degenerative  process. 
I.  Lumen  of  tlie  vessel  encroached  upon  one  side  only. 


PEEIARTERITIS.  513 

gangrene).  Apoplexy  may  occur,  and  some  ascribe  epilepsy  and  senile  de- 
mentia to  atheromatous  arteries.  The  different  organs  atrophy,  the  skin 
becomes  dry,  and  the  lungs  are  frequently  emphysematous.  Dissecting 
aneurisms  may  be  induced  after  a  rupture  of  an  atheromatous  abscess  ; 
persistent  anasarca  of  the  legs  in  old  men  is  often  due  to  calcified 
arteries. 

Diiferential  Diagnosis. — Aortitis  sometimes  gives  rise  to  symptoms  that 
can  establish  a  diagnosis.  These  are  acute  substernal  pain  with  oppres- 
sion, palpitation,  quick  and  feeble  pulse.  "With  these  symptoms  may  be 
associated  a  hard  systolic  murmur,  originating  at  the  seat  of  inflam- 
mation, and  transmitted  to  a  distant  point  of  the  aorta.  Paroxysms  of 
pain  like  angina  pectoris  are  sometimes  marked. 

Prognosis. — It  is  a  condition  which  cannot  be  cured. 

Its  treatment  is  altogether  hygienic. 

PERIAETEKITIS. 

In  periarteritis  the  adrentitia  and  very  soon  the  surrounding  cellular  tis- 
sue are  hypersemic,  swollen  and  infiltrated  with  cells.  The  external  coat 
becomes  homogeneous  and  gelatinous.  The  process  terminates  either  in 
connective-tissue  or  pus  formation.  In  purulent  infiltration  of  the  exter- 
nal coat  the  intima  is  not  affected  ;  but  should  the  middle  coat  become 
involved  pus  may  open  into  the  blood  current  and  an  aneurism  is  liable  to 
be  formed. 

Etiology. — Periarteritis  occurs  from  wounds,  extension  of  inflammation 
from  adjacent  parts,  or  during  the  course  of  pyaemia.'  Periarteritis  is  the 
first  step  in  the  formation  of  those  miliary  aneurisms  occurring  in  the 
cerebral  vessels,  and  which  are  always  found  preceding  cerebral  hemor- 
rhages. 

Fatty  degeneration,  apart  from  atheroma,  is  rare.  It  occurs  chiefly  in 
the  aorta.  In  the  internal  coat  the  fat  granules  occur  in  flat  layers,  and 
in  the  middle  coat  they  are  found  between  the  flbres,  and  when  very 
abundant  the  muscular  elements  cannot  be  distinguished.  Sometimes  the 
endothelium  alone  is  involved,  and  it  may  desquamate,  laying  bare  the 
tunica  intima.     This  is  said  to  accompany  erysipelas  and  relapsing  fever. 

Calcification  of  the  arteries,  independent  of  atheroma,  is  even  rarer  than 
fatty  degeneration. 

Amyloid  degeneration  occurs  in  the  small  arteries,  especially  in  the  renal 
glomeruli,  but  also  in  those  of  the  spleen,  liver,  intestines  and  lymph  glands. 
Its  causes,  gross  and  microscopical  appearances,  tests,  etc.,  are  fully  dis- 
cussed under  chronic  Bright's  disease. 

Cancer  only  attacks  the  adventitia. 

Tuberculous  granules  often  stud  the  external  coat  of  the  small  arteries. 

Syphilitic  Ai^ea^Q  of  the  arteries  chiefly  attacks  the  cerebral  vessels.  G-reat. 
thickening  and  nodose  swellings  are  due  to  gummatous  material  infiltrating 

'  Kusfmaul  and  Maier  describe  a  periarteritis  nodosa  wliich  is  usually  fatal,  and  Gull  and  Sutton  have: 
called  the  hyaline  fibroid  appearance  of  the  external  coat  of  the  arterioles  arterio-ccqnllary  fibrosis. 

33 


514  DISEASES    OF   THE   BLOOD-VESSELS. 

the  outer  coats.  The  walls  are  opaque  and  the  lumen  is  considerably 
diminished.  Later,  cellular  growths  occur  in  the  internal  coat.  Throm- 
bosis and  cerebral  softening  are  often  the  result.  This  neoplastic  formation 
has  been  called  arterioma.  When  such  a  condition  is  suspected,  mercury 
and  iodide  of  potash  are  to  be  given. 

General  dilatation  of  arteries  may  be  due  to  atony  or  paralysis  of  their 
muscular  coat,  or  to  atheroma  or  degeneration  of  their  walls.  The  aorta 
and  the  pulmonary  arteries  are  those  most  frequently  involved.  Sometimes 
the  aorta  and  its  branches  are  the  seat  of  congenital  uniform  stenosis.  This 
occurs  in  females  chiefly,  and  is  associated  with  other  malformations.  The 
■  symptoms  are  a  small  pulse,  frequent  palpitation,  cold  extremities,  tendency 
to  syncope,  and  menorrhagia.  Gastric  ulcers  are  common.  The  aorta  may 
be  contracted  and  nearly  obliterated  at  its  junction  with  the  ductus 
arteriosus. 

PHLEBITIS. 

Phlebitis  may  be  acute  or  chronic. 

Morbid  Anatomy. — In  acute  phlebitis  the  adventitia  maybe  first  involved 
and  the  inflammation  extend  inward,  a  clot  forming  in  the  calibre  of  the  vein; 
or  the  inflammation  may  commence  within,  in  connection  with  surrounding 
inflammation  and  extend  outward.  If  there  is  extensive  connective-tissue 
infiltration  around  the  vein,  adhesive  obliteration  of  the  vein  I'esults ; 
should  the  clot  soften  and  disintegrate,  pus  formations  result.  The 
presence  of  a  clot  may  be  regarded  as  an  essential  accompaniment  of  all 
forms  of  phlebitis,  except  the  adhesive  or  chronic. 

In  cJironic  plilehitis  the  external  coats  of  the  veins  are  very  much  thick- 
ened, while  the  intima  may  be  normal.  The  connective-tissue  around  the 
vein  is  greatly  increased,  there  is  hypertrophy  of  its  muscular  tissue,  and  the 
vasa  vasorum  are  very  much  dilated.  In  rare  cases  thickening,  fatty 
<iegeneration,  and  calcification  (''^atheroma")  of  the  innermost  venous 
coats  are  found.  In  these  cases  the  outer  layers  will  almost  invariably  ex- 
hibit ''sclerotic"  changes.     This  has  been  called  "chronic  endophlehitis." 

Etiology. — The  commonest  cause  of  phlebitis  is  the  formation  of  a 
thrombus.  Periphlebitis  may  be  induced  by  wounds,  ulcers,  abscesses, 
chronic  visceral  disease,  phlegmonous  erysipelas,  separation  of  the  placenta, 
osteo-myelitis,  amputation,  ligation  of  veins,  pyaemia  and  septicgemia,  cel- 
lulitis from  any  cause,  and,  according  to  some,  by  varicosity  or  permanent 
dilatation. 

Symptoms. — If  the  vein  is  within  reach  of  observation,  it  will  be  found 
hard,  swollen,  and  tender  ;  prominences  occur  at  the  sites  of  the  valves, 
pains  dart  along  its  course,  and  the  limb  may  become  stiff.  When  super- 
ficial, the  veins  can  be  felt,  and  the  skin  over  them  is  livid  red.  When 
deep  main  trunks  are  involved  the  limb  is  swollen,  and  the  skin  pale,  tense, 
and  shining  over  it.'  Abscesses  in  the  course  of  the  vessel,  which  may  or 
may  not  communicate  with  its  interior,  are  of  common  occurrence.  Should 

1  See  phlegmasia  alba  dolens  in  works  on  Obstetrics. 


VARIX. — THROMBOSIS.  515 

the  tissues  become  oedematous  and  should  constitutional  hectic  or 
pyaemic  symptoms  supervene,  suppurative  phlebitis  (peri-phlebitis)  may 
be  suspected. 

Gouty  phlebitis  occurs  in  those  with  hereditary  gouty  tendencies ;  the 
skin  over  a  vein  becomes  dusky  or  livid  red,  the  vein  is  hard,  and  the  limb 
is  somewhat  oedematous.  All  the  symptoms  may  suddenly  disappear, 
quickly  to  reappear  in  some  distant  part  (metastatic  iDhlebitis).  Varicose 
veins  in  the  gouty  are  especially  liable  to  these  manifestations,  although 
loss  of  tone  and  local  erythema  are  more  to  be  blamed  than  gout  for  these 
venous  inflammations. 

Differential  Diagnosis. — Phlebitis  is  distinguished  from  lymphangitis  by 
the  fact  that  in  the  latter  the  glands  are  tender  and  enlarged  from  the  out- 
set ;  and  bright  red  streaks  are  very  numerous. 

In  erysipelas,  redness  is  in  the  form  of  a  general  blush ; — in  phlebitis 
there  is  only  a  dusky  red  localized  streak. 

Prognosis. — This  is  bad  only  in  the  suppurative  variety. 

Treatment. — Absolute  Best,  splints  to  confine  and  render  the  affected 
limb  immovable,  and  hot  fomentations  over  the  parts  are  the  first  indica- 
tions. Abscesses  should  be  opened  early,  and  when  oedema  occurs  the  parts 
must  be  bandaged. 

VAEIX. 

Varix  or  dilatation  of  the  veins  occurs  most  in  obstructive  diseases  of  the 
right  heart.  In  a  few  cases  the  veins  become  dilated  and  varicose  without 
any  obstruction,  the  cause  of  the  dilatation  under  such  circumstances  being 
very  obscure. 

Morbid  Anatomy. — When  veins  dilate  they  elongate  ;  the  dilatation  is 
most  marked  immediately  above  the  valves  and  the  affected  vein  assumes 
an  irregular  outline.  The  walls  are  thickened  from  hypertrophy  of  their 
middle  coat  at  some  points,  and  dilated  at  others.  Dilatation  may  take 
place  in  the  largest,  the  smallest,  or  in  the  medium  sized  veins;  calcareous 
plates  not  infrequently  form  in  their  walls,  and  phlebolites  and  venous 
calculi  often  develop  in  the  pouch-like  protrusions  in  the  veins,  where  the 
circulation  is  slowed.  Local  or  general  obstruction  and  a  varicose  condi- 
tion of  the  veins  serve  primarily  as  important  aids  in  diagnosis  and  rarely 
require  medical  treatment.     They  are  mainly  surgical  disorders. 

THEOMBOSIS. 

Thromlosis  is  coagulation  of  the  blood  in  the  heart,  or  blood-vessels,  dur- 
ing life.  The  clot  or  coagulum  is  called  a  tliromhus,  and  is  most  com- 
monly met  with  in  the  veins.  Parietal  thrombi  are  those  clinging  to  the 
wall  of  a  vessel  and  not  completely  obstructing  the  flow.  Occluding 
thrombi  are  those  absolutely  obstructing  the  flow. 

Morbid  Anatomy, — In  rapidly  formed  thrombi  a  considerable  number  of 
red  blood  discs  are  entrapped  and  the  color  is  first  dark  red  ;   in  such  clots 


616 


DISEASES   OF   THE   BLOOD-VESSELS. 


the  fibrin  at  once  completely  fills  the  vessel,  and  the  thrombosis  is  uniform 

or  non-laminated.  These  are  the  usual  charac- 
teristics of  obliterating  thrombi.  In  slowly  formed 
thrombi  fewer  red  blood  discs  are  entangled, 
hence  the  color  is  lighter,  sometimes,  indeed, 
the  clot  is  absolutely  colorless.  The  structure 
is  laminated  or  stratified;  and  the  mass  adher- 
ing to  the  wall  of  the  vessel  does  not  wholly  ob- 
struct the  current,  or  at  least  in  its  early  stages. 
These  primitive  thrombi  usually  extend  along 
the  vessel  to  a  branch  whose  blood  current  is 
sufficiently  strong  to  arrest  their  progress.  The 
projecting  conical  end  of  the  coagulum  becom- 
ing softened,  small  pieces  may  be  detached  and 
thus  enter  the  circulation. 

A  thrombus  may  organize  or  undergo  shrink- 
ing, softening,  or  suppuration. 

Organization    occurs     oftenest    in     uniform 

magram  showing  the  manner  of  de-  thrombi  situated  in  arteries.     The  leucocytes  in 

iachment  of  small  iwrtions  oj  a  J 

venms  thrombus  A,  by  the  blood  the  clot  or  thosc  from  the  vasa  vasorum  develoT* 

current  of  a  small  venous  branch,  .  -■ 

£.    0,  Detached  portions  of  co-  ncw  connectivc-tissuc,  and  vessels  permeate  the 
.    new  structure  in  whose  meshes  lies  the  d6bris  of 
the  clot.     Progressive  dilatation  of  the  new  vessels  ultimately  renders  the 
original  channel  pervious: — "canalization  of  the  throtnbus.'"  * 

Instead  of  organization  a  thrombus  may  soften.  Stratified  thrombi 
usually  soften.  Molecular  disintegration  commences  at  the  centre  of  the 
clot,  which  will  be  found  filled  with  a  purulent-looking  milky  or  pulpy 
material,  containing  albuminous  granules,  molecular  fat,  granular  detritus, 
and  changed  red  and  white  corpuscles.  This  is  not  suppuration  of  the 
thrombus,  nor  should  it  be  called  puriform  softening.  Large  cardiac 
thrombi  suifering  these  changes  resemble  cysts.  Those  thrombi  that  break 
down  into  granular  matter  containing  bacteria  and  pus  cells,  are  specific 
or  infectious  thrombi  {vide  Pyaemia).  A  non-infectious  thrombus,  after 
softening,  may  be  wholly  absorbed  ;  or,  as  central  softening  occurs,  fibrin  is 
deposited  upon  the  periphery.  Pus  may  enter  such  a  thrombus  from  without. 

Supiniration  is  occasionally  seen  in  the  thrombi  of  veins  surrounded  by, 
or  leading  from,  inflamed  parts  ;  a  multiplication  of  leucocytes  takes  place 
in  the  thrombus  either  by  proliferation  or  immigration,  and  the  whole 
softens  down  into  a  purulent  fluid.  In  these  cases  the  wall  of  the  vein  itself 
is  always  inflamed.  These  softened  and  broken  down  thrombi  are  a  common 
cause  of  embolism.  When  the  middle  coat  of  the  vein  is  involved  and  in- 
tensely inflamed,  true  suppuration  of  the  coats  may  occur,  and  thus  throm- 
bosis may  be  a  cause  of  abscess  of  the  external  coats  of  a  vein.  It  is  impor- 
tant to  distinguish  between  thrombi  and  post-mortem  coagula  : — the  latter 


1  Cornil  and  Ranvier  assert  that  there  is  merely  an  outgrowth  of  vascular  granulations  from  the  tunica 
intima,  that  penetrate  the  thrombus  ;— and  that  the  latter  gradually  disnppears  without  taking  part  in  the 
formation  of  the  reticulated  tissue  which  occupies  its  place  ("  obliterating  endarteritis  ").   - 


embolism:.  517 

are  soft,  divisible  into  two  layers — a  colored  and  an  uncolored — are  never 
laminated,  their  texture  is  looser,  they  never  entirely  fill  the  vessel,  and  they 
do  not  adhere  to  its  wall.  Heart  clots  that  form  during  the  death  agony 
are,  in  color  and  consistence,  midway  between  the  two  just  mentioned. 
They  are  entangled  with  the  columnae  carnese  and  chordae  tendineae,  but 
can  be  separated  with  a  little  care. 

Etiology. — Any  abnormality  of  the  vessels,  but  especially  of  the  tunica 
intima,  will  induce  the  formation  of  a  thrombus  (atheroma,  phlebitis,  endar- 
teritis, etc.,  etc.).  Any  neoplasm  in  a  vessel  may  cause  it.  Wounds,  blows, 
ligation,  dilatation  of  the  vessels  or  of  the  heart,  and  anything  that  will 
diminish  heart  power,  or  induce  slowing  of  the  Mood  current,  will  induce 
thrombosis.  Hence  we  find  it  occurring  in  phthisis,  cancer,  old  age,  etc., 
etc.  The  veins  of  the  pelvis  and  lower  limbs,  and  in  children  the  cerebral 
sinuses  are  the  favorite  seats  of  these  "  mar  antic  ^^  thrombi. 

Compression  thrombosis  results  from  slowing  of  the  current  from  mechan- 
ical causes  outside  the  wall.  In  the  heart  thrombosis  may  be  caused  by 
endocarditis.  Lymphatic  thrombosis  has  chiefly  been  observed  in  the  puer- 
peral condition.  In  leucocythaemia  the  capillary  circulation  being  inter- 
fered with  from  the  vast  number  of  white  corpuscles,  clots  readily  form  in 
the  veins.  Finally,  venous  thrombi  are  especially  liable  to  form  in  the  jjockets 
of  the  valves. 

Symptoms. — The  symptoms  depend  upon  the  extent  of  the  obstruction  to 
the  circulation  and  the  size  and  situation  of  the  vessel : — for  instance^ 
when  the  femoral  vein  is  plugged,  phlegmasia  alba  dolens  results.  Throm- 
bosis of  the  cerebral  vessels  gives  rise  to  special  cerebral  manifestations. ' 
Thrombosis  of  the  portal  vein  is  followed  by  the  grave  symptoms  of  py- 
lephlebitis. Moist  gangrene,  ascites,  hydrothorax,  oedema  and  cyanosis  of 
the  face  and  neck,  hemorrhage  from  stomach,  intestine  or  kidney — each 
may  be  a  consequence  of  the  plugging  of  the  main  vein  issuing  from  the 
part.  The  special  danger  of  venous  thrombosis  is  the  possible  detachment 
of  a  portion  of  the  thrombus,  its  transportation  by  the  circulation  to  the 
heart,  and  its  arrest  there  or  in  one  of  the  branches  of  the  pulmonary  ar- 
tery (embolism).  The  result  of  arterial  thrombi  is  ansemia  of  the  part  sup- 
plied, necrosis,  or  hemorrhagic  infarction. 

EMBOLISM. 

An  emholus  is  any  plug  in  a  vessel  which  has  previously  had  another 
site  or  has  been  moving  in  the  circulation.  Thus  it  is  seen  that  arteri- 
oles and  capillaries  are  the  usual  seats  of  emboli,  since  in  these  vessels  the 
current  is  toward  ever-diminishing  branches.  In  general  an  embolus 
is  part  or  all  of  a  dislodged  thrombus  ;  for  ex'ample  :  a  clot  in  the  femoral 
vein  (milk-leg)  crumbles  ;  particles  are  swept  into  the  ascending  cava, 
then  through  the  right  heart  into  the  pulmonary  artery,  and  some  of  the 
latter's  branches  having  a  calibre  smaller  than  the  diameter  of  the  par- 
ticles they  will  be  plugged. 

1  See  Brain  :  Art.  Embolism. 


518 


DISEASES   OF  THE   BLOOD-YESSELS. 


Morbid  Anatomy.— When  small  arteries  are  plugged  the  anastomoses 
may  prevent  any  visible  lesion  from  occurring, 
When  a  vessel  of  any  size  is  plugged,  the  first  re. 
suit  is  anaemia  of  the  district  supplied  by  the 
branches  of  the  blocked  vessel.  Then  there  is 
backward  pressure  and  regurgitation  of  blood  from 
the  veins,  through  the  capillaries  into  the  arteri- 
oles, whose  vitality  is  impaired  because  of  this  venous 
substitution.  Exudation  and  ultimate  necrosis  of 
vascular  walls  are  followed  by  hemorrhage,  and  the 
blood  coagulates  forming  a  hemorrhagic  infarc- 
tion. When  an  embolus  causes  anaemia  and  ne- 
crosis without  hemorrhage,  it  produces  what  is 
cq\\q6l  Sb  white  or  a ^^(em^c  infarction.  The  primary 
and  essential  change  in  a  white  infarction  is  coagu- 
lation-necrosis. The  shape  of  an  infarct  is  conical 
Diagram  showino:  the  establish-  bccausc  of  the  tree-like   branching  of  the  arteries 

inent  of   circulation  by  anas-  .  «     , 

tomotic  vessels  after  an  Em-  and  Capillaries  bcyond   the    Site  of  the  embolus; 
.   „  , "       ,     .         „  ,     and  it  is  usually  situated  with  its  base  toward  the 

A,  Embolus  plugging  small  Ar-  ,   •' 

J^ry.  surface   and  its  apex   toward   the    centre   of   the 

B,  Anastomotic  branch  supply-  ,t  •/»i--i»;- 

ing  blood  to  the  area  c.  Organ.      In  non-iniectivc  infarctions  the  mass  be- 

comes decolorized,  changing  from  dark  red  to  dirty 
yellow,  and  then  to  white.  At  the  same  time  it  shrinks  and  finally  may 
leave  a  depressed  fibrous  patch  or  cicatrix.  In  larger  masses  molecular 
disintegration  and  softening  first  occur  and  a  pulpy  granular  puriform 
fluid  forms,  which  becomes  enclosed  in  a  fibrous  capsule,  and  finally  be- 
comes cheesy  or  calcareous.  In  both  cases  there  is  a  circumscribing  zone 
of 


Fig.  111. 


congested  vessels. 


When  a  vessel  is  plugged,  wholly  or  partly,  and  the  vessel  is  a  terminal 
artery,  hemorrhage  does  not  necessarily  occur,  and  there  occurs  a  white  or 
anaemic  infarction,  which  is  to  be  distinguished  from  a  decolorized  hemor- 
rhagic infarction  by  microscopical  examination.  Some  emboli  are  always 
followed  by  necrosis,  others  by  hemorrhage.  In  the  brain  anaemic  softening 
without  hemorrhage  is  common.  Necrcsis  may  rapidly  ensue  after  embol- 
ism (gangrene),  or  it  may  come  on  slowly  as  a  withering  or  softening.  The 
vessel  wall  at  the  site  of  the  embolus  undergoes  changes  similar  to  those 
described  as  resulting  from  thrombi.     If  an  embolus  does  not  completely 

1  Cohnheim  states  that  in  order  to  produce  hemorrhagic  infarction  the  artery  must  be  a  terminal  artery, 
t.  e.,  giving  off  no  anastomotic  branches  before  its  final  capillary  distribution,  and  the  veins  must 
not  have  valves,  and  that  these  conditions  are  met  with  in  the  spleen,  kidney,  brain,  certain  branches  of 
the  pulmonary  artery,  and  the  central  artery  of  the  retina.  Litten  has  opposed  these  views,  and  states 
that  in  genuine  terminal  arteries  hemorrhagic  infarction  does  not  occur,  and  that  infarction  may  take 
place  afte?^  ligature  of  the  vein.  Hence  venous  reflux  cannot  be  its  cause.  Prom  his  experiments  it 
would  seem  that  congestion  and  infarction  following  embolism  are  due  to  afflux  of  arterial  blood  into 
the  territory  from  collateral  channels  ;  his  views  more  nearly  correspond  to  Virchow's  original  theory. 
— Zeitschriftfiir  Klinische  Medicin,  vol.  i. 

2  The  changes  that  occur  in  infective  or  specific  emboli  are  described  under  P3'£emia.  Cornil  and  Ran- 
vier  regard  the  decolorization  which  marks  the  white  infarct  as  the  result  of  fatty  degeneration  of  the  pa- 
renchymatous cell  elements  of  the  organ  involved.  The  connective-tissue  about  them  is  infiltrated  with 
white  blood  discs.  But  Litten  regards  white  infarctions  as  due  to  coagulation-necrosis  of  the  proto 
plasm  of  the  cells,  having  a  remarkable  tendency  to  calcification. 


THORACIC   ANEURISM,  519 

fill  a  vessel  a  secondary  thrombus  forms,  by  deposition  of  fibrin,  and  this 
extends  till  a  strong  current  of  blood  arrests  its  progress.  Emboli  coming 
from  venous  thrombi  usually  induce  pulmonary  infarction  ;  emboli  from 
the  left  heart,  arterial  aneurisms,  arterial  neoplasms,  etc.,  produce  infarc- 
tions in  spleen,  kidneys  and  brain,  as  a  rule. 

When  emboli  produce  death  of  part  of  an  organ  without  true  gangrene, 
Virchow  gives  the  name  necrobiosis.  An  embolic  abscess  is  the  same  as 
a  pysemic  abscess.  The  influence  of  embolism  in  the  production  of 
aneurism  is  to-day  recognized,  even  when  the  particle  that  plugs  the  vessel 
is  not  a  sharp  calcareous  or  atheromatous  mass. 

THOKACIC    AIS'EUEISM. 

An  aneurism  is  a  more  or  less  abrupt  dilatation  of  the  calibre  of  an  ar- 
tery ;  the  tumor  thus  formed  must  communicate  with  the  channel  of  the 
vessel.  Thoracic  aneurism  includes  all  those  tumors  which  arise  from  the 
aorta  and  its  branches  within  the  thorax,  or  from  the  pulmonary  artery. 

Morbid  Anatomy. — The  convexity  of  the  ascending  portion  of  the  arch 
of  the  aorta  is  the  most  frequent  seat  of  the  aneurismal  development,  next 
the  transverse  portion  of  the  arch  ;  next  the  descending  portion  of  the 
arch,  and  least  frequent  of  all  the  descending  aorta.  Aneurisms  of  that 
portion  of  the  aorta  which  is  embraced  by  the  pericardium  are  of  small  size 
and  are  apt  to  pass  unrecognized. '  The  junction  of  the  ascending  and  trans- 
verse portions  of  the  arch  at  the  sinus  magnum  is  a  favorite  seat  of  aneu- 
rism, it  being  nearly  at  right  angles  to  the  blood-stream  from  the  heart.  ^ 

The  only  logical  clinical  classification  of  aneurisms  is  based  on  their 
shape. 

The  whole  surface  of  the  artery  may  be  dilated,  and  the  aneurismal  tu- 
mor be  cylindrical,  fusiform  or  globular  in  shape. 

There  may  be  a  lateral  bulging  or  sacculation  of  a  portion  of  the  circum- 
ference of  the  artery  : — a  sacculated  aneurism.  In  both  of  these  classes  the 
arterial  coats  may  be  all  intact,  or  any  one  or  two  of  them  may  be  absent 
or  diseased. 

When  the  walls  of  an  aneurism  are  made  up  of  the  surrounding  tissue, 
it  is  called  a  consecutive  diffuse  aneurism  ;  and  when  blood  finds  its  way 
between  the  coats  of  an  artery,  it  is  called  a  dissecting  aneurism. 

The  post-mortem  appearances  of  aneurism  will  vary  with  its  location, 
size  and  variety.  In  some  cases  nothing  abnormal  will  be  found  except  an 
unruptured  aneurismal  tumor  ;  in  others  the  tumor  will  be  found  ruptured, 
the  pericardium  filled  with  blood,  or  extravasated  blood  will  be  found  either 
in  the  bronchi,  trachea,  stomach,  or  pleural  cavity,  or  an  external  rupture 
may  have  been  the  immediate  cause  of  death.  Aneurisms  arising  fi-om  one 
of  the  sinuses  of  Valsalva,  within  the  range  ci  the  valves,  rarely  attain  a  size 
larger  than  that  of  a  small  billiard-ball.   They  are  sacculated  and  not  infre- 

>  Of  703  cases  of  Sibson's  (Medical  Anatomy),  87  were  within  the  pericardium,  i.  e.,  about  12  per  cent. 

2  Anatomically,  aneurisms  are  divided  into  irve  and  false.  True  aneurisms  are  those  in  which  all  the 
coats  of  tlic;  artery  are  found  in  the  walls  of  the  aneurismal  sac.  False  aneurisms  are  those  in  which  a  rup- 
ture of  one  or  more  coats  of  the  artery  has  occurred. 


520  DISEASES    OF   THE    BLOOD-VESSELS. 

quently  pedunculated,  communicating  with  the  aorta  by  a  small  orifice. 
The  J  further  exhibit  a  remarkable  tendency  to  descend  in  the  progress  of 
growth,  involving  in  their  course  the  heart  or  the  root  of  the  pulmonary 
artery.  By  their  position  they  are  sheltered  from  direct  influx  from  the 
ventricle,  whilst  they  are  exposed  to  the  maximum  force  of  reflux  from  the 
aorta.  When,  however,  the  orifice  is  partially  or  entirely  above  the  level 
of  the  valves,  the  main  pressure  sustained  by  the  sac  is  that  during  influx 
from  the  ventricle ;  hence  the  direction  of  growth  is  upward. 

Aneurisms  near  the  sinus  magnum  produce  erosion  of  the  ribs  and  their 
cartilages,  the  sternum  and  the  right  clavicle  : — sections  of  the  bones  show 
the  lesions  of  osteitis.  The  adjacent  muscular  and  connective-tissue  is  ex- 
tensively infiltrated.  The  descending  cava  and  the  left  innominate  vein 
may  be  so  compressed  as  to  have  their  channel  completely  closed.  The  left 
recuiTcnt  laryngeal,  the  left  sympathetic,  or  the  trunk  of  the  vagus  may 
be  compressed,  atrophied,  or  entirely  destroyed.  The  thoracic  duct  may 
be  compressed  and  ruptured  into.  Should  aneurisms  about  the  arch  enlarge 
backward,  the  trachea,  oesophagus,  and  right  lung  will  suffer  from  the 
pressure. 

In  aneurism  of  the  descending  arch,  or  thoracic  aorta,  the  spinal  extrem- 
ity  of  the  ribs  and  the  bodies  of  the  vertebrae  in  the  dorsal  region  may  be 
destroyed,  and  the  left  bronchus  may  be  obliterated,  causing  consolidation 
of  the  entire  lung.  The  dorsal  spinal  nerves  and  sympathetic  trunk  may 
be  destroyed  by  pressure.  All  the  secondary  changes  in  thoracic  aneurism 
are  "pressure  effects,"  and  they  are  never  alike  in  any  two  cases. 

The  aneurismal  sac  also  varies  greatly  in  the  appearance  it  presents  at 
the  autopsy.  All  the  tunics  of  the  artery  may  be  preserved  ;  but  in  large 
aneurisms  while  the  external  and  internal  coats  can  be  traced  all  over  the 
tumor,  the  middle  coat  ceases  abruptly  where  the  sac  opens  into  the  artery. 

When  an  aneurism  begins  with  rupture  or  dis- 
ease of  the  inner  coat  of  the  artery,  a  lining 
membrane  of  new  formation  meets  and  coalesces 
with  the  intima,  so  that  the  appearance  is  the 
same  as  if  no  rupture  or  change  had  occurred. 
The  aneurismal  walls  may  undergo  fatty  or  cal- 
careous degeneration.  The  contents  vary  with 
the  size  and  shape  of  the  sac  and  with  the  rapid- 
ity with  which  it  has  formed.  The  sac  may  be 
nearly  filled  with  concentric  layers  of  firm  lami- 
^^'^-  ■'^^-  nated  fibrin  containing  small  calcareous  plates  ; 

Diagram  illustrating  the  anatomy  .,  ,  ,.    ,,        „,,     -,         ^,^      ^  i 

of  spontaneous  Arterial  Aneurism.   Or   it    may    DC    partially    filled    With    lOOSCr  layCrS 

A.  Internal    coat    of    Artery;  of  fibrin  inclosing  recent  coaarula.      Sometimes 

B.  Middle  coat  of  same  ;  C.  Ex-  °_.^^,P 

ternaicoat.  ircsh  coagula  and  fluid   blood  are  alone  round. 

D  and  E.  External  and  internal  rm  i-  j^    n-i     •  in  •  i 

coats  of  the  aneurismal  tianoj-  ihose  lammse  01  nbrm  nearest  the  aneurismal 

showing  the  absence  of  the  middle         ■,-,  i.i       ji  j. 

arterial  coat.  Wall  are  the  firmest. 

Etiology. — The  chief  predisposing  cause  of 
aneurism  is  disease  of  the  arterial  walls,  the  most  common  of  which  are 
chronic  endarteritis  and  atheroma.     Age  and  occupation  may  also  be  re- 


THORACIC    ANEURISM.  521 

garded  as  predisposing  causes,  the  period  between  forty  and  fifty  being 
the  favorite  period  of  its  development.  It  is  a  question  whether  aneurisms 
occurring  in  middle  life  are  the  result  of  senile  changes  or  violent  physical 
exertion.  Atheroma  and  calcareous  degenerations  are  commonest  after 
sixty;  hence  muscular  effort  probably  has  much  to  do  in  developing  the 
more  frequent  aneurisms  in  those  who  are  younger,  although  it  is  doubtless 
aided  by  commencing  degeneration  of  the  arterial  wall.  Mechanics,  por- 
ters, soldiers,  and  those  liable  to  sudden  and  violent  physical  exertion  are  fre- 
quent subjects  of  aneurism  ;  the  irregularity  and  violence  of  the  action  is  to 
be  considered,  rather  than  its  severity.  Habits  of  life,  intemperance  m  eating 
and  drinking,  chronic  alcoholismus  and  tight  fitting  garments  (uniforms) 
predispose  to  aneurismal  developments.  The  majority  of  these  who  de- 
velop aneurism  before  forty-five  will  give  a  syphilitic  history ;  hence  syjah- 
ilis  must  be  ranked  as  a  predisposing  cause.  Chronic  Bright's,  rheuma- 
tism, gout,  lead  and  mercurial  poisoning  are  included  in  the  predisposing 
causes  to  arterial  diseases,  and  consequently  to  aneurism.  In  aortic  insuf- 
ficiency the  hypertrophied  left  ventricle  throws  a  larger  column  of  blood 
with  abnormal  force  against  aortic  walls ;  chronic  aortitis  results  and  an 
aneurism  may  follow. 

The  exciting  causes  are  blows,  falls  from  heights,  wounds,  excess  or  pro- 
longed venereal  excitement,  and  sudden  violent  strains,  exerted  on  a  de- 
generated artery. 

Symptoms. — The  early  rational  symptoms  of  thoracic  aneurism  vary  with 
the  site  of  the  tumor.  If  the  aneurism  is  near  the  sinuses  of  Valsalva,  it 
will  give  rise  to  no  symptoms  until  rupture  discloses  its  existence.  If  a 
second  murmur  is  heard  over  the  pulmonary  artery  it  may  be  caused  by  dis- 
placement of  the  valve,  or  diminution  in  the  calibre  of  the  pulmonary 
artery  from  pressure  of  an  aneurismal  tumor,  and  if  it  is  accompanied  by 
venous  stasis  and  congestion  of  the  upper  half  of  the  body,  an  aneurism 
may  be  suspected.  "With  all  aneurisms  within  the  pericardium  there  will  be 
some  hypertrophy  of  the  left  ventricle.  The  development  of  an  aneurism 
near  the  sinus  magnum  is  usually  accompanied  by  very  positive  symptoms. 
The  patient  often  states  that  after  some  violent  effort,  some  blow,  or  during 
an  excess  of  some  kind,  "  he  felt  something  suddenly  give  way,"  and  then 
followed  a  '^boring  "  pain  near  the  sternum  with  dyspnoea,  palpitation,  and 
perhaps  haemoptysis. 

As  a  rule  there  are  no  subjective  signs  of  thoracic  aneurism  until  the 
tumor  presses  on  the  adjacent  parts.  By  the  direction  of  the  pressure  the 
seat  of  the  tumor  may  be  determined.  Aneurism  of  the  ascending  arch 
usually  presses  forward,  upward,  and  to  the  right ; — of  the  transverse 
arch,  backward  and  upward  ;  and  of  the  descending  portion  of  the  arch, 
backward  and  to  the  left.  In  whatever  direction  an  aneurism  presses,  pain 
is  its  first  symptom.  The  pressure  may  be  exerted  upon  (1)  the  nerves ; 
(2)  the  bloodvessels ;  (3)  the  trachea,  oesophagus,  the  large  bronchi,  the  lung- 
tissue,  the  thoracic  duct,  and,  indirectly  on  the  heart. 

The  pain  when  present  is  constant.  It  is  increased  by  acceleration  of  the 
circulation,  and  is  localized  in  the  region  of  the  tumor ;  usually  it  is  asso- 


522  DISEASES    OF   THE   BLOOD-VESSELS. 

ciated  with  a  sense  of  constriction.  The  pressure  pain  may  be  neuralgic, 
paroxysmal  and  wandering.  It  radiates  to  the  neck  and  shoulder  and 
may  shoot  down  either  arm.  If  the  intercostal  nerves  are  pressed  on,  there 
will  be  attacks  of  excruciating  intercostal  neuralgia.  If  erosion  of  verte- 
brae, sternum,  or  ribs  occurs,  there  is  a  peculiar,  constant  "  boring  "  pain. 
When  one  or  both  vagi  or  recurrent  laryngeal  nerves  are  pressed  on,  spasms 
and  partial  or  complete  paralysis  of  the  laryngeal  muscles  cause  dyspnoea 
and  voice-changes  ;  the  voice  becoming  husky.  Sometimes  there  is  com- 
plete aphonia.  Violent  paroxysms  of  dyspnoea  are  liable  to  occur,  attended 
by  a  congested,  anxious  countenance,  and  violent  respiration  followed  by  ex- 
haustion. Cases  are  recorded  where  vomiting  and  pjrrosis  resulted  from 
pressure  on  the  pneumogastric.  Pressure  on  the  pulmonary  plexus  gives 
rise  to  a  harsh  metallic  '^ brassy"  cougli.  Pressure  on  the  vagus  may  be 
followed  by  congestion  of  the  lungs,  oedema  and  gangrene.  An  inequality 
of  the  pupils  may  come  from  irritation  or  pressure  on  the  cervical  sympa- 
thetic :  irritation  causes  dilatation  of  the  pupil ;  and  pressure  (when  annul- 
ling the  function)  causes  its  contraction  on  the  affected  side.  Disordered 
vision  may  thus  become  a  symptom  of  thoracic  aneurism. 

When  Mood-vessels  are  compressed  only  the  main  trunks  of  one  side  are 
involved,  hence  a  delayed,  even  a  suppressed  radial  pulse  will  be  found 
only  on  that  side.  In  a  few  cases  I  have  found  no  pulsation  in  either  carotid 
or  subclavian  on  the  affected  side.  Then  cerebral  anaemia  and  signs  of  im- 
paired nutrition  in  the  limb  on  that  side  were  present.  The  effect  of  im- 
peded venous  return  may  lead  to  a  diagnosis  of  the  seat  of  an  aneurism. 
When  an  aneurism  near  the  sinus  magnum  enlarges  forward,  the  upper 
half  of  the  body  shows  congestion  and  oedema  ;  there  is  headache,  drowsi- 
ness and  other  cerebral  symptoms,  and  the  eyeballs  protrude.  Aneurism 
of  the  innominata  or  of  the  right  common  carotid  in  the  thorax,  presses 
on  the  external  jugular,  and  hence  the  right  side  of  the  head  and  neck  is 
turgid.  Such  a  condition  on  the  left  means  aneurism  of  the  left  common 
carotid. 

When  tracheal  symptoms  are  urgent,  they  point  to  aneurism  of  the 
transverse  portion  of  the  arch  enlarging  backward.  The  flattening  of  the 
trachea  induces  difficult  breathing,  then  follows  a  stridulous  cough  (with 
no  expectoration),  having  a  metallic  ring,  like  a  ^'nervous  cough."  Such 
compression  may  result  from  an  accumulation  of  mucus  which  cannot  be 
expectorated  ;  hence,  dyspnoea  arises.  The  pressure  may  even  produce 
gangrenous  patches,  which  lead  to  rupture  and  fatal  hemorrhage.  It  is 
readily  seen  why  congestion  of  the  lungs  and  pneumonia  sometimes  fol- 
low compression  of  the  trachea.  The  signs  of  pressure  on  a  large  tronclius 
are,  principally,  a  metallic  cough,  with  tenacious  mucous  sputa,  at  times 
blood-streaked,  and,  possibly,  evidences  of  pneumonia  and  gangrene. 
Pleurisy  may  be  excited  by  a  tumor's  pressure,  and  it  is  always  an  important 
sign  taken  in  connection  with  signs  of  pressure  upon  the  trachea  and  bron- 
chus. 

Dysphagia  may  be  induced,  but  the  oesophagus  is  rarely  ruptured  into 
by  an  aneurism.     Dyspepsia,  reflex  in  origin,  may  be  a  symptom  of  thoracic 


THORACIC   ANEURISM.  533 

aneurism.  The  lower  third  of  the  oesophagus  is  said  to  be  widely  dilated  in 
some  cases  of  this  kind.  Enlargement  of  the  lymphatics  below  the  sac 
results  from  pressure  of  an  aneurism  on  the  thoracic  duct.  Symptoms  of 
mal-assimilation,  wasting  and.  inanition  would  also  be  present  in  such  cases. 

All  these  symptoms  are  never  present  together  in  any  one  case,  but  when 
three  or  four  of  the  prominent  ones  exist,  they  are  strong  evidence  of 
thoracic  aneurism. 

Physical  Signs. — Inspection. — If  the  aneurism  press  on  the  cava  descen- 
dens,  the  face,  neck  and  upper  extremity  will  be  swollen,  livid,  or  oedem- 
atous,  the  veins  being  turgid  and  varicose.  Sometimes  there  is  a  thick, 
fleshy  collar  around  the  lower  part  of  the  neck,  due  to  capillary  turges- 
cence.  Bulging  is  seen  at  some  spot  on  the  chest,  probably  along  the 
course  of  the  aorta,  and  this  may  be  as  large  as  a  cocoanut,  or,  again,  may 
be  perceptible  only  after  careful  inspection.  Non-existence  of  a  tumor 
does  not,  however,  disprove  the  existence  of  an  aneurism  ;  aneurismal  tu- 
mors deeply  seated  will  not  produce  bulging.  AVhen  the  visible  tumor  is 
large  it  is  generally  conical.  The  skin  over  it  is  smooth,  tense  and  shining. 
Inspection  may  reveal  pulsation  in  it,  which  is  synchronous  with  the  car- 
diac systole,  and  when  this  bulging  occurs  on  the  anterior  surface  of  the 
chest  there  seem  to  be  two  beats  within  the  thorax  at  the  same  time. 
Pulsations  are,  at  times,  only  detected  by  bringing  the  eye  to  a  level  with, 
and  looking  across  the  chest.  Aneurisms  of  the  ascending  arch  usually 
enlarge  first  to  the  right  of  the  sternum  near  the  second  costal  cartilage, 
but  if  it  is  very  large  it  may  extend  into  hoth  the  mammary  and  infra- 
clavicular region.  Aneurisms  of  the  transverse  arch  protrude  above  the 
sternum,  those  of  the  descending  arch  to  its  left.  In  the  latter  case  a 
visible  tumor  is  uncommon.  Aneurisms  of  the  descending  aorta  enlarge 
to  the  left,  rarely  to  the  right,  of  the  spine.  They  may  sometimes  give 
rise  to  violent  pulsations  near  the  heart  and  simulate  extensive  cardiac  hy- 
pertrophy. 

Palpation  discovers  more  accurately  the  size  and  the  condition  of  the 
walls  of  the  aneurism.  The  pulsation  imparted  to  the  hand  is  like  that 
of  a  blow  from  the  centre  outward  in  all  directions,  dilating  or  expansile  ; 
there  may  be  a  diastolic  pulsation  as  well  as  systolic.  The  impulse  is  some- 
times perceptible  only  when  one  hand  is  pressed  over  the  sternum  and  the 
other  over  the  interscapular  space.  When  the  transverse  arch  is  involved 
the  aneurismal  thrill  may  be  communicated  to  the  hand  by  pressing  the 
fingers  down  behind  the  sternum.  Palliation  should  be  employed  to  de- 
tect lung  changes,  fremitus,  expansion,  etc.,  etc.;  it  is  noteworthy  that  con- 
solidation of  lung  substance  induced  by  thoracic  aneurism  is  characterized 
by  absence  of  vocal  fremitus. 

Percussion  elicits  circumscribed  dulness  at  some  point  along  the  line  of 
the  aorta,  corresponding  to  the  seat  and  size  of  the  aneurism.  A  resistance, 
peculiar  to  aneurism,  and  increased  by  the  force  of  the  percussion -blow, 
will  be  noticed  over  all  large  aneurisms.  Consolidation  of  adjacent  lung- 
tissue  may  increase  the  area  of  dulness. 

Auscultation. — The  heart  sounds  accompanied  by  "  murmurs"  peculiar 


524  DISEASES    OF   THE    BLOOD-VESSELS. 

to  aneurism  may  at  times  be  audible  over  the  seat  of  the  tumor,  or  both  heart 
sounds  may  be  replaced  by  murmurs,  the  character  of  which  varies.  They 
may  be  sawing,  rasping,  or  grating.  A  diastolic  murmur  is  rarer  than  a 
systolic,  and  is' usually  softer.  With  aneurisms  near  the  sinus,  the  murmur 
is  booming  or  splashing,  and  is  accompanied  by  a  thrill  not  transmitted  in 
any  direction.  When  a  large  bronchus  is  compressed,  the  respiratory  mur- 
mur is  weak  or  suppressed  on  one  side  and  exaggerated  on  the  other. 
There  is  loss  of  vocal  resonance  over  the  aneurism  and  over  the  side  on 
which  the  bronchus  is  compressed. 

Differential  Diagnosis. — It  is  always  of  the  first  importance  to  determine 
at  what  point  in  the  course  of  the  aorta  an  aneurism  is  developed. 

An  aneurism  near  the  sinuses  of  Valsalva  may  be  mistaken  for  aortic  in- 
sufficiency. The  latter  is  distinguished  by  the  previous  history,  absence  of 
arterial  degeneration,  transmission  of  the  murmur  to  the  xiphoid  cartilage, 
absence  of  a  murmur  over  the  pulmonary  artery,  and  the  existence  of  left 
ventricular  hypertrophy  and  dilatation.  Should  the  sinus  of  the  right 
auricle  be  pressed  on,  loth  cavae  will  be  obstructed  and  the  liver  will  show 
evidences  of  congestion. 

The  diagnosis  between  aneurism  of  the  arch  of  the  aorta  and  of  the  in- 
nominate artery  is  difficult.  In  the  latter  the  tumor  appears  earlier  in  the 
neck,  and  on  the  right  side  at  the  sternal  end  of  the  clavicle  ;  while  aneu- 
risms of  the  arch  are  usually  limited  to  the  second  right  intercostal  space,  or 
appear  at  the  manubrium  sterni  or  in  the  episternal  notch,  frequently  ex- 
tending to  the  left  of  the  median  line.  Pressure  on  the  right  subclavian 
or  common  carotid  does  not  lessen  the  pulsation  in  aneurism  of  the  arch  ; 
while  if  the  innominate  alone  is  involved,  the  impulse  will  be  markedly 
diminished.  Impaired  venous  return  and  neuralgic  pains  are  confined  to 
the  right  side  in  innominate  aneurism,  while  the  venous  congestion  is 
bilateral  and  pain  is  on  both  sides  in  aneurisms  of  the  arch.  The  hruit  of  an 
innominate  aneurism  is  less  intense  than  that  of  an  aortic.  The  radial 
pulse  is  seldom  altered  in  aortic  aneurism,  while  a  suppressed  radial  pulse 
on  the  right  side  is  a  common  and  important  sign  of  aneurism  of  the  in- 
nominate. The  larynx  and  trachea  are  often  pushed  to  the  left  by  an  in- 
nominate aneurism  ;  rarely  by  an  aortic. 

Cancer  of  the  pleura,  mediastinal  tumors,  iony  exostoses,  pulsating  em- 
pyema, abscesses  between  oesophagus  and  trachea,  laryngeal  disease,  in- 
tercostal neuralgia,  angina  pectoris,  consolidation  of  the  lung  near  the  apex, 
and  hydropericardium, — all  may  be  mistaken  for  a  thoracic  aneurism. 

In  cancer  of  the  pleura  the  personal  and  hereditary  history  is  impor- 
tant. The  pain  in  cancer  is  constant ;  in  aneurism  it  is  wandering,  and 
shifts  with  change  in  direction  of  the  tumor.  Anything  increasing 
heart  action  increases  the  pain  of  an  aneurism  ;  this  is  not  so  in  cancer. 
The  pulsation  is  dilating  in  aneurism  ;  heaving  and  lifting  in  cancer. 
A  harsh  double  Iruit  is  present  in  aneurism ;  while  if  one  is  present  in 
cancer  it  is  soft  and  blowing.  In  aneurism  the  centre  of  dulness  and  the 
point  of  maximum  dulness  coincide  ;  this  is  not  the  case  in  cancer. 
Enlarged  veins  and  glands  (axilla,  neck,  etc.)  accompany  cancer ;  they  are 


THORACIC   ANEUEISM.  525 

not  present  in  aneurism.  In  aneurism  there  is  a  subjective  sense  of 
throbbing,  never  present  in  cancer.  Infiltrated  cancer  of  the  lung  induces 
retraction  of  the  chest-walls,  and  is  not  likely  to  be  confounded  with  tho- 
racic aneurism. 

Localized  empyema  which  pulsates  must  occupy  the  cardiac  area  and  push 
the  heart  to  the  right,  and  it  has  no  murmur.  Besides,  the  peculiar 
wandering  pain  of  aneurism  is  absent  in  empyema,  and  in  this  condition 
the  pulse  is  not  altered.  Irregular  diurnal  fever,  chills,  and  sweatings 
occur  in  empyema,  never  in  aneurism.  The  exploring  needle  will  settle 
the  question. 

An  abscess  between  the  trachea  and  oesophagus  is  attended  by  no  hruit, 
no  pulsation  of  an  expansile  character,  no  shifting  pain,  no  pulse-difference. 
Deep-seated  fluctuation,  chills,  fever,  and  sweats  accompany  it,  however. 

An  exostosis  below  the  sterno-clavicular  articulation  may  pulsate,  but 
the  pulsation  is  lifting,  not  expansile,  and  there  is  no  bruit. 

Laryngeal  disease  may  be  recognized  by  the  vocal  changes.  A  physical 
examination  of  the  chest,  and  the  laryngoscope  will  enable  one  to  make  a 
correct  diagnosis. 

Tn  intercostal  neuralgia,  the  three  diagnostic  points  of  tenderness,  i.  e., 
at  the  exit  of  the  nerve  from  the  spme,  midway  between  this  and  the 
sternum,  and  at  the  edge  of  the  sternum  where  the  terminal  branches  be- 
come superficial,  will  decide  between  it  and  aneurism. 

Angina  pectoris  may  occur  with  thoracic  aneurism.  But  in  all  such  cases 
valvular  disease  or  degeneration  of  the  heart- walls  will  be  found  to  co-exist. 
Hence  the  diagnosis  rests  on  the  signs  of  a  tumor  in  the  one  case,  and  the 
symptoms  of  structural  heart-disease  in  the  other. 

Pulmonary  consolidation  at  one  apex,  with  a  murmur  in  the  subclavian 
or  pulmonary  artery,  will  be  attended  by  the  signs  of  phthisis  and  not  by 
those  of  a  tumor.  Fluid  in  the  pericardium  gives  a  triangular  outline  of 
dulness  never  met  with  in  aneurism. 

Prognosis. — Although  cases  of  thoracic  aneurism  have  apparently  recov- 
ered, the  rule  is  that  they  terminate  fatally.  The  average  duration  is  about 
two  and  one-half  years  : — some  terminate  in  a  few  months,  others  live  five 
or  six  years.  There  is  always  a  liability  to  sudden  death.  The  better  the 
general  health  and  the  smaller  the  swelling,  the  better  the  prognosis.  The 
prognosis  in  aneurism  of  the  ascending  arch  is  better  than  in  any  other 
form  of  thoracic  aneurism.  Death  may  occur  from  jaressure  on  important 
organs,  or  from  rupture  of  the  sac. 

The  sac  may  open  into  one  of  the  serous  cavities  from  sloughing,  erosion 
or  laceration  of  its  wall ;  or  it  may  open  externally,  or  into  a  mucous  canal. ' 
When  the  sac  bursts  into  the  pericardium  or  j)leura,  it  ruptures  at  the 
thinnest  part ;  if  into  the  oesophagus,  trachea,  or  a  bronchus,  it  breaks  at 
some  point  of  adhesion  between  the  two,  which  has  subsequently  become 
thinned.  External  openings  are  produced  by  gradual  atrophy  from  press- 
ure, or  by  sloughing  of  the  skin  over  the  tumor.     Pneumonia,  pleurisy, 

'  In  twenty-six  ruptures,  ten  were  into  the  pericardium,  Ave  into  the  left  lung  or  pleura,  four  into  the  tra- 
chea, three  into  the  right  lung  or  pleura,  three  into  the  left  bronchus  or  oesophagus,  one  extei-nally. 


526  DISEASES    OF   THE   BLOOD-VESSELS. 

bronchitis  and  gangrene  may  occur  as  complications  to  cause  death.  Press- 
ure  on  nerves,  lymphatics  or  ducts  may  induce  death  from  exhaustion. 
Emboli  may  arise  and  become  a  cause  of  death. 

Treatment. — The  treatment  of  thoracic  aneurism  is  divided  into  those 
measures  which  come  strictly  within  the  province  of  the  physician,  and  the 
more  recent  Gurgical  procedures.  In  both,  absolute  rest  is  one  of  the  essen- 
tials. Anything  that  accelerates  or  increases  the  force  of  the  heart's  action 
will  do  harm,  in  accordance  with  the  simple  physical  law  that  every  abnor- 
mal dilating  force  applied  to  the  walls  of  an  aneurismal  sac  must  favor  its 
growth  and  hasten  the  fatal  issue.  Blood  rich  in  nutritive  elements  more 
readily  deposits  its  fibrin,  thus  favoring  that  formation  of  laminated  layers 
of  fibrin  within  the  aneurismal  sac  which  is  the  first  step  in  the  curative 
process.  Fluids  must  be  taken  in  minimum  quantities.  Mr.  Tuf nell  re- 
stricts the  food  taken  to  two  ounces  of  bread  and  butter,  and  two  ounces  of 
milk  for  breakfast ;  two  or  three  ounces  of  bread  with  two  or  three  ounces 
of  meat  for  dinner,  with  two  to  four  ounces  of  milk  or  claret  wine  ;  and 
two  ounces  of  bread  and  butter  and  milk  for  supper.  Mr.  Tufnell  says 
that  this  dietetic  treatment,  combined  with  absolute  rest  in  a  recumbent 
position  for  two  or  three  months,  resulted  in  cure  in  a  large  percentage  of 
cases.  These  statements  have  not  been  sustained  by  the  experience  of 
American  observers.  While  this  treatment  has  arrested  the  progress  of  an 
aneurism  in  quite  a  number  of  cases,  I  have  never  yet  seen  a  cure  effected ; 
and  in  almost  every  instance,  just  as  soon  as  the  patient  began  to  show  evi- 
dences of  anaemia,  which  are  certain  to  appear  after  six  or  eight  weeks,  the 
aneurismal  tumor  rapidly  increased  in  size,  and  the  cases  advanced  quickly 
to  a  fatal  issue.  I  very  much  question  if  the  absolute  restriction  of  diet 
and  movement  prescribed  by  this  plan  is  necessary  or  serviceable. 

Various  internal  remedies  have  been  used  to  favor  the  formation  of  a 
coagulum  within  the  aneurismal  sac,  either  by  increasing  the  coagulating 
power  of  the  blood,  or  by  acting  in  some  specific  manner  upon  the  walls  of 
the  aneurism  itself  or  upon  the  adjacent  arterial  walls.  The  principal 
drugs  used  for  this  purpose  are  ergot,  iodide  of  potassium,  acetate  of  lead, 
and  the  vegetable  astringents.  Iodide  of  potassium  and  ergot  are  the  only 
ones  that  have  stood  the  test  of  experience.  Both  are  used  at  the  present 
time,  and  seem  to  have  power  in  staying  the  growth  of  aneurisms  and  re- 
lieving painful  phenomena. 

The  only  remedy  to  be  relied  on  for  relief  of  the  excruciating  pain  attend- 
ing aneurismal  development  is  the  hypodermic  use  of  morphine.  It  not 
only  relieves  pain,  but  by  its  quieting  and  regulating  influence  on  the  heart 
it  delays  the  growth  of  the  aneurism.  It  also  diminishes  restlessness  and 
impatience,  and  enables  persons  who  are  naturally  irritable  to  obtain  the 
necessary  rest  which  is  so  important  a  factor  in  any  plan  of  treatment.  The 
external  application  of  belladonna  to  the  aneurismal  tumor  will  often  aft'ord 
temporary  relief  to  the  local  pain.  The  continued  application  of  an  ice- 
bag  to  an  external  aneurismal  tumor  will  often  afford  temporary  relief  of 
the  pain  and  reduce  the  tegumentary  inflammation  ;  its  use  should  not  be 
continued  too  long.     When  a  patient  with  aneurism  has  an  undue  fulness 


ABDOMINAL    ANEURISM.  527 

of  the  vessels,  free  purgation  with  salines  will  be  attended  by  marked  relief 
for  a  time. 

Surgical  Treatment  of  Thoracic  Aneurism. — Thoracic  aneurism  seldom 
presents  features  which  justify  surgical  measures.  The  methods  employed 
are  ligation  of  one  or  more  of  the  great  vessels  in  the  neck,  galvano- 
puncture,  the  injection  of  coagulating  substances  into  the  sac,  and  the  in- 
troduction of  solid  bodies  with  the  object  of  starting  consolidation.  The 
two  latter  methods  have  only  been  employed  in  a  few  desperate  cases,  and 
death  has  always  followed  so  rapidly  that  no  deductions  can  be  made.  On 
theoretical  grounds  it  is  improbable  that  either  method  could  do  good, 
except  in  cases  of  pouched  aneurism.  Experience  shows  injection  of  coag- 
ulating fluids  to  be  very  dangerous,  usually  inducing  suppuration  of  the 
sac.  The  permanent  introduction  of  wire,  horse-hair,  and  catgut  has  never 
been  followed  by  good  results ;  but  in  at  least  one  case  of  (ileo-femoral) 
aneurism  no  harm  resulted.  The  temporary  introduction  of  several  acu- 
puncture needles  and  their  retention  from  one  to  two  days  has  been  tried 
with  good  results  in  a  few  cases  ;  it  is  less  dangerous  than  the  other  methods 
mentioned.  Gralvano-puncture  has  been  employed  by  Ciniselli  in  twenty- 
three  cases,  with  five  cures.  The  same  method  has  been  tried  by  other 
surgeons,  but  the  clot  is  liable  to  break  down  and  cause  inflammation  of  the 
sac.  This  plan  has  been  adopted  when  rupture  of  the  sac  was  impending, 
to  delay  for  a  time  the  fatal  result.  In  some  cases  of  supposed  innominate 
aneurism,  which  proved  to  be  aortic,  ligation  of  the  carotid,  or  of  the 
subclavian,  has  been  followed  by  marked  relief.  In  two  cases  of  aneurism 
involving  the  transverse  arch,  the  left  carotid  has  been  tied  and  the  disease 
cured  or  arrested  for  a  v&ry  long  time.  It  would  seem  best  to  perform  this 
when  the  sac  involves  only  the  arch.  Tracheotomy  may  be  performed  only 
to  insure  a  quiet  death. 

abdomi:n^al  aisteueism. 

An  aneurism  of  the  abdominal  aorta,  or  of  any  of  its  branches  situated 
within  the  abdominal  cavity,  is  called  an  abdominal  aneurism.  The  coeliac 
axis,  the  mesenteries,  the  renal,  and  the  common  iliacs  are  the  branches 
usually  involved.  The  morbid  changes  are  similar  to  those  of  thoracic 
aneurisms,  except  that  the  pressure  effects  are  different.  The  splanchnic 
nerves,  semilunar  ganglia,  and.  the  solar  plexus  may  be  involved.  The  bile- 
duct  or  the  renal  vessels,  the  stomach  and  the  duodenum  may  be  pressed 
on  and  narrowed.  The  bodies  of  the  vertebrae  may  be  eroded.  Abdominal 
aneurisms  are  not  so  often  caused  by  "  atheromatous  "  changes  in  the  walls 
of  the  artery  as  are  thoracic  aneurisms. 

Etiology. — Its  development  is  always  preceded  by  some  form  of  arterial 
degeneration.  It  is  rare  before  thirty-five,  and  is  met  with  in  men  oftener 
than  in  women. 

Symptoms. — Intermittent,  paroxysmal  pain  is  its  prominent  symptom. 
Agonizing  ^am  in  the  bach  darts  along  the  branches  of  the  lumbar  plexus. 
This  pain  is  apt  to  be  continuous,  and  indicates  erosion  of  the  spinal  column. 


528  DISEASES   OF  THE   BLOOD-VESSELS. 

l^ausea  and  vomiting  may  result  from  pressure  on  the  stomach  ;  dyspha- 
gia from  pressure  on  the  oesophagus  ;  jaundice  from  pressure  on  the  bile- 
duct  ;  changes  in  the  urine  from  pressure  on  the  renal  vessels  ;  and  anasarca 
of  the  lower  limbs  from  pressure  on  the  inferior  cava,  or  in  one  limb  from 
pressure  on  one  of  the  iliac  veins.  Aneurisms  here  may  burst  into  the 
peritoneal  cavity,  the  retroperitoneal  tissue,  the  spinal  canal,  or  into  the 
substance  of  the  mesentery,  meso-colon,  or  great  omentum,  and  in  the 
last-named  instances  there  will  be  more  or  less  obstruction  about  the  region 
of  the  pylorus.  They  may  also  open  into  the  intestinal  canal,  the  lung, 
the  pleura,  the  inferior  cava,  the  pelvis  of  the  kidney,  the  ureter,  bile- 
passages,  or  the  oesophagus.     Earely  are  the  liver  and  heart  displaced. 

Physical  Signs. — Palpation  discovers  in  some  instances  a  smooth,  elastic 
tumor  to  the  left  of  the  median  line.  It  has  an  expansive,  dilating  impulse 
(rarely  double),  and  synchronous  with  the  radial  pulse. 

There  is  dulness  over  the  tumor. 

On  auscultation  a  single  prolonged  post-systolic  murmur  may  be  heard. ' 
A  double  murmur  over  the  aneurism  in  front  is  rare.  Seldom  can  any 
murmur  be  heard  when  the  patient  is  in  any  other  than  a  recumbent  pos- 
ture, 

DiiFerential  Diagnosis. — If  an  abdominal  aneurism  is  of  considerable  size, 
the  constant  pain  in  the  back  and  the  presence  of  a  dilating  tumor  will 
establish  a  diagnosis  ;  forcible  pulsation  of  the  aorta  may  simulate  an 
aneurism,  but  the  throbbing  is  felt  along  the  entire  course  of  the  aorta 
and  its  branches,  and  is  not  localized  as  in  aneurism  ;  then  the  absence  of 
pain  and  of  the  "  expansive  "  impulse  and  murmur  will  establish  the  diag- 
nosis. A  cancerous  or  other  solid  tumor  may  have  a  pulsation  communi- 
cated to  it  by  the  underlying  aorta  ;  but  the  knee-chest  position  will  re- 
move doubts.  In  thin  subjects  especially,  by  grasping  the  solid,  uneven 
mass,  it  is  easy  to  decide  for  or  against  an  aneurism. 

Prognosis. — Hayden  gives  fifteen  days  to  eleven  years  as  the  extremes  ;  a 
year  or  eighteen  months  is  the  average  duration.  After  rupture  the  pa- 
tients have  lived  for  some  time  ;  but  death  is  certain  sooner  or  later. 

Treatment. — Posture,  rest,  a  restricted  diet,  and  mild  laxatives  are  advo- 
cated in  the  treatment  of  abdominal  aneurism  by  Bellingham.  Tufnell's 
plan  may  also  be  followed.  Iodide  of  potassium  and  ergot  reduce  vascu- 
lar tension  and  are  highly  recommended.  Aconite  is  highly  recommended 
by  English  surgeons.  Pressure,  ligation,  tourniquets,  etc.,  etc.,  are  meas- 
ures resorted  to  by  surgeons. 

MEDIASTIlSrAL    TUMORS. 

Cancer  and  sarcoma  are,  independent  of  aneurism,  the  most  frequent 
mediastinal  tumors.  In  rare  instances  lymphadenomata,  lipomata,  cysts, 
enlarged  lymphatics,  fibromata  and  osteomata  may  develop  in  the  medias- 
tinum.    The  lymphatic  glands  in  the  anterior  mediastinum  are  most  fre- 

1  If  the  patient  be  placed  in  the  knee-elbow  position,  and  a  murmur  still  persists,  then  the  tumo"  if:  in 
all  probability  an  abdominal  aneurism,  not  a  tumor  to  which  aortic  pulsations  have  been  transmitted. 


THE    URINE.  529 

qiiently  the  seat  of  these  developments,  although  they  may  originate  in  any 
mediastinal  tissue.  In  exceptional  cases  the  thymus  gland  is  the  original 
seat  of  the  new  growths.  The  primary  cause  of  their  development  is  un- 
known ;  they  occur  at  any  age,  but  are  most  frequently  met  with  between. 
twenty  and  forty. 

The  symptorns  of  mediastinal  tumors  are  those  of  pressure,  e.g.,  aphonia, 
dysphagia,  cyanosis,  pain,  and  a  sense  of  constriction  about  tlie  chest. 
Displacement  of  the  heart  without  any  other  recognizable  cause  is  an  almost 
diagnostic  symptom. 

The  physical  signs  vary  with  the  size  and  site  of  the  tumor,  which  may 
pulsate  and  have  a  distinct  hruit.  Mediastinal  tumors,  mediastinal  ab- 
scesses, aneurism,  pericardial  or  pleuritic  effusions  and  chronic  pneumonia 
all  produce  symptoms  which  are  strikingly  similar  ;  and  the  diagnosis  of  a 
mediastinal  tumor  is  arrived  at  mainly  by  exclusion.  The  exploring  trocar 
is  often  the  only  means  by  which  a  diagnosis  can  be  reached. 

Prognosis. — Mediastinal  tumors  sooner  or  later  terminate  fatally.  Lebert 
states  that  their  average  duration  is  thirteen  months.  In  a  case  of  Jac- 
coud's,  death  occurred  on  the  eighth  day. 

The  ^rm^mew^  is  palliative. 

DISEASES  OF  THE  KIDNEYS. 

THE    UEESTE. 

The  urine  in  health  is  a  clear,  amber  colored  liquid  of  acid  reaction, 
saline  taste,  and  having  a  peculiar  aromatic  odor.  The  amount  voided  in 
twenty-four  hours  ranges  between  forty  and  fifty  ounces.  Its  specific 
gravity  varies  from  1.012  to  1.030  ;  the  average  being  about  1.020.  After 
exposure  to  the  air  the  acidity  of  the  urine,  which  is  due  mainly  to  the 
presence  of  the  acid  phosphates,  continues  for  a  few  days,  and  then  an  acid 
or  alkaline  fermentation  takes  place.  The  former  is  caused  by  the  growth 
of  a  round  cell  vegetable  ferment,  and  is  accompanied  by  the  ci-ystallization 
of  uric  acid  and  the  precipitation  of  the  acid  urate  of  soda.  The  alkaline 
change  is  the  result  of  the  growth  of  the  micrococcus  urea,  and  is  marked 
by  decomposition  of  the  urea  and  the  formation  of  carbonate  of  ammonia 
and  the  triple  phosphates. 

Normal  Cotistitnents  of  the  Urine. — Generally  speaking,  these  may  be 
regarded  as  the  products  of  the  metamorphosis  of  the  tissues  of  the  body  ; 
the  most  important  organic  constituents  are  urea,  uric  acid,  hippuric  acid, 
oxalic  acid,  kreatinin,  xanthin,  and  the  coloring  and  extractive  materials. 

Urea. — This  substance  represents  the  result  of  the  retrograde  metamor- 
phosis of  the  nitrogenous  body  tissues  and  the  excess  of  the  nitrogenous  ele- 
ments of  the  food.  It  is  formed  in  the  tissues,  taken  up  by  the  blood  and 
lymph,  filtered  by  the  kidneys,  and  appears  in  the  urine  to  the  amount  of 
five  to  six  hundred  grains  daily.  Urea  is  abnormally  increased  in  amount 
in  all  febrile  and  nervous  affections,  in  pyaemia  and  diabetes  ;  it  is  abnor- 
mally diminished  in  nephritis,  anasmia,  cholera,  and  starvation,  and  maj 
34 


530  DISEASES    OF   THE    KIDNEYS. 

be  entirely  absent  in  acute  yellow  atrophy  of  the  liver.  TJrea  is  a  feeble 
base,  extremely  soluble,  and  cannot  be  detected  except  by  chemical  exami- 
nation. 

Uric  acid  is  generally  found  in  the  urme  combined  with  some  base, 
especially  lime  or  soda.  Its  origin  is  similar  to  that  of  urea.  In  health 
six  to  nine  grains  are  passed  every  twenty-four  hours  ;  this  amount  is  in- 
creased by  a  highly  albuminoid  diet  and  in  certain  febrile  conditions.  It 
is  diminished  by  out-door  exercise.  Uric  acid  appears  in  the  urine  as  a 
crystalline  deposit,  which  will  be  described  hereafter.  Besides  the  above 
constituents,  the  urine  normally  contains  small  quanti- 
ties of  kreatinin,  hippuric  acid  and  xanthin,  which  may 
be  said  to  represent  the  less  completely  oxidized  products 
of  tissue  change. 

Coloring  and  extractive  materials. — The  normal  color  of 

the  urine  is  due  to  tbe  presence  of  a  pigment,  called  urohse- 

matin  ;  a  substance  closely  allied  to  the  coloring  matter 

of  the  bile,  and  derived  from  the  blood  by  the  action  of 

Fig.  113.  the   livcr  and   spleen.     Another  normal  pigment  of   the 

ippuric   ci  .  X  250.  ^^j,jj^g  ^g  iiifjicai;,^  a  peculiar  substance  which  under  certain 

conditions  gives  rise  to  indigo-blue.     The  extractives  are  certain  volatile 

organic  acids  which  give  to  the  urine  its  peculiar  aromatic  odor. 

The  inorganic  constituents  of  the  urine  are  chlorine,  sulphuric  acid, 
phosphoric  acid,  potassium,  sodium,  calcium,  magnesium,  oxygen,  hydro- 
gen and  nitrogen. 

Chlorine. — The  average  amount  of  chlorine  passed  daily  is  about  one 
hundred  grains  ;  an  increase  in  this  amount  has  no  special  significance,  but 
a  diminution  or  absence  has  been  noticed  in  all  acute  febrile  diseases  with 
the  one  exception  of  intermittent  fever. 

Sulphuric  Acid. — The  amount  daily  passed  averages  about  thirty 
grains.  Sulphuric  acid  in  the  urine  arises  from  the  animal  and  vegetable 
food  taken  into  the  system,  and  from  changes  in  those  tissues  which  con- 
tain sulphur  and  sulphates. 

Phosphoric  Acid. — About  fifty  grains  of  this  acid  are  eliminated  in 
the  twenty-four  hours.  It  is  abnormally  increased  in  all  inflammatory 
diseases  of  the  nervous  system,  in  severe  nerve  lesions  and  in  rickets.  It 
is  abnormally  diminished  in  most  febrile  and  inflammatory  diseases,  es- 
pecially in  pneumonia  and  Bright's  disease.  The  rest  of  the  inorganic  con- 
stituents of  the  urine,  which  amount  to  about  one  hundred  grains  daily, 
will  be  considered  under  the  head  of  urinary  sediment,  as  they  generally 
appear  in  that  form. 

Albumen. — ^When  albumen  appears  in  the  urine  it  may  have  its  origin 
in  the  kidneys  or  depend  upon  the  presence  of  pus  or  free  blood ;  this 
question  can  only  be  settled  satisfactorily  by  the  microscope.  Albuminous 
urine  is  generally  of  low  specific  gravity.  In  diseases  of  the  kidney  the 
serum-albumen  which  is  found  in  the  urine  has  its  origin  in  the  blood, 
and  either  by  the  increase  or  diminution  of  the  blood  pressure  within  the 
glomeruleSj,  the  albumen  is  transuded  within  the  capsule  of  Bowman,  and 


THE   UEINE.  531 

then  is  waslied  along  the  uriniferous  tubules  with  the  urine.  When  albu- 
men appears  in  the  urine  in  acute  and  chronic  Bright's  disease  some 
structural  change  in  the  kidney  is  indicated  ;  but  it  may  appear  independ- 
ent of  any  structural  lesions  under  the  following  conditions,  viz.  :  febrile 
and  inflammatory  diseases,  impediments  to  the  circulation  of  the  blood, 
pregnancy  and  the  puerperal  state,  saturnine  intoxication,  hydraemia  and 
atony  of  the  tissues,  after  the  use  of  certain  drugs,  and  in  some  people  after 
taking  certain  articles  of  food. 

Urinary  Sugar. — When  the  urine  contains  much  sugar  it  is  of  a  pale, 
yellow  color,  sweetish  taste,  and  increased  in  amount.  Its  specific  gravity 
is  always  high,  generally  between  1.030  and  1.040,  although  cases  are  occa- 
sionally met  in  which  it  is  as  low  as  1.008.  Sugar,  except  in  a  very  small 
quantity,  is  not  found  in  normal  urine,  so  when  it  is  constantly  present 
in  large  amounts  a  grave  pathological  lesion  is  indicated.  Diabetes  mel- 
litus  is  the  only  disease  in  which  sugar  is  found  in  the  urine  in  large  quan- 
tities, but  traces  of  it  appear  after  disturbances  of  the  abdominal  circula- 
tion, after  injuries  to  certain  portions  of  the  nervous  system,  after  inter- 
ference with  respiration,  in  the  urine  of  women  just  after  weaning  a  child, 
and  sometimes  it  is  temporarily  present  without  any  assignable  cause. 

Bile. — Urine  containing  bile  varies  in  color  from  a  deep  reddish  brown 
to  a  dark  green,  and  generally  has  an  acid  reaction  and  high  specific  gravity. 
The  coloring  matter  of  the  bile,  such  as  bilirubin,  biliverdin,  and  bili- 
prasin,  is  the  portion  which  usually  appears  in  the  urine  in  disease.  It  is 
especially  noticed  in  those  who  are  jaundiced.  The  bile  salts  are  some- 
times present. 

Lactic  acid  has  been  found  in  the  urine  in  diabetes,  acute  yellow  atrophy 
of  the  liver,  trichinosis  and  osteomalacia. 

i^a^.  — Fat  is  not  very  often  found  in  the  urine,  but  when  it  is  present  it 
gives  to  that  fluid  a  milky  appearance,  for  it  is  held  in  the  form  of  an 

emulsion  by  the  albumen  present.    The 
O     Q  (-\        urine  shows  a  tendency  to  spontaneous 

^0  0  oo      coagulation,  and  in  a  short  time  a  white 
^rsO'oO     l^y^^'  I'ises  to  the  top  which  disappears 

® J:  o  o    o       on  the  addition  of   ether.     Under  the 
O 

Q  o  Q  rnicroscope  mmute  globules  of  fat,  some- 
times with  blood  and  lymph  corpuscles, 
are  seen. 

Fat  globules  from  -r  •  •\      m  •  mi 

chylous  nrine.  Lcucin    and    lyrosm. — The    urine 

often  contains  large  quantities  of  these 
substances,  which  arise  from  the  prolonged  action  of  ^i*^-  "s. 

the  pancreatic  ferment  upon  the  nitrogenous  elements       Leucm  andTyrosm. 

of  the  food.  A.  Globules  of  Levcin. 

B.   Tyrosm.    x  250. 

Leucin  appears  either  in  the  form  of  white  crystal- 
line scales  freely  soluble  in  water,  or  as  small,  round,  yellow  bodies  looking 
something  like  spherical  fat  cells. 

TyroHin  is  in  the  form  of  white  masses  consisting  of  long  shiny  needles 
arranged   in  star-shaped  groups.       Leucin  and  tyrosin  appear  in   those 


532 


DISEASES   OF   THE   KIDKETS. 


diseases  in  whicli  oxidation  is  very  greatly  impaired,  such  as  acute  yellow 
atrophyof  the  liver,  typhoid  fever,  small-pox,  and  in  hepatic  diseases 
generally. 

UEINAEY     SEDIMENTS. 


A 


Many  deposits,  in  crystallizd  and  non-crystallized  forms,  appear  in  the 
urine,  some  of  which  are  passed  with  it,  and  others  are  separated  from 
it  aiter  its  passage.    The  following  are  the  most  important : 

Ui'ic  Acid. — The  strong  acids  which  appear  in  the  urine  during  the 
stage  of  acid  fermentation  quickly  decompose  the  urates,  and  set  the  uric 
acid  free.     This  is  deposited  in  the  form  of  yellowish-red  colored  crystals 

which  assume  a  multitude  of  forms.  „The 
most  common  are  lozenge-shaped  and  rhom- 
boidal  crystals, having  angles  more  or  less  round- 
ed ;  they  also  appear,  especially  when  abun- 
dant, as  aggregated  or  flat  stellate  crystals. 
Should  any  doubt  arise  as  to  the  character  of 
the  crystals,  dissolve  the  sediment  in  a  drop  of 
potassic  hydrate,  then  add  a  little  hydrochloric 
acid,  and  the  uric  acid,  if  present,  will  recrystal- 
lize  into  one  of  its  numerous  forms.  The  clinical 
importance  of  uric  acid  crystals  has  already 
been  referred  to. 

Urates. — When  the  urine  contains  abundant 
amorphous  urates  it  is  generally  turbid,  but 
becomes  clear  on  heating.  On  careful  obser- 
vation a  fine  powdery  sediment  will  be  seen, 
which  clings  to  the  glass  and  varies  in  color 
from  a  light  fawn  to  a  pink.  The  urates  are  in  a 
state  of  solution  in  normal  urine,  but  when 
that  fluid  becomes  concentrated 
or  has  lost  the  temperature  of 
the  body,  the  urate  of  soda  will 
become  deposited  in  an  amor- 
phous condition, appearing  under 
the  microscope  as  mossy  granu- 
les. Urate  of  ammonia  appears 
only  after  the  urine  becomes 
alkaline,  occurring  as  brown- 
ish spherical  bodies,  with  or  with- 
out fine  proiecting  spiculaj.     The  ^'■^^e  of  Ammonia. 

.  A    Cluster  of  BTcywn 

urates    may  be   deposited    after     'spiwruies. 
slight  indigestion,  great   mental     'vie!°withmcuia-^^ 
and  physical    exertion,  and    in    %staif'''f^^!' 
acute   febrile   and  inflammatory 
diseases  ;  they  are  often  the  forerunner  of  urinary  calculi,  and  of  derange- 
ments of  the  liver  and  of  the  other  chylopoetic  viscera. 


Fig.  116. 

Uric  Acid. 

A.  The  most  crmimon  form. 

B.  Disintegr  'ted  crystals. 

C.  Formaiion  of  7'ounded  masses . 

X  350. 


Pig.  118. 


Fig.  117. 
Urate  of  Soda. 

A.  AmorpfwMS  granvles  in  clusters 
resemhling  moss. 

B.  Granules  in  strings  sometimes 
mistaken  fm^  granular  casts. 

X  250.  ■ 


UEINARY   SEDIMENTS. 


533 


o 
o  c? 


(P 


.oo 


Fig.  119. 


Oxalate  of  Calcium. 
The  octahedra,  most  fre- 
quently present,  are 
seen  on  the  left.  The 
comparatively  rare 
form  of  dumb-bells  is 
also  shown,     x  250. 


Oxalate  of  Calcium. — Calcium  oxalate  is  often  held  in  solution  in  the 
urine,  but  when  it  is  precipitated  it  takes  one  of  two 
forms,  either  as  small,  colorless,  sharp- edged,  octa 
hedral  crystals  resembling  envelopes,  or  as  dumb- 
bell shaped  crystals,  entangled  with  mucus.  The 
presence  of  the  oxalate  of  lime  crystals  is  due 
to  the  reduction  of  the  compounds  of  oxalic  and 
carbonic  acids  which  are  normal  to  the  urine,  or  to  the 
ingestion  of  certain  articles  of  food.  "When  oxalate  of 
calcium  occurs  constantly  in  the  urine  it  produces  the 
so-called  oxaluria  or  oxalic  acid  diathesis,  and  is  apt  to 
lead  to-  the  formation  of  the  mulberry  calculi,  and  in 
time  exert  its  poisonous  effects  on  the  brain  and  spinal 
cord.  The  crystals  of  calcium  oxalate  are  found  in  the  urine  in  cases 
of  disturbed  respiration,  emphysema  of  the  lungs,  rachitis,  and  after 
epileptic  convulsions. 

Earthy  Phosphates. — The  earthy  phosphates  are  the  most  common  sedi- 
ment met  with  in  the  urine,  in  fact,  when  the  urine  is  alkaline  they  are 
never  absent ;  they  present  themselves  as  the  am- 
monio-magnesian  or  triple  phosphates,  or  as  the 
phosphate  of  calcium.  During  the  stage  of  alkaline 
fermentation,  the  ammonia  produced  combines 
with  the  phosphate  of  magnesium  present,  and  the 
result  is  that  the  crystals  of  the  triple  phosphates, 
being  insoluble  in  an  alkaline  fluid,  are  thrown 
down  in  large  quantities,  as  also  are  the  crystals  of 
the  phosphate  of  lime,  the  separation  of  the  latter  de- 
pending upon  the  presence  of  one  of  the  fixed  alka- 
lies, as  the  carbonate  of  sodium.  The  crystals  of  the 
triple  phosphates  vary  according  as  they  are  the  re- 
sult of  rapid  or  slow  crystallization  :  in  the  former 
case  they  assume  a  feathery  form,  looking  some- 
Ammonio-Magnesian,  or  Triple  thing  like  two  fcms  crossing  at  an  acute  angle  ;  in 
Phosphate.  ^j^^  latter  case  they  appear  as  triangular  prisms  with 

A.  Larqe  colorless  prisms.  t^.         ,  ,,  »,.  „ 

B.  Forms  rapidly  deposited,     bevelled  edgcs.     ihe  pliosphatc  01  lime  lorms  an 

amorphous  transparent  sediment  like  the  urates, 
but  is  distinguished  from  them  by  the  action  of  heat,  which  causes  an 
increased  precipitation,  and  by  that  of  nitric  acid,  a  few 
drops  of  which  clear  up  the  urine.  A  sediment  of  the 
earthy  phosphates  does  not  of  necessity  indicate  that  there 
is  an  abnormal  amount  in  the  urine,  but  it  does  show  the 
alkaline  state  of  the  urine  and  the  possible  results  of  such 
a  condition,  and  it  points  out  the  danger  of  the  formation 
of  phosphatic  calculi.  An  increase  of  the  earthy  phos- 
phates has  been  noted  in  certain  diseases  of  the  bones,  such 
as  rachitis. 

Cystine,  which  is  a  crystalline  body   derived  from  the 


Fig.  120. 


Fig.  121. 

Phosphate  of  Lime. 

X  350. 


534 


DISEASES   OF   THE    KIDJS'BYS. 


Fig.  122. 
Cystine,     x  250. 


liver,  is  not  often  found  in  the  urine,  but  when  it  is  it  presents  itself  in 
the  form  of  flat  hexagonal  plates,  which  are  of  neutral  reaction  and  can  be 
dissolved  by  the  caustic  mineral  alkalies.  When  this 
substance  occurs  in  the  urine  it  is  apt  to  give  rise  to  cal- 
culi.    Cj^stinuria  seems  to  run  in  families. 

Organized  Sediments. — Mucus  and  EpitJielium.  All 
urine  contains  a  varying  amount  of  mucus,  derived  from 
the  urinary  passages  and  from  the  bladder,  which  sepa- 
rates in  the  urine  as  a  light,  flaky  cloud.  Under  the 
microscope  mucus  presents  itself  in  one  of  two  forms, 
either  as  mucous  corpuscles  in  the  form  of  small,  round 
granular  cells  containing  one  or  more  nuclei,  or  as  trans- 
parent masses  of  mucous  coagula,  which  look  very  much  like  granular 
casts  and  for  this  reason  have  been  called  mucoid  casts.  An  abnormal 
amount  of  mucus  in  the  urine  shows  that  there  is  irritation  at  some  point 
along  the  urinary  tract ;  this  may  be  the  re- 
sult either  of  a  local  inflammation  or  of  a 
general  constitutional  disease,  such  as  pneu- 
monia or  typhoid  fever  ;  when  there  is  a  mu- 
cous sediment  in  the  urine,  there  is  always 
found  entrapped  in  it  a  large  number  of 
epithelial  cells  of  different  varieties,  which 
for  convenience  of  description  may  be  di- 
vided into  three  classes.  First,  round, 
spherical  cells  having  distinct  nuclei  de- 
rived from  the  tubules  of  the  kidney,  or  from 
the  deep  layers  of  the  mucous  membrane  lin- 
ing the  pelvis  or  from  the  male  urethra. 
Second,  columnar  and  ciliated  cells  derived 
from  the  cervix  of  the  uterus.     Third,  flat 


cells  with  large  distinct  nuclei  which  have 


their  origin  in  the  bladder  or  vagina  ;  in  the 
former  case  they  are  much  larger  and  granu- 
lar.    The  situation  of  an  inflammation  con- 


0? 


Fig.  123. 
Epithelium  from  Urinary  Deposits. 
.  --.  Large,  flat  bladder  cells. 

fined   to    some    portion    of   the    urinary  tract  B"^.  From  Uadder— deeper  layers. 
,       -  .  .  ,        y-  Cells  from  vagina. 

may  sometimes  be  determined  by  noting  the  v.  cmated  cells  from  cervix  of  uterus. 

1  ,  «,,  -iiTi       n  T-iT        C*.  From  mucosa  of  uterus. 

character  oi  the  epithelial  cells  passed  m  the  p.  cdisfrainpeMsofkidney. 
urine  whenever  it  can  be  determined  whether  g.  F7wn!prostatvcport^  of  urethra. 
the  cells  came  from  the  tubules  or  pelvis  of        ""  ^^' 
the  kidney,  or  from  the  bladder  or  lower  part  of  the  urinary  passage. 

Blood  may  appear  in  the  urine  in  varying  amounts,  and  may  come  from 
any  portion  of  the  tract ;  when  the  urine  contains  blood  it  will  have  a 
reddish  or  smoky  appearance,  and  deposit,  on  standing,  a  coffee-ground  like 
sediment,  and  will  show  by  chemical  analysis  the  presence  of  both  albumen 
and  fibrin.  The  appearance  of  the  urine,  the  amount  of  blood,  and  the 
cause  of  its  presence  will  vary  greatly  according  to  the  portion  of  the 
urinary  passages  from  which  it  comes  -.—first,  when  the  quantity  of  blood 


URINARY   SEDIMENTS.  535 

is  small,  and  it  is  equally  diffused  throughout  the  urine,  in  all  probability, 
it  is  derived  from  the  parenchyma  of  the  kidneys,  and  especially  from  the 
Malpighian  tnfts ;  this  condition  is  met  with  as  the  result  of  Bright's  dis- 
ease, congestion  of  the  kidney,  injury,  the  use  of  certain  drugs,  such  as 
cantharides,  the  formation  of  abscesses  secondary  to  renal  infarctions,  and 
from  the  presence  of  adventitious  growths.  Second,  when 
the  urine  contains  much  blood  and  distinct  clots  are  visi- 
ble, it  is  safe  to  infer  that  the  blood  is  derived  from 
the  pelvis  of  the  kidney,  from  the  ureters,  or  from  the 
bladder ;  in  the  former  case  it  is  generally  the  result  of 
pyelitis,  renal  calculi,  parasites,  or  morbid  growths  ;  in  the 
latter  case  it  is  present  as  the  result  of  vesical  calculi,  or 
erosions  and  ulcerations  of  the  mucous  membrane.  Blood 
may  appear  in  the  urine  as  the  result  of  disease  of  the 
urethra,  but  then  the  cause  of  its  presence  can  easily  be  ^.  sivoUen  red  cor- 
determined.  Certain  constitutional  causes  may  give  rise  to  uHnfo/Zws^ 
bloody  urine,  for  it  appears  in  the  following  diseases :  ^  cfmateT^^'^lmr/us- 
fevers,  scurvy,  purpura,  cholera,  myelitis,  and  in  the  ^les  from  dense 
hemorrhagic  diathesis. 

Pus,  when  present  in  the  urine,  gives  to  it  a  milky  appearance,  and,  on 
standing,  a  yellowish-green  sediment  is  precipitated  which,  as  long  as  the 
urine  is  acid,  can  easily  be  mixed  with  it,  but  when  the  urine  becomes 
alkaline,  the  sediment  will  have  a  gelatinous,  ropy  appearance  and  soon 
undergo  ammoniacal  decomposition.  Albumen  is  always  found  in  urine  con- 
taining pus,  and  varies  in  quantity  with  the  amount  of  pus  present.  The 
microscopical  appearance  of  pus  is  sufficient  to  determine  its  presence  ;  for 
the  shape,  size  and  granular  appearance  of  the  pus  corpuscles,  with  their 
granular  nuclei  rendered  more  distinct  by  the  addition  of  acetic  acid,  cannot 
mi  g^  #  ^®  mistaken  for  anything  else.  Pus  appears  in  the 
t-  #*"         urine  either  as  the  result  of  some  suppurative  inflam- 

^#?^        ^bi  ®  ^       mation  along  the  genito-urinary  tract  or  from  the  rup- 
ture of  some  neighboring  abscess,  but  it  must  be  re- 
membered that  in  women  it  may  be  derived  from  the 
^        genital  organs.      The  significance  of  pus  in  the  urine 
^         ^  depends  upon  its  source,  which  may  be  determined  by 

^  ©  @   remembering  the  following  points  :— if  the  urine  is 
®  ©    acid,  when  voided,  the  pus  probably  has  its  origin  in 

®  the  kidneys  ;  if  it  is  alkaline,  its  origin  is  in  the  blad- 

^Puf ^'  ^®^  5  ^^  ^^^  presence  is  accompanied  by  slight  colicky 

A.  Pits  corpuscles  as  ordi-  pains  ovcr  the  course  of  the  ureters,  probably  suppu- 

B.  TfTfLTjrM"'wUh  ration  is  going  on  in  them.    In  inflammations  of  the 

acetic  acid,  x  300.  urethra  pus  can  be  pressed  out  of  the  meatus. 
Casts  are  peculiar  cylindrical  bodies  consisting  of  exudative  material  or 
coagulated  matter  formed  in  the  urinary  tubules  of  the  kidney  as  the 
result  of  disease,  and  then  washed  out  by  the  urine  secreted  behind  them. 
They  vary  in  size  and  number  according  to  the  nature  of  the  disease  which 
gives  rise  to  them,  but  it  may  be  rightly  stated  that  the  more  numerous  the 


536 


DISEASES    OF   THE    KIDN"EYS. 


Pig.  126. 

EpiiheJial  Casts. 

X  250. 


casts  and  the  longer  time  they  are  present,  the  more  extensive  will  be  the 
Etructural  lesions  in  the  kidney.  The  following  are  the  principal  varieties 
of  casts  met  with  in  the  urine  : 

Epitlielial  castn  consist  of  tubular  masses  of  renal  epithelium,  especially 
from  the  tubules  of  Bellini  in  the  medullary  por- 
tion of  the  kidneys  ;  they  are  also,  at  times,  de- 
rived from  the  epithelial  lining  of  the  pelvis 
and  calices  of  the  kidney.  Occasionally  the 
epithelial  cells  present  a  normal  condition,  but 
generally  they  show  granular  degeneration.  This 
variety  of  casts  indicates  desquamative  nephritis. 
When  they  are  found  mingled  with  pus  cor- 
puscles a  serious  inflammatory  condition  is  in- 
dicated. 

Hyaline  casts  are  structureless,  transparent  cyl- 
inders, having  a  tendency  to  fracture  transversely, 
and  are  derived  from  the  fibrinous  exuduation 
which  has  passed  through  the  degenerated  walls 
of  the  renal  vessels  and  coagulated  in  the  tubules 
of  the  kidney.  Large  hyaline  casts  are  met  with 
in  the  atrophied  stage  of  all  forms  of  Bright's 
disease.  Small  hyaline  casts  are  found  in  the 
acute  stage,  and  sometimes 
when  no  lesion  can  be  appreci- 
ated. 
Granular  Casts. — These  casts  are  solid,  fibrinous  cyl- 
inders, which  have  a  finely  granular  appearance  caused 
by  the  presence  of  the  debris  of  the  degenerated  renal 
epithelium.  Blood  and  pus  corpuscles  and  granular  cells 
are  often  found  embedded  in  this  granular  matter.  These 
casts  are  most  often  found  in  the  advanced  stages  of 
Bright's  disease,  and  indicate  the  large  white  or  granular 
kidney,  or  that  extensive  destruction  of  the  paren- 
chyma of  the  kidney  is  taking  place. 

Fatty  casts  are  made  up  of  a  material  supposed  to 
be  mixture  of  olein  with  cholesterin,  and  some  al- 
buminous matter ;  fat  globules,  varying  greatly  in 
size,  and  also  some  epithelial 
cells  and  granular  material 
may  be  found  in  them.  These 
casts  show  that  the  degenera- 
tive changes  in  the  kidney  are 
fatty,  and  they  indicate  the 
same  conditions  as  granular 
casts. 

Blood  casts  consist  of  coagu- 
lated fibrin  and  red  blood  corpuscles.     By  some  they  are  thought  to  indi' 


Fig.  137. 
Hyaline  Casts. 

A.  Bellcate  hyaline  casts. 

B.  Dense,  so-called  waxy  casts. 


Pig.  128. 
Granular  Casts. 

A.  Large  granular  casts. 

B.  8mall  finely  granular 

casts.     X  250. 


Pig.   130. 
Blood  Casts. 

A.  Collecting -tube  blood  casts. 

B.  Mucous  casts. 


ACUTE    UEtEMIA. 


537 


cate  the  disease  of  the  renal  blood-vessels,  especially  amyloid  or  fatty  de- 
generation of  the  Malpighian  tuft. 

Spermatozoa  are   occasionally  met   with    in   the 

urine,  and  give  to  it,  when  present  in  abundance,  a 

milky  white  appearance.     If  a  drop  of  the  urine 

be  placed  under  the  microscope  the  characteristic 

tadpole   appearance  of  the  spermatozoa   can  easily 

be  recognized.     Spermatozoa  appear  in  the  urine 

after     coitus,    involuntary    nocturnal      emissions, 

and    occasionally    after     defecation.     They    have 

also  been    found  in    the  urine   of    typhoid  fever 

patients. 

Animal  and  Vegetable  Organisms. — Fully 
developed  hydatids  and  echinococci,  or  only 
portions  of  these,  may  appear  in  the  urine, 
having  been  developed  at  some  portion  of  the 
genito-urinary  tract  or  poured  into  it  by  tlie 
rupture  of  some  hydatid  cyst.  A  small  uni- 
sexual parasite,  the  Bilharzia  haematobia,  has 
been  found  in  the  urine,  especially  during  the 
epidemics  of  hfematuria  occurring  in  North- 
ern Africa.  Bacteria,  or  fermentation  spores, 
form  in  urine  which  is  undergoing  decom- 

A.ToruiacerevisicR.—B.PenicUmmgiau-  position.     Sarcinas  have  been  observed  in  al- 

cum.—  C.  Sarcince  Vent,     x  300.  i    t  ■  t-»      •    -t  i  t         i 

kalme  urine,  renicilium  glaucum  has  been 
found  in  acid  albuminous  urine.  Torula  cerevisise  often  forms  in  diabetic 
urine. 


Pig.  132. 


ACUTE    UE^MIA. 


Under  the  tei*m  acute  uraemia  may  be  grouped  two  classes  of  symptoms, 
which  differ  in  their  mode  of  development  and  in  their  attendant  phenom- 
ena. In  the  one,  nausea,  vomiting,  and  headache  usher  in  twitchings  and 
epileptiform  convulsions  of  the  voluntary  muscles,  a  state  which  has  re- 
ceived the  name  of  nrcemic  convulsions.  In  the  other,  headache  and  drowsi- 
ness, a  gradually  advancing  torpor  or  convulsions  usher  in  a  state  of  insen- 
sibility, which  has  received  the  name  of  nrmmic  coma. 

The  primary  cause  of  both  these  conditions  is  to  be  found  in  a  failure  of 
the  kidneys  to  perform  their  normal  function  of  elimination,  and  the  con- 
sequent accumulation  in  the  circulation  of  some  or  all  of  the  poisonous  ele- 
ments of  the  urine.  This  condition  may  occur  in  the  course  of  any  disease 
in  which  suppression  of  the  renal  secretion  takes  place  ;  such  arrest  of  the 
function  of  the  kidneys  most  frequently  occurs  in  the  different  forms  and 
stages  of  Bright's  disease,  in  the  puerperal  state,  in  connection  with  the 
surgery  of  the  urethra,  cystic,  tubercular  and  cancerous  disease  of  the  kid- 
ney, and  in  suppurative  nephritis  ;  by  far  the  largest  number  occur  in  acute 
Bright's  disease. 


538  DISEASES   OF   THE   KIDNEYS. 

A  number  of  theories  have  been  advanced  in  regard  to  the  exact  element 
which  acts  as  the  poisonous  agent  in  uraemia.  The  earliest  accepted  view 
is  that  which  attributes  the  symptoms  of  uraemia  to  retained  urea.  Although 
this  view  at  different  times  has  been  discarded,  and  apparently  disproved  by 
the  experiments  of  distinguished  observers,  to-day  it  is  the  one  generally 
received.  French's  theory  was  that  urea,  as  urea,  was  innocuous,  and 
that  the  poisonous  agent  was  carbonate  of  ammonia  resulting  from  decom- 
position in  the  blood  of  urea  into  carbonate  of  ammonia  and  water,  which  de- 
composition was  ascribed  to  the  action  of  a  ferment  in  the  blood  ;  this  theory 
has  been  disproved.  Another  hypothesis  which  has  attracted  much  attention 
is  that  the  phenomena  of  ursemia  are  due  to  cerebral  anaemia  and  the  attend- 
ing cerebral  oedema.  This  is  the  mecMnical  theory.  Still  more  recent  ex- 
perimenters have  claimed  that  urea  is  formed  in  the  kidneys  from  nitroge- 
nous matter  m  the  blood,  and  that  uremic  manifestations  mainly  depend 
upon  the  accumulation  in  the  blood  of  kreatin  and  kreatinin.  Again, 
others  have  claimed  that  the  phenomena  of  uraemia  are  due  to  the  retention 
in  the  circulation  of  the  products  of  nerve  waste.  It  has  also  been  claimed 
that  some  forms  of  uraemia  may  be  associated  with  structural  changes  in 
the  brain  similar  to  those  which  occur  in  the  retina  in  cases  of  neuro-ret- 
initis. 

Mahomed  (Brit.  Med.  Jour.,  1877,  ii.  10-43)  calls  attention  to  the  cer- 
ebral lesion  which,  he  says,  accounts  for  the  epileptiform  convulsions  of 
uraemia,  viz.,  numerous  punctiform  hemorrhages  in  the  gray  matter  of  the 
cerebral  convolutions.  They  are  true  hemorrhages.  He  ascribes  other  cer- 
ebral symptoms  to  oedema  of  the  brain  following  increased  tension.  Simi- 
lar to  oedema  is  the  ''hyaline  exudation  into  nervous  tissue  "found  by 
Gull  and  Sutton.  Similarly,  headache  results  from  increased  tension  with- 
out exudation.  Gubler  (Paris,  1878)  describes  the  ''diminished  number 
and  impaired  respiratory  capacity  of  the  red  blood-corpuscles  "  in  ursemia, 
due  (G.  states)  to  kreatinin  and  ammonium  carbonate.  Hence  there  is 
more  or  less  "asphyxiation  of  the  nerve  centres."  He  also  believes «r^erm? 
spasm  to  result  in  sudden  retention  of  effete  products.  He  regards  the 
dyspnoea  as  at  times  due  to  kreatinin,  at  times  to  ammonium  carbonate  : 
in  one  the  breathing  is  hurried,  in  the  other  it  is  the  "  Clieyne- Stakes' 
respiration.'^ 

The  experiments  and  facts  upon  which  these  theories  are  based,  lead  to 
the  following  conclusions  :  that  ursemic  toxaemia  depends  upon  a  complete 
or  partial  arrest  of  the  urinary  secretion.  A  qualitative  analysis  of  the 
constituents  of  the  urine  goes  to  show  that  urea  is  its  only  actively  poison- 
ous ingredient,  and  that  it  is  not  the  special  product  of  any  particular  tis- 
sue or  organ,  but  the  united  product  of  all  nitrogenized  effete  matter. 
That  the  tissue-changes  found  in  the  brain  in  acute  uraemia  are  the  results 
of  the  action  of  this  poison.  Sometimes  ten  to  fifteen  times  as  much  urea 
is  found  in  the  blood  in  uraemia  as  in  health.  Again,  in  severe  cases  the 
amount  may  be  so  small  as  to  be  scarcely  determinable  (Jacobson).  And 
large  amounts  of  urea  may  be  found  in  the  blood  witJiout  the  symptoms  of 
acute  uraemia. 


ACUTE    URAEMIA.  539 

Symptoms. — An  acute  ursemic  attack  is  usually  preceded  by  certain  pre- 
monitory signs,  such  as  oedema  in  various  parts  of  the  body,  restlessness 
or  an  almost  irresistible  desire  to  sleep,  vertigo,  headache,  delirium,  nau- 
sea, vomiting,  diarrhoea,  and  impaired  vision.  The  countenance  has  a  pale, 
waxy  or  dingy  appearance,  and  the  urine  is  scanty,  high-colored,  bloody, 
albuminous,  and  contains  casts  ;  the  body  and  extremities  may  become 
violently  convulsed,  or  the  patient  may  pass  rapidly  into  a  state  of  coma. 

The  convulsions  may  consist  of  a  single  paroxysm,  or  a  succession  of 
paroxysms  may  follow  one  anotlier  at  intervals  of  a  few  minutes  or  several 
hours,  the  patient  during  the  interval  lying  in  a  state  of  more  or  less  pro- 
found insensibility.  They  may  almost  exactly  simulate  epilepsy,  or  they 
may  be  unattended  by  loss  of  consciousness.  During  the  convulsions 
the  face  becomes  livid,  the  eyes  are  glassy,  and  the  pupils  are  contracted 
or  dilated  ;  at  the  commencement  of  the  convulsive  attack,  they  are  gener- 
ally contracted.  Frothy  mucus,  which  is  sometimes  bloody,  collects  around 
the  mouth,  and  there  is  a  strong  urinous  odor  emanating  from  the  per- 
spiration. The  pulse  is  accelerated,  and  the  temperature  is  raised  in  some 
instances  as  high  as  107°  F.  A  low  temperature  may  be  present  in  the 
aged.  Sudden  coma  may  occur  with  convulsions.  Eestless  delirium  is  the 
chief  symptom  in  many  cases.  Intense  dyspnoea,  and  articular  symptoms 
are  very  rare. 

Urmmic  coma  may  come  on  gradually,  twenty-four  or  forty- eight  hours 
elapsing  before  the  stupor  is  complete,  or  the  patient  may  fall  suddenly 
into  a  state  of  profound  coma,  its  advent  resembling  an  attack  of  cerebral 
apoplexy.  Headache,  giddiness,  disorders  of  vision,  vomiting,  or  delirious 
excitement  may  precede  the  coma.  There  are  periods  when  the  coma  is  so 
profound  that  nothing  arouses  the  patient ;  at  other  times  he  is  easily 
aroused,  or  arouses  himself  and  attempts  to  speak  and  sit  up,  swallowing 
fluids  with  difficulty.  If  the  system  has  become  accustomed  to  the  pres- 
ence of  the  urinary  poisons,  a  considerable  excess  of  urea  and  effete  uri- 
nary products  may  exist  in  the  blood  for  a  long  period  without  giving  rise 
to  any  but  the  premonitory  symptoms  of  acute  uremia.  When  once  this 
balance  is  destroyed  and  a  certain  excess  of  urea  and  its  allies  in  the  blood 
is  reached,  the  kidneys  become  embarrassed  by  the  excessive  demand  made 
on  their  excreting  power,  and  rapid  and  intense  renal  congestion  follows,  but 
either  convulsions,  coma,  or  both,  result  in  this  way ;  acute  uraemia  may 
be  developed  in  the  chronic  as  well  as  the  acute  stage  of  renal  disease. 
Ursemic  coma  is  always  accompanied  by  stertor.  The  stertor  is  peculiar  : 
it  is  not  the  ^'snoring"  of  apoplexy,  but  a  sharp,  hissing  sound  produced 
by  the  rush  of  expired  air  against  the  teeth  or  hard  palate.  At  first  the 
respirations  are  accelerated,  but  they  soon  become  slow  and  labored  ;  the 
pupils  are  dilated,  but  they  are  not  irregular  ;  they  may  be  normal  ;  they 
react  slowly  to  light.  The  pulse  is  increased  in  frequency  and  lacks  firm- 
ness ;  at  first  the  temperature  is  raised,  but  after  a  time  it  falls  below  the 
normal  standard  ;  the  face  is  pale. 

Differential  Diagnosis. — Acute  uraemia  simulates  in  some  of  its  phenom- 
ena those  diseases  in  which  convulsions  and  coma  are  prominent  symptoms. 


540  DISEASES    OF   THE   KIDNEYS. 

The  phenomena  of  an  epileptic  seizure  are  almost  identical  with  those 
of  an  uraemic  convulsion,  and  it  is  exceedingly  difficult  to  distinguish  one 
from  the  other.  If  the  previous  history  is  known,  the  chronic  character 
of  the  epilepsy  will  in  some  instances  distinguish  it  from  acute  ursemia, 
and  an  examination  of  the  urine  will  generally  determine  the  ursemic  char- 
acter of  the  convulsions  ;  in  epilepsy  one  side  is  convulsed  more  violently 
than  the  other  ;  while  in  ursemia  both  sides  of  the  body  are  equally  con- 
vulsed. In  epilepsy  the  temperature  is  not  elevated,  and  although  there 
is  a  loss  of  consciousness,  reflex  sensibility  continues  from  the  beginning 
to  the  end  of  the  paroxysm,  which  is  not  the  case  in  ursemia.  Immedi- 
ately following  urgemic  convulsions  there  is  deep  coma ;  following  an 
epileptic  seizure  there  is  merely  a  deep  sleep,  from  which  the  patient  may 
be  aroused.  The  initial  cry  and  corpse-like  pallor  of  the  face  in  epilepsy 
are  wanting  in  uraemia. 

In  cerebral  apoplexy  coma  always  precedes  convulsions,  and  with  the  con- 
vulsions there  is  facial  paralysis  and  hemiplegia  ;  there  is  also  clonic 
spasm  of  the  parsflyzed  parts.  The  urinary  symptoms  of  uraemia  are  ab- 
sent and  the  stertor  is  less  sharp  and  hissing. 

In  hysterical  convulsions  the  patient  falls  with  a  scream  into  a  convul- 
sive, tetanic  or  cataleptic  condition.  Close  inspection  shows  that  the 
patient,  is  not  unconscious,  and  the  pupils  are  normal,  as  are  the  pulse  and 
temperature.  The  limbs  are  jerked  irregularly,  the  breathing  is  spasmodic 
and  is  attended  by  a  choking  sensation  ;  opisthotonos  is  very  common. 
There  is  no  lividity  of  the  face,  nor  distention  of  cervical  blood-vessels, 
and  the  close  of  the  paroxysm  is  usually  accompanied  by  the  discharge  of 
a  large  quantity  of  pale  urine, — non-albuminous  and  free  from  casts. 

OTiolcemic  convulsions  very  closely  resemble  ursemia,  but  may  be  dis- 
tinguished from  them  by  the  jaundice  which  precedes  or  accompanies  their 
development,  and  by  the  antecedent  history  of  hepatic  disease.  Convul- 
sions originating  in  meningitis  and  other  cerebral  affections  are  distin- 
guished by  the  accompanying  characteristic  symptoms  of  these  affections. 

The  points  in  the  differential  diagnosis  of  urcemic  coma  are  similar  to 
those  of  ursemic  convulsions.  It  may  be  distinguished  from  the  coma  of 
apoplexy  by  the  absence  of  paralysis. 

From  opium  poisoning  it  may  be  distinguished  by  the  rise  in  temperature. 
The  temperature  in  opium  poisoning  is  often  below  the  normal.  In  opium 
coma  the  respiration  is  slow  and  peculiar,  and  the  pupils  are  uniformly  con- 
tracted. Ursemic  coma  is  distinguished  from  epileptic  coma  by  the  ante- 
cedent history  of  the  patient,  the  presence  of  bloody  froth  about  the  mouth, 
and  the  indentations  on  the  side  of  the  tongue  ;  from  alcoholic  coma,  by  the 
temperature,  and  the  character  of  the  breathing,  which  is  "puffy"  in  alco- 
holic coma,  and  a  hissing  stertor  in  uremia.  In  all  cases  of  coma,  an  ex- 
amination of  the  urine  is  important  before  reaching  a  diagnosis. 

Prognosis. — From  experiments  as  well  as  from  the  clinical  history  of  acute 
ursemia,  it  is  evident  that  the  primary  cause  of  death  is  a  poison,  the  exact 
nature  of  which  is  obscure,  but  which  resembles  in  its  action  narcotic 
poisons.     This  poison  acts  primarily  on  the  nerve  centres,  and  produces* 


ACUTE   TJE^MIA.  541 

changes  in  the  blood  which  interfere  with  or  arrest  oxygenation.  This 
action  is  followed  by  certain  structural  changes  in  the  different  tissues  of 
the  body.  When  this  poison  is  introduced  into  the  circulation  in  small 
quantities,  so  that  its  elimination  can  be  effected  in  a  short  time,  it  only 
temporarily  disturbs  the  functions  of  organic  life ;  but  when  it  is  intro- 
duced in  large  quantities,  oxygenation  of  the  blood  is  arrested,  and  it  under- 
goes certain  changes  which  render  it  incapable  of  supporting  life.  The 
prognosis,  then,  in  each  case  will  depend  upon  the  amount  of  the  poison, 
and  the  length  of  time  the  system  is  under  its  influence. 

If  the  symptoms  of  excessive  ursemic  toxaemia  are  present,  and  there  are 
evidences  that  the  poisoning  has  been  going  on  for  a  considerable  time,  the 
prognosis  is  much  more  unfavorable  than  when  the  acute  uraemic  symptoms 
are  mild  and  of  recent  date. 

Treatment. — It  is  claimed  that  the  most  important  thing  to  be  accom- 
plished in  the  treatment  of  acute  uraemia,  is  to  secure  as  rapidly  as  possible 
a  free  eliminative  action  of  the  skin,  bowels,  and  kidneys.  The  favorite 
method  of  elimination  is  by  diaphoresis,  accomplished  by  the  hot-air  baths. 
Pilocarpin  has  recently  been  used  to  accomplish  the  same  results.  In  con- 
nection with  diaphoresis,  a  vicarious  action  of  the  bowels  is  induced  by  the 
administration  of  drastic  j)urgatives,  such  as  elaterium,  pulvis  purgans  and 
scammony.  The  testimony  in  regard  to  the  use  of  diuretics  is  conflicting. 
Many  object  to  their  use,  on  the  ground  that  inflamed  organs  should  not 
be  stimulated. 

Digitalis  acts  efficiently — is  diuretic  without  stimulating  the  kidneys. 
It  increases  the  power  of  the  heart's  action  and  increases  the  tension  in  the 
Malpighian  tufts.  The  diminished  secretion  of  urine  is  due  to  obstruction 
in  the  capillary  circulation  of  the  kidneys.  Digitalis,  by  increasing  the 
heart  power,  overcomes  such  obstruction.  To  obtain  its  effects  in  such  con- 
ditions, larger  doses  are  required  than  are  usually  administered.  My  rule 
of  practice  in  these  cases  is  to  give  half  an  ounce  of  the  infusion  every  three 
hours  for  twenty-four  hours,  or  at  least  until  its  specific  effect  is  produced. 
In  the  majority  of  severe  cases  of  acute  ureemia,  when  the  patient  is  in 
convulsions  or  coma,  the  excretory  functions  of  the  skin,  bowels  and  kid- 
neys are  completely  arrested,  so  that  diaphoresis  cannot  be  induced,  or,  if 
induced,  it  is  not  eliminative,  and  the  bowels  do  not  respond  to  purgatives 
although  the  patient  may  swallow  them  in  large  doses,  and  digitalis  in 
large  doses  fails  to  restore  the  urinary  secretion.  At  one  time  under  such 
circumstances  free  general  blood-letting  was  used  extensively,  but  the  result 
was  unsatisfactory. 

If  there  is  acute  uraemia,  the  avenues  of  elimination  are  shut  off,  and  the 
question  arises: — what  means  have  we  to  counteract  this  uraemic  poison,  and 
open  again  the  avenue  of  its  elimination,  or,  at  least,  to  hold  the  patient  until 
the  normal  eliminating  process  shall  be  re-established  ?  The  first  indication 
is  to  diminish  reflex  sensibility,  and  subdue  spasmodic  muscular  paroxysms, 
for  these,  if  continued,  will  either  directly  terminate  life,  or  end  in  equally 
fatal  insensibility.  The  remedy  which  for  some  years  has  been  employed 
for  the  accomplishment  of  these  results  is  chloroform.     It  has  been  exten- 


542  DISEASES   OF   THE    KIDNEYS. 

sively  used,  and,  I  believe,  is  regarded  as  the  safest  and  most  reliable  means 
for  controlling  nrsemic  convulsions.  Hydrate  of  chloral  and  bromide  of 
potash  are  also  more  recently  recommended,  but  their  action  is  not  swift  or 
powerful  enough.  Although  many  authorities  recommend  the  use  of  chlo- 
roform in  uraemic  eclampsia,  few  make  mention  of  its  employment  in  acute 
uraemia  independent  of  the  puerperal  state.  Its  only  known  clinical  effect 
is  to  control  muscular  spasm,  and  in  a  large  projaortion  of  cases  it  fails  to 
give  more  than  temporary  relief  to  those  patients  who  pass  from  successive 
convulsions  into  a  state  of  complete  coma,  and  die  without  any  apparent 
neutralizing  effect  from  the  chloroform.  In  the  few  cases  in  which  I  have 
administered  chloroform  in  non-puerperal  ursemic  convulsions,  it  has 
seemed  to  me  to  have  no  other  effect  than  to  arrest  convulsive  movements 
by  rapidly  hastening  the  patient  into  a  state  of  insensibility.  In  no  in- 
stance have  I  known  its  administration  to  be  immediately  followed  by  di- 
aphoresis or  a  return  of  the  urinary  secretion.  It  has  seemed  to  be  more 
diflBcult  to  establish  diaphoresis  or  diuresis  by  diaphoretics  and  diuretics  in 
patients  with  urgemia  to  whom  chloroform  had  been  administered,  than  in 
those  who  had  not  taken  it. 

Therefore,  I  believe  that  while  chloroform  temporarily  controls  muscular 
spasm,  it  prejudices  the  chances  of  ultimate  recovery  by  the  changes  its  in- 
halation produces  in  the  blood,  which  changes  increase  rather  than  retard 
the  development  of  the  ursemic  toxaemia.  With  these  impressions  one  nat- 
urally seeks  an  agent  which  not  only  has  the  power  to  control  muscular 
spasm,  but  shall  also  at  the  same  time  tend  by  its  action  to  reopen  the  ave- 
nues of  elimination,  either  by  counteracting  the  effects  of  the  ursemic  poi- 
son on  the  nerve  centres,  and  thus  facilitating  the  action  of  diuretics  and 
diaphoretics,  or  by  acting  itself  directly  as  an  eliminative. 

I  believe  morphine  administered  hypodermically  to  be  such  an  agent. 

There  are  two  questions  that  very  naturally  present  themselves  in  con- 
nection with  the  use  of  morphine  in  acute  uraemia. 

First.  Can  morphine  in  full  doses  be  administered  without  danger  to 
patients  with  acute  uraemia  ? 

Secondly.  What  are  the  effects  of  such  administrations  ? 

If  one  turns  to  recognized  authorities  for  an  answer  to  the  first  of  these 
inquiries,  he  will  find  that  nearly  all  make  mention  of  the  use  of  opium  in 
urasmic  toxaemia  only  to  warn  against  the  danger  attending  its  administra- 
tion. During  the  first  years  of  my  professional  life,  I  regarded  opium  as 
one  of  the  most  dangerous  remedial  agents  that  could  be  administered  to 
urgemic  patients,  rarely  daring  to  give  more  than  five  grains  of  Dover's 
powder  to  a  patient  with  albuminous  urine,  and  if  fatal  coma  followed 
such  administration,  more  than  once  do  I  remember  to  have  felt  that  a  Do- 
ver's powder  which  I  had  administered  might  have  been  the  cause  of  the 
fatal  coma.  In  1868  I  administered  my  first  hypodermic  injection  of 
morphine  to  a  patient  with  acute  uraemia.  The  effects  which  followed  its 
administration  in  this  case  taught  me  that  in  some  cases  with  marked  urae- 
mic symptoms  morphine  could  be  administered  hypodermically  not  only 
safely,  but  with  apparent  advantage.     Since  that  time  I  have  used  mor- 


REKAL   HYPEREMIA.  543 

phine  hypodermically  in  the  treatment  of  these  patients,  not  only  during 
the  premonitory  stage,  but  also  during  the  active  manifestations  of  ursemic 
intoxication,  and  its  administration  has  been  uniformly  followed  by  good 
results.     In  no  instance  have  I  caused  a  fatal  narcotism. 

From  the  histories  of  quite  a  large  number  of  puerperal  and  non-puerpe- 
ral cases  of  acute  uraemia,  in  which  morphine  was  successfully  used,  T  have 
reached  the  following  conclusions  :  ^— first,  that  morphine  can  be  adminis- 
tered hypodermically  to  some  if  not  to  all  patients  with  acute  uraemia  with- 
out endangering  life.  Secondly,  that  the  almost  uniform  effect  of  morphine 
so  administered,  is,  first,  to  arrest  muscular  spasms  ;  secondly,  to  establish 
profuse  diaphoresis  ;  thirdly,  to  facilitate  the  action  of  cathartics  and 
diuretics,  especially  the  diuretic  action  of  digitalis.  Thus,  morphine 
administered  hypodermically  becomes  a  powerful  eliminating  agent.  The 
rule  is  to  give  small  doses  at  first,  not  to  exceed  one-sixth  of  a  grain.  If 
convulsions  threaten,  and  a  small  dose  does  not  arrest  the  muscular  spasm, 
it  may  be  increased  to  one-quarter  or  one-half  of  a  grain,  and  the  hypo- 
dermics may  be  repeated  as  often  as  every  two  hours.  It  must  be  given 
in  suflBcient  quantities  to  control  convulsions ;  neither  the  contraction  of 
the  pupils  nor  the  number  of  the  respirations  is  a  reliable  guide  in  its 
administration. 

I  would  not  discard  all  (perhaps  none)  of  those  means  which  have  been 
relied  on  for  the  relief  of  patients  in  acute  uraemia,  but  would  urge  that 
hypodermic  injections  of  morphine  not  only  control  muscular  spasms,  but 
aid  in  establishing  the  eliminating  processes,  and  thus  become  another 
means  of  saving  life  in  these  often  fatal  cases.  Dry  and  wet  cupping,  leech- 
ing and  poulticing  over  the  loins  may  be  employed  to  aid  in  this  re-estab- 
lishment of  the  suppressed  renal  function. 

DISEASES    OF    THE    KIDNEYS 

will  be  considered  in  the  following  order  : 

I.  Renal  Hyper cBinia.  VII.   Cystic  Kidney. 

II.   Renal  HemorrJiage.      (Embo-  VIII.  Reiial  Calculi. 

lism  and  Infarction. )  IX.  New  Groiuths.     (Cancer,  etc. ) 

III.  BrigJifs  Diseases.  X.  Parasites.     (Hydatids.) 

IV.  Pyelitis.  XI.  Perinephritic  Abscess. 
V.  Acute  Suppurative  Nephritis.  XII.  Hcematuria. 

("Surgical  Kidney.")  XIII.   Chyluria. 

VI.  Hydronephrosis.  XIV.   Cystitis. 

EENAL    HYPEREMIA. 

{Congestion.) 

Eenal  hyperaemia  may  be  active  or  passive.  Passive  renal  hyperaemia,  or 
congestion,  is  almost  always  due  to  a  mechanical  obstruction  of  the  venous 
circulation,  and  is  sometimes  called  ''chronic  renal  congestion." 

Morbid  Anatomy. — Active  renal  hyper cemia  has  its  seat  mainly  in  tho 

1  New  York  Med.  Rec,  Aug.  1,  1873. 


544 


DISEASES    OF   THE   KIDN'EYS. 


renal  arteries  and  in  the  Malpighian  tufts.  The  kidneys  are  much  increased 
in  size  ;  the  hyperaemia  may  involve  the  cortical  or  medullary  portion,  and 
may  be  more  intense  in  one  portion  than  another  ;  it  is  usually  most  marked 
at  the  base  of  the  pyramids.  The  kidneys  are  of  an  unnaturally  dark  color, 
their  capsule  is  non-adherent,  their  surface  is  smooth,  and  they  are  softer 
and  moister  than  normal. 

071  section,  dark  spots  are  noticed  scattered  over  the  cut  surface  which 
correspond  to  the  Malpighian  tufts,  and  the  vessels  of  the  cones  are  filled 
with  blood.  A  dark  fluid  follows  the  section,  which  is  partly  serum  and 
partly  blood.  The  stars  of  Verheyen  are  prominent.  A  microscopical  ex- 
amination shows  that  these  changes  are  due  to  an  engorgement  of  the  blood- 
vessels, and  a  more  or  less  abundant  infiltration  of  serum  into  the  inter- 
tubular  structure  of  the  kidneys. 

Passive  liypercemia,  or  '^chronic  renal  congestion,"  has  its  seat  in  the 
veins,  which  are  overfilled  with  venous  blood,  while  the  amount  of  blood 
contained  in  the  arteries  may  be  even  less  than  normal.  The  kidneys  are 
but  slightly,  if  at  all,  increased  in  size,  are  firmer  than  normal,  their  cap- 
sule is  non-adherent,  and  their  surface  is  smooth  and  of  a  uniform  red  color. 
In  chronic  cases  the  surface  is  uneven.  The  tubular  epithelium  is  gran- 
ular, opaque  and  fiattened  from 
coagulated  fibrin  which  may 
partially  fill  the  lumen  of  the 
tubes.  The  convoluted  tubules 
may  be  filled  with  blood.  The 
stroma  is  unaltered.  Hypersemia 
of,  and  hemorrhages  into  the 
mucous  membrane  of  the  pelvis 
and  ureters  may  occur  in  A'ery 
severe  cases. 

Upon  section,  it  will  be  noticed 
that  the  medullary  portion  is  of 
a  darker  color  than  the  cortical, 
that  the  cortical  portion  has 
streaks  of  red  rather  than  an 
uniform  redness.  The  Malpig- 
hian tufts  are  not  prominent. 
The  veins  are  dilated,  tortuous, 
and  varicose,  the  abnormal  hard- 
ness of  the  kidney  being  due  to 
the  constant  distended  condi- 
tion of  the  efferent  capillary 
vessels.  The  epithelium  of  the 
convoluted  tubes  may  have  a 
peculiar  stiff  appearance,  not 
the  result  of  an  inflammatory 
process.  Coagula  of  yellowish  hyaline  material  are  sometimes  found  in  the 
glomeruli,  arranged  in  concentric  layers. 


Fig.  133. 
Eenal  Hj'pereemia. 
Vertical  section  of  part  of  a  Malpiqhian  Pyramid  in  Pass- 
ive Hypercemia. 

A,  A.  Collecting  tubes. 

B,  B.  Dilated,  tortious  vessels. 

C,  C  Collecting  tubules  containing  blood,     x  300. 


RENAL   HYPERiEMIA.  545 

Both  these  varieties  of  hypertemia  may  lead  to,  or  be  accompanied  by 
inflammatory  processes  in  the  tubular  and  intertubular  structures  of  the 
kidneys.  Active  hyperemia  may  be  the  stepping-stone  to  acute  parenchy- 
matous nephritis.  It  is  only  a  step  from  congestion  to  some  of  the  more 
chronic  inflammatory  forms  of  kidney  disease.  When  to  passive  hyperae- 
mia  there  is  added  inflammatory  swelling  of  the  epithelium,  of  the  tubules, 
the  kidneys  will  be  enlarged,  and  the  epithelium  of  the  convoluted  tubules 
will  be  swollen,  granular,  fatty,  and  disintegrated.  When  the  inflamma- 
tion extends  to  the  stroma  the  kidneys  will  be  diminished  or  enlarged,  but 
retain  the  stony  hardness  of  non-inflammatory  congestion.  The  capsule 
will  be  adherent,  and  on  section  the  cortical  portion  will  be  slightly  dimin- 
ished, and  there  will  be  patches  of  new  connective-tissue  throughout  its  sub- 
stance,— the  process  not  being  unlike  the  "cirrhotic"  form  of  Bright's. 
If  the  passive  hyperaemia  is  due  to  heart  disease,  the  kidneys  will  be  in- 
creased in  size,  the  capsule  will  be  non-adherent  and  the  surface  smooth. 
The  cortical  substance  will  be  pale  instead  of  red,  and  the  medullary  portion 
of  a  darker  color  than  normal,  the  gross  appearance  very  closely  resembling 
that  of  the  "large  white  kidney."  There  will  be  well  marked  changes 
in  the  epithelium  of  the  tubules,  in  the  stroma,  and  in  the  walls  of 
the  arteries.  These  are  the  large  stony  kidneys  of  chronic  heart  dis- 
ease. Chronic  passive  hyperaemia  is  sometimes  called  "cyanotic  indura- 
tion." 

Etiology. — Active  renal  hypercemia,  or  fluxion,  may  be  produced  by  ex- 
posing the  body  to  sudden  changes  of  temperature,  by  any  of  the  blood 
poisons  which  give  rise  to  the  acute  infectious  diseases,  by  malaria  (and  it 
is  sometimes  a  prominent  feature  of  a  violent  malarial  paroxysm),  by  the 
prolonged  and  excessive  use  of  certain  drugs  which  give  rise  to  irritation  of 
the  urinary  passages,  as  cantharides,  copaiba,  turpentine,  cubebs,  nitrate  of 
potash,  carbolic  acid,  etc.,  and  by  the  irritating  condition  of  the  urine  in 
diabetes,  cholsemia,  etc.  It  sometimes  accompanies  Basedow's  disease. 
The  early  stage  of  acute  inflammations  of  the  kidneys  is  attended  by  active 
renal  hyperemia.  Paralysis  of  the  vaso-motor  nerves  of  the  kidneys  (sup- 
posed to  occur  in  hysteria  and  allied  states,  polyuria,  etc. )  is  said  to  be  a 
cause  of  active  renal  hyperaemia. 

Passive  renal  Tiypercemia,  or  renal  congestion,  has  its  most  frequent 
cause  in  organic  disease  of  the  heart.  All  valvular  lesions  of  the  heart,  or 
structural  diseases  of  the  cardiac  valves  which  interfere  with  venous  return, 
come  under  this  head,  as  well  as  all  those  forms  of  pulmonary  disease 
which  interfere  with  the  pulmonary  circulation,  and  are  followed  by  dilata- 
tion of  the  right  heart,  e.  g.,  emphysema  and  fibroid  phthisis.  Congestion 
may  also  be  produced  by  pressure  on  the  emulgent  renal  veins  or  inferior 
vena  cava  in  pregnancy  and  by  other  abdominal  tumors.  The  formatioa 
of  a  thrombus  is  also  followed  by  it.  Some  of  the  cases  of  so-called  albu- 
minuria in  pregnancy  are  examples  of  passive  hyperaemia  from  the  pressure 
of  the  pregnant  uterus. 

Symptoms. — The  symptoms  of  both  varieties  of  renal  hypereemia  are  for 
the  most  part  confined  to  changes  in  the  urine.  In  active  hyperaemia  the 
35 


54:6  DISEASES    OF   THE    EID^TEYS. 

urine  is  scanty,  high  colored,  of  high  specific  gravity,  containing  a  large  per- 
centage of  albumen,  with  few  blood  casts  and  hyaline  tube  casts. 

In  passive  hyper mmia,  without  any  structural  changes  in  the  kidneys,  the 
quantity  of  the  urine  is  not  much  diminished,  its  specific  gravity  remains 
about  normal,  the  amount  of  albumen  is  small,  and  only  small  hyaline 
casts  are  present.  It  is  often  of  an  acid  reaction,  and  deposits  urates.  The 
amount  of  urea  is  a  little  below  normal.  The  simultaneous  appearance  of 
blood  and  albumen  in  the  urine  is  so  common  in  renal  congestion  that  the 
presence  of  albumen  alone,  without  blood  globules,  almost  excludes  it.  Be- 
sides the  changes  in  the  urine  in  active  hyperemia,  there  is  usually  slight 
oedema  of  the  face  and  lower  extremities,  with  nausea  and  a  persistent 
headache. 

Passive  hypersemia  is  often  produced  by  chronic  cardiac  or  pulmonary 
disease,  attended  by  a  cough  with  a  watery  blood-stained  expectoration,  and 
by  dyspnoea  that  often  becomes  so  severe  as  to  prevent  the  patient  from 
lying  down.  The  cougli  and  dyspnoea  depend  in  part  upon  the  accompany- 
ing heart  or  pulmonary  disease,  but  there  is  also  a  nervous  element  in  it 
which  is  characteristic  of  the  renal  complication.  There  is  loss  of  appe- 
tite, nausea  and  occasional  vomiting ;  there  is  a  continuous  headache,  rest- 
lessness and  insomnia,  which,  added  to  the  dyspnoea,  make  the  patient's 
condition  distressing.  There  is  loss  of  flesh  and  strength,  and  steadily  in- 
creasing ansemia.  These  symptoms  gradually  become  worse,  and  general 
dropsy  develops,  and  the  patient  may  die  from  the  general  anasarca,  or  from 
convulsions  and  coma. 

The  history  of  these  cases  varies  greatly  :  some  get  progressively  worse, 
others  pass  from  an  apparently  hopeless  condition  to  one  of  comparative 
comfort,  and  these  attacks  are  repeated  at  intervals  for  a  long  period. 
However  desperate  the  condition  may  appear,  a  return  of  a  comparatively 
comfortable  condition  is  always  possible.  That  form  of  renal  congestion 
which  is  so  often  met  with  in  pregnancy  is  usually  accompanied  by  the 
presence  of  albumen  and  casts  in  the  urine  before  any  other  symptoms  are 
developed ;  afterward  the  patients  become  anaemic,  and  suffer  from  per- 
sistent headache,  vomiting,  and  oedema  of  the  face,  feet  and  legs  ;  they 
become  "water-logged."  In  a  few  cases  the  first  symptom  may  be  a  con- 
vulsion. In  all  cases  the  thing  to  be  dreaded  is  the  onset  of  convulsions, 
which  rapidly  follow  each  other  until  coma  is  reached. 

Differential  Diagnosis. — Eenal  congestion  is  distinguished  from  Briglifs 
disease  by  the  general  condition  of  the  patient,  the  presence  or  absence  of 
cardiac  or  pulmonary  disease,  or  venous  obstruction.  The  urine,  though 
scanty,  is  above  normal  in  specific  gravity,  and  always  deposits  blood, 
renal  epithelium,  or  tube  casts. 

Prognosis. — The  prognosis  in  active  renal  hypersemia,  when  the  cause  is  of 
a  transient  character,  is  good.  Eenal  congestion  which  occurs  in  the  ad- 
vanced stage  of  cardiac  disease  and  pulmonary  emphysema  has  much  to  do 
with  causing  a  fatal  termination,  and  after  it  is  once  developed  it  is  never 
recovered  from.  That  form  of  active  hypersemia  which  occurs  in  congestive 
malarial  fevers  is  sometimes  so  intense  as  to  entirely  arrest  the  function  of 


RENAL   HYPERiEMIA.  547 

the  kidneys,  and  then  it  becomes  a  direct  cause  of  death.  The  renal  con- 
gestion of  pregnancy  is  usually  relieved  by  the  removal  of  its  cause,  which 
should  never  be  delayed  if  the  symptoms  become  urgent. 

Treatment. — The  most  important  thing  to  be  accomplished  in  tlie  treat- 
ment of  active  renal  hypersemia  is  to  find  out,  and  as  quickly  as  possible 
remove  its  cause.  The  treatment  is  to  be  addressed  to  the  kidneys.  Place 
the  patient  in  bed  in  a  room  with  a  temperature  of  80°  F.,  and  apply  a  dozen 
wet  cups  over  the  lumbar  region.  Administer  a  powerful  drastic  purge, 
induce  free  diaphoresis,  and  let  the  patient  drink  freely  of  diluted  muci- 
laginous drinks.  The  hot-air  or  warm  vapor-bath,  and  even  blood-letting 
in  intense  fluxion,  are  to  be  employed.  Camphor  is  advocated  in  some 
cases  of  active  hyperasmia.  In  passive  renai  hyperemia  the  main  thing  to 
be  accomplished  is  to  relieve  the  venous  congestion  ;  it  is  to  remembered 
that  there  is  too  much  blood  in  the  veins  and  too  little  in  the  arteries. 

There  are  three  ways  of  restoring  the  natural  state  of  the  circulation  : — 

1st.  By  general  bleeding. 

2d.  By  increasing  the  force  of  the  heart's  action. 

3d.   By  causing  the.  dilatation  of  the  capillary  arterioles. 

A  free  bleeding  from  one  of  the  large  veins  will  temporarily  relieve  the 
venous  congestion  and  cause  a  better  filling  of  the  arteries,  but  it  exhausts 
the  patient,  and  is  only  admissible  in  the  renal  congestion  of  pregnancy 
when  the  symptoms  are  urgent.  By  increasing  the  propelling  power  of  the 
heart,  the  amount  of  blood  in  the  arteries  is  increased  and  that  in  the  veins 
diminished.  This  is  the  usual  mode  of  procedure  in  the  passive  renal 
hypersemia  which  depends  upon  chronic  heart  and  lung  disease.  Digitalis 
is  the  drug  which  has  been  most  extensively  employed  to  accomplish  this. 
It  must  be  given  in  full  doses  and  continued  until  the  desired  effect  is  in- 
duced. The  best  mode  of  its  administration  is  in  the  infusion  ;  a  tablespoon- 
ful  of  the  infusion  of  the  leaves  may  be  given  every  three  or  four  hours  until 
its  specific  effect  is  produced  or  the  quantity  of  urine  is  greatly  increased. 
Eecently  the  fluid  extract  of  convallaria  in  half-drachm  doses  has  been 
recommended  as  a  substitute  for  digitalis.  My  exjoerience  with  it  has  been 
very  unsatisfactory  ;  its  action  is  not  only  temporary,  but  far  less  certain 
than  digitalis. 

The  drugs  that  seem  to  have  some  power  in  dilating  the  capillaries  and 
arterioles  are  nitrite  of  amyl  and  nitro-glycerine.  The  nitrite  of  amyl  may  be 
given  by  inhalation  in  doses  of  from  three  to  five  drops  every  four  hours. 
The  nitro-glycerine  may  be  given  in  a  one  per  cent,  alcoholic  solution,  one 
drop  every  three  or  four  hours.  It  is  now  two  years  since  I  first  used  nitro- 
glycerine in  renal  disease,  and  under  its  use  albumen  has  disappeared  from 
the  urine  in  quite  a  number  of  instances,  and  remained  absent  so  long  as  the 
patient  continued  the  drug. 

If  counter- irritation  is  employed  it  must  be  mildm  character — a  few  dry 
cups  over  the  lumbar  region,  or  some  mild  embrocation  is  all  that  is  neces- 
sary. The  intestines  should  be  occasionally  unloaded  by  a  full  dose  of 
calomel  combined  with  rhubarb.  When  the  venous  obstruction  is  directly 
mechanical,  as  in  pregnancy  and  fluid  accumulation  in  the  abdominal 


548 


DISEASES    OF   THE   KIDNEYS. 


cavity,  something  may  be  accomplished  by  so  changing  the  position  of  the 
patient  as  to  relieve  the  pressure  on  the  renal  veins. 

If  passive  renal  hyperemia,  especially  in  heart  disease,  is  attended  by 
great  restlessness  and  dyspnoea,  morphine  may  be  given  hypodermically  in 
sufficient  quantities  to  give  relief  and  make  the  patient  comfortable,  even 
though  but  a  small  quantity  of  urine  is  being  passed. 


EEKAL     HEMOREHAGE. 

{UmhoUsm  and  Infarction.) 
Eenal  congestion  and  renal  hemorrhage  are  very  often  associated,  for 
renal  hemorrhage  often  occurs  as  a  result  of  renal  congestion. 

Morbid  Anatomy. — The  anatomical  changes  in  a  kidney  which  is  the  seat 
of  renal  hemorrhage  do  not  differ  essentially  from  those  already  described 
as  present  in  a  renal  hypereemia,  unless  there  are  hemorrhagic  infarctions 
or  renal  calculi.  Blood  may  be  effused  into  the  uriniferous  tubules  or  the 
interstitial  tissue,  giving  rise  to  ecchymotic  spots  varying  in  size,  from 
which,  on  section,  blood  flows  freely.  The  vessels  will  be  found  ruptured, 
and  the  epithelia  and  stroma  of  the  kidney  are  stained  with  blood  pigment. 
The  epithelia  soon  become  opaque,  granular,  and  infiltrated  with  fat,  and 
finally  disintegrate.  Incident  to  the  great  increase  in  the  blood  pressure, 
diapedesis  of  the  red  corpuscles  may  occur ;  this  is  true  renal  hemorrhage, 
having  its  origin  in  the  Malpighian  tufts.  The  blood  escapes  between  the 
vascular  tuft  and  its  capsule,  which  is  slightly  dis- 
tended. ' 

The  most  frequent  form  of  renal  hemorrhage  is  that 
which  occurs  in  connection  with  renal  embolism  and  in- 
farction. Its  occurrence  is  marked  by  the  development 
of  hard  uniform  masses  in  the  cortical  portion  of  the 
kidney  ;  these  masses  are  usually  wedge-shaped,  and 
have  t]ieir  sharp  edges  toward  the  hilus  of  the  kidney 
and  their  base  toward  its  surface.^  They  vary  in  size 
according  to  the  size  of  the  vessel  obstructed  ;  they  may 
be  capillary,  and  then  are  of  very  small  size.  These  in- 
farctions when  first  formed  are  of  a  dark  red  color,  and 
are  as  firm  as  normal  kidney-tissue  ;  very  soon  they  be- 
gin to  change  in  color,  losing  their  dark  red  hue  and 
becoming  lighter,  and  their  centres  present  a  yellowish 
appearance  ;  sometimes  they  undergo  cheesy  change, 
which  always  commences  at  their  centres.  Around 
these  infarctions  a  zone  of  redness  is  formed  ;  this  zone 
is  in  the  normal  kidney-tissue,  beyond  the  infarction. 
mi  vessels  fc"'capmu;  A  Congestion  takes  place  in  the  vessels,  due  to  changes 
liumfmiringtunmid  in  the  urinifcrous  tubes  adjacent  to  the  capillaries  in 
^aitofS£ti/tuMi:  that  portion  of  the  kidney  which  surrounds  the  infarc- 
^l$ing  fmmlhf%tft  ^iou  ;  there  is  also  a  more  or  less  rapid  production  of 
ana  entenng  the  tubule,   eells  in  this  surrounding  zone.     If  the  infarction  does 


Fig.  134. 
Eenal  Hemorrhage. 
Diagram  showing  Hem- 
orrhage  from  the  vas- 
cular tufts  of   the  glo- 
meruli. 


1  Cornil  and  Kanvier. 


"  Rayer's  so-called  "  Bheiimatic  Nephritis.' 


RE]S"AL   HEMORRHAGE. 


549 


by  absorption,  this  zone-change  continues  until  there 
developed  about  the  infarction,  which 
contraction    of    the    tissue,    gradually 


not   disappear 

is  more  or  less  cicatricial  tissue 
shrinks  in  consequence  of  the 
diminishes  in  size,  and  after  a 
time  disappears  altogether,  leav- 
ing only  cicatricial  tissue  to  mark 
its  former  site.  The  surface  of  the 
kidney  may  be  depressed  over  an 
atrophied  infarction. 

On  the  other  hand,  the  produc- 
tion of  cells  may  be  so  rapid  and 
abundant  that  the  entire  mass 
undergoes  purulent  transforma- 
tion, producing  abscesses  which 
will  occupy  the  seat  of  the  infarc- 
tion. This  is  one  of  the  ways  in 
which  abscesses  are  formed  in  the 
kidneys.  In  these  cases  there  is 
always  a  certain  degree  of  sup- 
puration occurring  at  the  margin 
of  the  affected  area.  Again,  these 
infarctions  may  undergo  a  still 
more  rapid  degeneration,  increas- 
ing in  size  and  becoming  necrotic, 
so  that  at  the  autopsy  a  gangre- 
nous mass  is  found  as  the  result  of 
the  necrotic  change  which  has 
taken  place  in  the  infarction.  More  or  less  suppuration  also  attends  it. 
Again,  there  may  be  little  masses  found  scattered  throughout  the  substance 
of  the  kidney,  especially  in  the  cortical  portion,  looking  very  much  like 
ecchymotic  spots,  which  are  simply  capillary  thrombi  :  these  are  usually 
due  to  some  slowing  of  the  circulation  in  the  capillary  vessels.  These 
capillary  thrombi  may  be  very  numerous,  and  they  may  undergo  changes 
similar  to  those  which  take  place  in  the  larger  infarctions. 

At  the  autopsy  the  kidneys  may  be  found  studded  with  minute  abscesses  ; 
unquestionably  these  little  collections  of  pus  are  nothing  more  than  minute 
capillary  infarctions  or  thrombi  which  have  undergone  purulent  transforma- 
tion. Thus  a  single  abscess  or  many  abscesses  of  the  kidney  may  form  as 
the  result  of  infarctions.  This  form  of  renal  hemorrhage  is  especially  liable 
to  occur  in  passive  renal  hypersemia. 

Etiology. — Intense  hypersemia  of  the  kidney  is  a  cause  of  renal  hemor- 
rhage, especially  in  the  first  stage  of  acute  nephritis.  It  may  also  result 
from  injuries,  and  in  connection  with  the  development  and  passage  of  renal 
calculi.  It  may  also  occur  in  connection  with  the  development  of  morbid 
growths  in  the  kidney,  especially  cancer.  Blood  changes,  such  as  occur  in 
purpura,  scurvy,  etc.,  may  cause  it.     Passive  obstructive  hypersemia  from 


Fm.  135 

Renal  UGmorrhage. 

Diagram  illustrating  Renal  Infarction. 

A.  Embolus  in  an  interlobular  artery. 

B.  Cheesy  centime  of  the  infarct. 

C.  C.  Zone  of  redness. 


550  DISEASES    OF   THE    KIDNEYS. 

cardiac  disease  may  become  so  intense  as  to  give  rise  to  it,  witli  or  without 
the  occurrence  of  infarctions. 

Symptoms. — It  is  attended  by  no  constant  or  distinctive  subjective  symp- 
toms. Our  knowledge  of  its  occurrence,  during  life,  rests  almost  exclu- 
sively upon  the  results  of  an  examination  of  the  urine.  Its  existence  can-^ 
not  be  recognized,  unless  the  blood  is  effused  into  the  uriniferous  tubules 
or  into  the  hilus  of  the  kidney  and  discharged  in  the  urine.  At  autopsies, 
large  infarctions  of  the  kidney  are  often  found  which,  during  life,  have  given 
no  indication  of  their  existence,  because  there  was  no  extravasation  of  blood 
into  the  uriniferous  tubules,  and  consequently  no  blood  appeared  in  the 
urine. 

The  course  of  a  renal  hemorrhage  depends  to  a  great  extent  upon  the 
cause  which  produces  it.  When  dependent  upon  the  presence  of  a  renal 
calculus,  the  hemorrhage  occurs  after  every  violent  exertion.  When  it 
arises  from  cancer  or  other  tumors,  it  is  generally  profuse  and  persistent. 
The  bleeding  which  accompanies  inflammation  of  the  kidneys  in  the  infec- 
tious diseases  is  never  severe  ;  it  may  be  so  slight  as  only  to  be  recognized 
by  a  microscopical  examination  of  the  urine.  That  form  of  renal  hemor- 
rhage which  occurs  in  malarial  districts  in  hot  climates  is  usually  profuse 
and  occurs  periodically.  When  it  is  caused  by  an  infarction,  the  patient  is 
usually  seized  with  a  chill  at  the  time  the  infarction  occurs,  followed  by 
pain  in  the  back,  and  more  or  less  nausea  and  vomiting.  If,  therefore, 
these  symptoms  are  developed  in  connection  with  cardiac  disease  or  pyae- 
mia, it  is  evidence  that  renal  infarctions  have  occurred. 

When  valvular  disease  of  the  heart  exists  with  ulcerative  endocarditis  or 
extensive  calcareous  degeneration  of  the  arteries,  embolic  infarction  may  be 
suspected,  when  in  addition  to  the  sudden  appearance  of  blood  and  albu- 
men in  the  urine  there  is  fever  and  vague  pains  in  the  lumbar  regions. 
Small  abscesses,  the  sequelae  of  infarcts  and  circumscribed  spots  of  gangrene, 
cannot  be  diagnosticated. 

Prognosis. — The  prognosis  depends  upon  the  conditions  and  circum- 
stances under  which  the  hemorrhage  occurs.  If  it  occurs  in  connection 
with  renal  calculi  or  cancerous  disease  of  the  kidney,  the  prognosis  is  bad  ; 
life  is  endangered  under  these  circumstances  by  the  exhaustion  produced 
by  the  continued  loss  of  blood.  Occurring  in  connection  with  infectious  dis- 
eases, it  has  no  particular  significance  ;  it  merely  is  an  indication  of  intense 
renal  hyj^erEemia.  When  there  is  reason  to  believe  that  a  hemorrhagic  infarc- 
tion has  occurred  in  the  kidney,  the  event  must  always  be  regarded  as  at- 
tended with  danger  to  life  ;  not  that  it  is  necessarily  fatal,  or  that  the  prog- 
nosis is  necessarily  unfavorable,  but  the  fact  that  infarctions  exist  will  cause 
anxiety  as  to  the  development  of  the  other  degenerative  changes  in  the  kid- 
neys, and  as  to  the  lodging  of  emboli  in  other  parts,  particularly  the  brain. 

Treatment.— The  first  thing  to  be  accomplished  in  its  treatment  is  to  find 
out  and,  if  possible,  remove  its  cause.  In  many  cases  where  the  main  causa- 
tive disease  is  amenable  to  treatment,  the  hemorrhage  does  not  require  any 
special  attention.  During  the  occurrence  of  the  hemorrhage,  the  patient 
should  be  kept  absolutely  at  rest.     If  there  is  danger  of  exhaustion  from 


bright's  diseases.  551 

repeated  and  profuse  hemorrhages,  ice-bags  may  be  applied  to  the  lumbar 
region  and  styptics  administered  internally. 

The  remedial  agent  which  seems  to  have  the  greatest  control  over  these 
hemorrhages  is  tannic  acid,  it  being  expelled  from  the  system  through  the 
kidneys  in  the  form  of  gallic  acid  ;  a  powerful  astringent  is  thus  brought 
directly  in  contact  with  the  uriniferous  tubes  and  urinary  passages.  Ergot, 
muriate  of  iron,  alum,  the  acetate  of  lead,  and  turpentine  are  sometimes  of 
service.  Ergotin  given  hypodermically  in  connection  with  morphia  is  in- 
dicated if  hemorrhages  are  profuse.  If  the  hemorrhage  is  of  malarial  ori- 
gin, large  doses  of  quinine  and  arsenic  are  indicated.  The  danger  from 
acute  renal  inflammation  must  always  be  borne  in  mind  when  renal  hem- 
orrhage occurs  in  connection  with  the  infectious  diseases  ;  the  proper  meas- 
ures for  the  subduing  or  arresting  of  such  inflammations  must  be  promptly 
resorted  to. 


A  very  important,  and  at  the  same  time  a  very  common  group  of  dis- 
eases, are  classed  under  the  comprehensive  term  of  Bright' s  diseases  of  the 
hidneys.  Dr.  Bright  first  called  the  attention  of  the  profession  to  these 
diseases  in  the  year  V^'ri,  at  which  time  he  described,  and  represented  by 
colored  drawings,  various  morbid  appearances  of  the  kidneys,  which  he 
showed  were  of  every-day  occurrence,  and  were  frequently  associated  with 
general  dropsy.  He  was  the  first  systematic  investigator  in  the  field  of 
renal  pathology.  Dr.  Bright  regarded  granular  degeneration  as  the  prin- 
cipal, if  not  the  only  pathological  lesion  present  in  this  class  of  diseases  ; 
he  accordingly  designated  it  as  a  granular  nephritis. 

Eecent  and  more  extended  investigations  have  shown  that  there  are 
several  morbid  processes  in  the  kidneys  of  those  who  are  the  subjects  of 
this  class  of  diseases,  and  that  the  kidneys  in  the  course  of  these  morbid 
processes  present  a  great  variety  of  appearances. 

A  great  number  of  terms  claiming  to  be  exj)ressive  of  these  different 
morbid  appearances  have  been  employed,  such  as  the  large  white  kidney, 
the  large  granular  kidney,  the  small  fatty  granular  kidney,  the  large  and 
small  red  granular  kidney,  the  waxy  kidney,  and  the  cirrhotic  kidney ; 
all  these  different  varieties  are  described  by  different  writers  under  the 
head  of  Bright's  disease. 

Before  studying  the  morbid  changes  which  occur  in  this  group  of  dis- 
eases, it  is  important  to  remember  that  there  are  three  distinct  anatomical 
elements  in  the  kidney  which  are  primarily  or  secondarily  involved  in 
these  changes ;  namely,  the  uriniferous  tubules,  the  blood-vessels,  and  the 
intertubular  tissue  (or  stroma).  In  the  different  kidney  changes  included 
in  Bright's  diseases,  the  morbid  processes  begin  in  one  of  these  three  ele- 
ments, and  it  is  possible  to  divide  this  group  of  diseases  into  classes  which 
shall  correspond  to  the  anatomical  elements  primarily  affected.  Eor  in- 
stance, there  is  one  form  in  which  pathological  changes  commence  in  the 
uriniferous  tuhules  ;  another  in  which  they  commence  in  the  walls  of  the 


552  DISEASES   OF  THE   KIDTvTEYS. 

vessels,  and  another  in  which  they  commence  in  the  intertubular  tissue. 
All  these  morbid  changes  may  be  present  in  the  same  kidney,  but  by  care- 
ful investigation  one  is  enabled,  in  many  instances,  to  determine  in  which 
the  primary  morbid  processes  commenced. 

I  shall  describe  Bright's  diseases  under  the  following  heads  : — 

First.  A  form  in  which  the  morbid  changes  commence  in  the  uriniferous 
tubules,  designated  parenchymatous  nephritis,  tubular,  diffuse,  catarrhal, 
croupous,  and  desquamative  nephritis. 

Second.  A  form  in  which  the  morbid  changes  commence  in  the  inter- 
tubular tissue,  designated  the  cirrhotic  form  of  Bright's  disease,  the  hob- 
nailed, "gin-drinker's,"  gouty,  or  "red  granular"  kidney. 

Third.  A  form  in  which  the  morbid  changes  commence  in  the  walls 
of  the  blood-vessels,  designated  the  amyloid  form  of  Bright's  disease, 
waxy  or  lardaceous  degeneration  of  the  kidney ;  it  were  more  in  keeping 
with  modern  pathology  to  describe  this  variety  under  the  head  of  "  de- 
generations of  the  kidney." 

Clinically  there  can  be  readily  recognized  two  well-defined  varieties  of 
Bright's  disease, — the  acute  and  the  chronic. 

ACUTE    BEIGHt's    DISEASE. 

Acute  Bright's  disease  is  a  tubular  inflammation  which  may  be  wholly 
recovered  from,  prove  fatal,  or  lead  to  chronic  parenchymatous  nephritis. 

Morbid  Anatomy. — The  gross  and  microscopical  appearances  of  the  kid- 
neys in  acute  Bright's  disease  will  vary  according  to  the  intensity  and  char- 
acter of  the  processes  which  attend  its  development.  The  kidneys  are 
usually  increased  in  size,  their  capsule  non-adherent,  their  surface  smooth 
and  mottled,  presenting  an  irregular  combination  of  red  vascular  engorge- 
ment and  unnatural  pallor ;  sometimes  they  are  of  a  dark  purplish  color 
dotted  here  and  there  with  spots  of  ecchymosis.  The  stars  of  Verheyen 
are  more  or  less  dilated  and  the  kidneys  are  softer  than  normal. 

On  section,  the  cortical  portion  is  relatively  increased  in  size,  and  is  dot- 
ted over  its  entire  cut  surface  with  dark  or  bright  red  points,  which  cor- 
respond to  the  situation  of  the  Malpighian  tufts,  which  in  some  instances 
stand  out  prominently  upon  its  cut  surface.  The  cortical  substance  be- 
tween the  Malpighian  tufts  may  be  of  a  paler  color  than  natural.  Some 
distinguish  between  a  "red"  and  a  "pale"  kidney  in  acute  Bright's. 
The  engorgement  will  usually  be  most  marked  at  the  base  of  the  pyramids, 
at  the  junction  of  the  cortical  and  medullary  substance — in  the  arterial 
arcade.  The  medullary  portion  will  be  of  a  darker  color  than  normal, 
darker  even  than  the  cortical  portion  ;  sometimes  it  will  present  a  stria- 
ted appearance  (red  and  white  lines  alternating),  the  lighter  lines  corre- 
sponding to  the  changed  uriniferous  tubes. 

The  lining  membrane  of  the  pelvis  of  the  kidney  is  usually  congested. 
The  inflammation  of  the  mucous  membrane  of  the  pelvis  and  calicos  is 
attended  by  exudation  of  a  turbid  fluid  containing  cells. 

When  such  a  kidney  is  examined  microscopically ,  it  may  be  found  to  pre- 


ACUTE   BRIGHT'S    DISEASE. 


553 


First,  the  epithelial  lining  of  the  tu- 


sent  quite  a  variety  of  appearances, 
bales  may  become  partially  or 
completely  lifted  from  its  nor- 
mal situation,  and  the  tubules 
become  more  or  less  filled  with 
cells — the  changes  correspond- 
ing to  those  which  occur  in  ca- 
tarrhal inflammations  of  the  mu- 
cous surfaces.  The  cells  of  the 
convoluted  tubes  of  the  cortex 
will  have  undergone  cloudy 
swelling  ;  and  in  them  and  in 
the  looped  tubes  of  H  e  n  1  e 
the  epithelia  are  granulo-fatty. 
These  changes  are  common  in 
the  acute  Bright's  of  fevers. 
By  pressing  on  the  top  of  a  Mal- 
pighian  pyramid  a  turbid  fluid 

exudes,  containing  granular  and  Acute  Bright's  Disease. 

fattv     eoithelial      cells      hvaline  ^^^^^on  of  the  cortex  of  a  Kidney  sJiowing  ^^  cloudy  swell- 
J         ir  '        J         _  iwg',"  etc. 

casts   and  pus  cells.      There  will       a.  Part  of  a  capsule  of  a  lUalpigMan  body. 

11  1  1-1     •     ni     JB,  S.  Convoluted  tr/bes  showing  the  cloudy,  swollen  epithe- 

also    be    more  or    less    cell    mhl-  Uum.    The  nuclei  are  obscured. 

+      J-'^-r,    r.-..^n-,v^/-l    +!> /^    4-1-1 1-> n  1 /^c     4 r",  ^  Ascendtng  Umb  of  Henh^ s  loop. 

tration    arouna    tne   lUDUieS     in        2>.  SUgU  round-cetl  infUtralion  in  intertubular  tissue. 

the  intertubular  tissue.'     Some  ""  ^^' 

cases  are  very  mild,  the  epithelia  are  "cloudy,"  and  red  and  white  cor- 
puscles and  hyaline  casts  are  found  in  the  tubes. ^ 

Again,  in  another  class  of  cases  the  centre  of  the  uriniferous  tubes  will 
contain  a  hyaline  material  which  resembles  coagulp  ,ed  fibrin  ;  this  hyaline 
material  may  have  mingled  with  it,  or  may  be  surrounded  by,  epithelium 
and  blood  globules,  and  it  resembles  fibrinous  inflammatory  exudation.' 

Again,  in  another  class  of  cases  the  epithelial  cells  of  the  uriniferous 
tubes  become  cloudy,  their  nuclei  disappear,  and  they  become  distended 
and  granular  ;  desquamation  follows,  and  the  tubes  become  filled  with 
broken-down  epithelium  and  fatty  matter.  The  epithelia  in  a  few  cases 
undergo  simple  atrophy.  In  some  cases  of  acute  Bright's  disease  all  these 
processes  may  be  present  at  the  same  time  in  the  same  kidney.  In  addition 
to  these  tubular  changes,  more  or  less  cell  development  takes  place  in  the 
intertubular  structure.  In  scarlatinal  nephritis  exudative  processes  co- 
exist ;  *  small  cells  and  nuclei  form  abundantly  in  the  vascular  tuft  of  the 
glomerulus,  and  at  its  centre  or  upon  the  vascular  loops  a  compact  ball  is 
formed,  wherein  the  small  vessels  of  the  glomerulus  are  matted  together  by 
an  embryonic  connective-tissue,  infiltrated  with  lymph  cells  In  the  latter 
part  of  this  stage,  if  the  inflammatory  stimulus  is  constant,  the  contents 

•  Celt  accumulations  about  the  glomeruli  and  tubuli  contorti  are  said  by  Traube  to  be  primary,  and  the 
epithelial  changes  to  be  secondary. 
2  Wagner  calls  this  "  hemorrhagic  catarrhal  nephritis,"  and  Cohnheim  calls  it  "  glomerulo-nephritis." 
'  Reinhardt  compared  this  form  of  acute  Bright's  disease  to  pneumonia.— 4«n«/.  d.  Gharite,  Berlin- 
♦Kelsch  and  Klebs  describe  peculiar  morbid  occurrences  in  scarlatinal  nephritis. 


554 


DISEASES    OF   THE    KIDNEYS. 


Fig.  137. 
Acute  Bright's  Disease. 

Section  of  the  Coi'tical  portion  of  a  Kidney,  show- 
ing advanced   degenerative   changes  in   the 
parenchyma. 
A,  A.  Convoluted  t-ubules  filed  with  broken-down 
epithelium  and  gramdo-fatty  matter. 

B.  Swollen  epithelium  of  one  of  Henle^ s  tubes. 

C.  A  collecting  tnlnde.     Epithelium  nearly  nor-    occasionally 


mal. 


350. 


of  the  tubules  become  clianged  into  an  amorphous  mass.     In  some  cases 
swarms  of  micrococci  are  found  in  the  blood-vessels.     In  most  cases  these 

processes  quickly  terminate  either 
in  recovery  or  death  ;  in  a  few  they 
become  chronic.  When  blood  extra- 
vasations are  abundant  in  acute 
Bright's  the  name  ''  hemorrhagic 
nephritis  "  has  been  given  to  it. 

Etiology. — Its  most  common  cause 
in  the  adult  is  exposure  of  the 
surface  to  sudden  changes  of  tem- 
perature, as  is  indicated  by  the  class 
of  subjects  in  which  it  is  most 
liable  to  occur — bakers,  firemen, 
moulders,  and  those  whose  occu- 
pation subjects  them  to  sudden, 
repeated  changes  of  temperature. 
Again,  it  occurs  among  those  whO' 
are  addicted  to  the  use  of  alcohol : 
they  may  not  be  habitual  drinkers 
or  greatly  intemperate,  but  they 
go  on  a  spree,"  and 
while  in  a  state  of  intoxication  expose 
their  surface  to  sudden  changes  of  temperature,  or  to  prolonged  cold 
after  violent  exercise.  Under  these  circumstances  it  is  not  the  alcohol 
that  develops  the  tubular  inflammation,  but  the  sudden  changes  of  tem- 
perature to  which  these  persons  subject  themselves  in  consequence  of 
such  indulgence.  The  daily  use  of  alcohol  may  be  indulged  in  for  years 
without  leading  to  acute  Bright's  disease,  provided  the  individual  exercises 
care  in  regard  to  exposure,  and  therefore  it  should  not  be  included  in  the 
list  of  its  direct  causes. 

Occasionally  it  happens  that  a  very  trifling  exposure  to  sudden  changes 
in  temperature  is  sufficient  to  develop  it,  such  as  sitting  in  a  draught  of  air 
and  exposing  the  lightly  covered  loins  to  a  current  of  cold  air  while  the  in- 
dividual is  in  a  heated  condition.  In  this  climate,  the  failure  to  wear  flan- 
nel next  the  body  throughout  the  year  involves  the  risk  of  developing  at 
some  time  an  inflammatory  process  in  the  uriniferous  tubules.  It  is  not 
clear  how  such  exposure  excites  tubular  inflammation,  Runeberg  states 
that  congestion  (e.  g.,  passive  hypergemia)  and  the  consequent  slowed  cir- 
culation and  diminished  pressure  in  the  glomeruli  is  the  cause  of  the  al- 
buminuria or  tubular  inflammation.  The  theory  that  the  nephritic  in- 
flammation is  due  to  the  reflex  influence  of  the  nervous  system — there  being 
a  connection  between  the  sympathetic  nervous  system  and  the  surface  of 
the  body — rests  on  the  same  basis  which  is  employed  to  explain  the  occur- 
rence of  pneumonia  and  bronchitis  after  exposure  to  cold. 

Another  very  common  cause  of  acute  Bright's  disease  is  the  circulation 
of  morbid  elements  in  the  blood ;  such  elements  are  very  numerous,  em- 


ACUTE   BEIGHT's    DISEASE.  555 

bracing  all  those  poisons  which  give  rise  to  specific  forms  of  infectious  dis- 
eases. The  infection  of  scarlet  fever  is  one  of  its  most  frequent  causes, 
especially  in  childhood.  Every  epidemic,  however,  is  not  attended  by 
renal  complications,  for  there  are  some  seasons  when  a  type  of  scarlatina 
prevails,  in  which  scarcely  a  case  will  have  renal  complications  ;  while  dur- 
ing other  seasons  almost  every  case  will  be  attended  by  them.  Such  vari- 
ations can  only  be  accounted  for  by  regarding  the  occurrence  of  nephritic 
complications  as  dependent  upon  a  difference  in  the  scarlatinal  infection. 

Another  class  of  causes  is  included  under  the  head  of  renal  irritants 
which  may  be  introduced  into  the  stomach  :  among  these  are  the  balsam 
of  copaiba,  spirits  of  turpentine,  cantharides,  phosphorus,  arsenic,  and 
lead.  The  prolonged  use  of  these  remedies,  or  their  administration  in  over- 
doses, not  infrequently  gives  rise  to  tubular  nephritis.  Another  cause  is 
acute  internal  inflammations,  especially  inflammation  of  the  lungs  :  one 
should  always  be  on  the  watch  for  its  occurrence  during  a  pneumonia. 

Another  frequent  cause  is  pregnancy.  It  was  formerly  supposed  that 
pregnancy  produced  Bright's  disease  by  interference  with  the  renal  circu- 
lation from  pressure  on  the  renal  veins  ;  but  probably  this  is  rarely  its 
cause.  During  pregnancy  there  is  an  abnormal  quantity  of  excrementi- 
tious  material  to  be  carried  out  of  the  system  by  the  kidneys,  which  not 
only  calls  upon  these  organs  for  increased  labor,  but  the  material  elimi- 
nated acts  as  an  irritant  on  the  uriniferous  tubes,  and  tubular  inflammation 
is  the  result.  It  may  occur  at  any  period  of  pregnancy,  but  it  is  rare  be- 
fore the  third  month,  and  is  of  more  frequent  occurrence  during  the  later 
months.  In  connection  with  pregnancy,  this  form  of  kidney  disease  rarely 
terminates  in  chronic  Bright's.  It  often  disappears  rapidly  and  never  re- 
curs, or  it  may  appear  in  successive  pregnancies,  and  finally  lead  to  the  de- 
velopment of  chronic  Bright's  disease.  Again,  passive  renal  hy^DerEemia 
dependent  upon  obstruction  to  the  return  circulation  from  cardiac  or  pul- 
monary lesions,  may  cause  acute  Bright's  disease. 

There  is  a  degeneration  of  the  epithelium  of  the  uriniferous  tubes  which 
occurs  under  certain  circumstances  independent  of  inflammation.  It  is 
not  amyloid  ;  it  is  not,  strictly  speaking,  a  fatty  change  ;  but  it  occurs  dur- 
ing the  degenerative  processes  of  old  age.  This  epithelial  degeneration  of 
the  uriniferous  tubules  is  a  result  of  senile  change.  In  this  sense,  extreme 
old  age  may  be  regarded  as  a  cause  of  tubular  epithelial  degeneration  in  the 
kidneys. 

Symptoms. — The  presence  of  urea  and  its  allies,  kreatin,  kreatinin,  etc., 
in  the  blood  in  abnormal  quantities  gives  rise  to  the  phenomena  which  at- 
tend the  development  of  acute  Bright's  disease.  The  symptom  which  usu- 
ally first  attracts  the  attention  of  a  j)atient  is  oedema  of  the  face.  There 
may  have  been  signs  of  gastric  disturbance  prior  to  its  occurrence,  but  they 
have  not  been  distinctive  in  character.  After  exposure  to  sudden  varia- 
tions in  temperature,  or  after  an  attack  of  some  form  of  acute  infec- 
tious disease,  or  withor.t  any  known  cause,  there  is  noticed  a  slight  puffi- 
ness  about  the  eyes  in  the  morning  ;  if  the  patient  is  anaemic,  the  oedema 
may  appear  in  the  feet  and  ankles  at  the  same  time      This  oedema  usually 


556  DISEASES   OF   THE    KIDN^EYS. 

increases  very  rapidly.  With  the  occurrence  of  the  oedema  there  is  great 
restlessness.  Toward  evening  there  is  a  little  quickening  of  the  pulse  and 
a  slight  rise  in  temperature — never  typical  ;  the  patient  complains  of  head- 
ache, which  increases  in  severity  from  hour  to  hour ;  at  times  he  is  very 
drowsy.  Complete,  sudden,  but  temporary  blindness  may  occur  at  its  very 
onset,  the  ophthalmoscope  showing  no  morbid  appearances. 

If  the  patient  is  closely  questioned,  he  will  state  that  he  has  recently 
noticed  some  change  in  his  urine,  that  it  has  been  scanty  and  high  colored, 
and  he  has  had  a  frequent  desire  to  pass  it.  Perhaps  he  has  had  some  pain 
in  the  back  and  loins  ;  he  may  complain  of  nausea  and  perhaps  of  vomit- 
ing ;  the  latter  is  sometimes  so  troublesome  that  the  physician  may  direct 
his  attention  to  the  stomach  as  the  seat  of  the  disease,  and  treat  the  pa- 
tient for  some  form  of  gastric  lesion.  There  is  more  or  less  acceleration 
of  the  pulse,  which  is  irritable  in  character.  The  skin  is  usually  unnatu- 
rally dry  ;  occasionally  it  is  moist,  but  when  it  is  so  the  perspiration  has  a 
peculiar  urinous  odor.  These,  in  brief,  are  the  symptoms  which  attend 
the  development  of  a  mild  form  of  acute  Bright's  disease. 

In  a  favorable  case,  after  the  patient  has  reached  the  condition  described, 
he  begins  to  improve  ;  the  urine  is  increased  in  quantity,  the  oedema  grad- 
ually disappears,  the  headache  moderates,  the  gastric  disturbances  disap- 
pear, and  in  the  course  of  two  or  three  weeks  he  has  entirely  recovered. 

In  a  certain  proportion  of  cases,  instead  of  improving,  the  patient  steadily 
grows  worse  ;  the  oedema  steadily  increases  until  the  cellular  tissues  of  the 
entire  body  become  oedematous.  As  a  result  of  the  pulmonary  oedema  there 
is  dyspnoea.  Dyspnoea  in  this  connection  is  not  always  dependent  upon  an 
oedematous  condition  of  the  lung,  for  uraemic  dyspnoea  may  occur  inde- 
pendent of  any  change  in  the  lung-tissue.  When  there  is  general  ana- 
sarca the  dyspnoea  is  usually  due  to  pulmonary  oedema  ;  it  may  be  accom- 
panied by  more  or  less  pulmonary  congestion,  giving  rise  to  a  watery  expec- 
toration, which  may  be  streaked  with  blood.  If  the  disease  progresses,  the 
anasarca  will  gradually  increase  until  the  patient  becomes  "  water-logged." 
With  the  general  anasarca  the  surface  of  the  body  assumes  a  peculiar,  pale, 
waxy  appearance  ;  there  is  oedema  of  the  scrotum  and  penis,  or  labia,  and 
more  or  less  eifusion  into  the  peritoneal,  pleural,  and  pericardiac  cavities. 
Hydrothorax  may  so  impede  respiration  as  to  cause  death. 

As  the  uraemia  becomes  more  profound,  a  series  of  nervous  phenomena 
are  developed  :  the  patient  becomes  exceedingly  restless,  muscular  twitch- 
ings  occur,  and  these  may  soon  be  followed  by  convulsions,  coma,  and 
death.  If  this  class  of  patients  do  not  die  from  the  direct  toxic  ejffect  of 
the  urea,  they  may  have  complications,  such  as  meningitis,  pericarditis,  en- 
docarditis, pneumonia,  etc.,  which  may  rapidly  lead  to  a  fatal  issue.  This 
is  the  most  unfavorable  of  all  the  types  of  acute  parenchymatous  nephritis. 
Such  cases  sometimes  follow  scarlet  fever.  The  same  type  of  cases  is  also 
met  with  in  connection  with  other  infectious  diseases. 

There  is  still  another  type  of  acute  Bright's  disease  which  is  occasionally 
met  with.  It  is  ushered  in  by  violent  symptoms  :  the  patient  is  seized 
with  a  chill,  intense  pain  in  the  back  and  along  the  ureter,  with  retraction 


ACUTE    BRIGHT's   DISEASE.  657 

of  both  testicles ;  there  is  delirium,  great  nervous  disturbance,  urgent  cere- 
bral symptoms,  and  the  patient  may  pass  quickly  into  a  state  of  coma  and 
die  within  two  or  three  days.  The  chill  in  these  cases  is  followed  by  high 
temperature  ranging  from  104°  F.  to  106°  F.;  there  is  often  almost  com- 
plete suppression  of  urine,  perhaps  not  more  than  two  ounces  being  se- 
creted in  twenty-four  hours.  The  delirium  which  is  present  so  closely  re- 
sembles that  of  meningitis  that  it  is  often  difficult  to  differentiate  between 
the  two  conditions.  In  these  cases  there  is  intense,  active  renal  hyperaemia, 
and  the  tubules  are  extensively  filled  with  an  inflammatory  exudation. 
Very  soon  after  the  accession  of  the  ushering-in  symptoms,  oedema  of  the 
face  will  be  developed,  and  soon  after  its  occurrence  the  patient  will  pass 
into  a  state  of  coma,  which  is  usually  followed  by  death.  If  these  patients 
recover  from  the  acute  stage,  the  kidneys  will  be  permanently  damaged,  and 
they  will  afterward  present  the  symptoms  of  chronic  Bright's  disease. 

Connected  with  the  history  of  acute  Bright's,  there  are  symptoms  which 
are  of  special  imjoortance,  and  which  I  shall  consider  more  in  detail ;  these 
are  the  changes  in  the  iirine,  the  dropsy,  and  the  nervous  phenomena. 
These  are  present  to  a  greater  or  less  degree  in  all  cases,  and  their  exist- 
ence is  necessary  for  its  diagnosis. 

The  urine  in  all  varieties  is  diminished  in  quantity,  high  colored,  and 
sometimes  smoky  in  appearance  ;  it  is  of  high  specific  gravity,  perhaps  as 
high  as  1.030.  A  sediment,  in  which  there  are  red  and  white  blood-corpus- 
cles, forms  soon  after  the  urine  is  voided.  The  amount  of  urea  eliminated 
in  the  twenty-four  hours  is  diminished  to  one-half  or  one-quarter  the  nor- 
mal amount.  When  tested  for  albumen,  from  one-third  to  one-half  of  the 
entire  bulk  of  the^  urine  will  coagulate.  In  testing  for  albumen  it  is  well 
to  employ  both  heat  and  nitric  acid.  Albuminous  urine  is  usually  coagu- 
lated by  heat  below  the  boiling  point,  and  by  nitric  acid.  If  both  of  these 
tests  are  carefully  used,  one  will  rarely  be  led  into  error  ;  but  mistakes  are 
often  made  when  only  one  of  these  agents  is  employed,  for  the  reason  that 
heat  alone  Avill  not  coagulate  albumen  in  urine  which  is  neutral  or  alkaline  ; 
in  such  cases  the  addition  of  nitric  acid  coagulates  and  precipitates  the  al- 
bumen. In  true  albuminuria,  where  serum-alhumen  appears  in  the  urine, 
there  is  some  kidney  change.  In  false  albuminuria,  where  albumen,  not 
serum-albumen,  appears  in  the  urine,  the  kidneys  maybe  healthy.'  Ee- 
cently,  opinions  have  changed  in  regard  to  albuminuria.^  If  a  |)ortion  of 
the  urinary  sediment  be  microscopically  examined,  casts  will  be  found  which 

'  See  text-books  on  "  Urinary  Analysis '"  for  modes  of  determining  the  different  albumens  ;  also  Appen- 
dix to  Foster's  "  Physiology." 

2  Albuminuria  itself  is,  according  to  Gull's  statements,  as  common  in  young  men  and  boys  as  spermator- 
rhoea ;  Moxon  confirms  this.  Young  girls  from  fourteen  to  seventeen  have  it.  Depressing  mental  emo- 
tions cause  a  lowered  pressure  in  the  vessels,  and  this,  according  to  Runeberg's  ingenious  theory,  is  the 
one  cause  of  albuminuria.  Leube  and  Purbruger  incline  to  the  opinion  of  an  individual  permeability  of 
membrane.  Temporary  nervous  innervation  may  in  some  instances  induce  transient  albuminuria,  with  or 
without  healthy  kidneys.  Drs.  Brunton  and  Power  (St.  Barthol.  Hosp.  Rep.,  1877)  take  issue  with  Burtel's 
statement  that  albuminuria  is  always  of  renal  origin.  There  are  different  albumens,  some  derived  from 
the  blood,  others  from  the  digestive  organs.  Diminution  and  increase  of  blood-pressure  in  the  glom. 
eruli  have  both  been  advanced  as  prime  causes  of  the  albuminuria.  Probably  blood-pressure  plays  but  an 
unimportant  part.  Cohnheim  legards  changes  in  the  epithelium  covering  the  glomeruli  as  an  important 
factor.  These  changes  are,  no  doubt,  in  part  produced  by  the  stagnant  inflammatory  current.  The  vessels 
of  the  glomeruli  unquestionably  allow  most  of  the  albumen  (in  acute  albuminuria)  to  exude. 


558  DISEASES   OP  THE  KIDKETS. 

correspond  to  the  contents  of  the  urinif  erous  tubes  already  described  ;  these 
casts  consequently  vary  in  appearance  and  composition.  Tliose  which  are 
most  characteristic  are  the  epithelial  casts,  which  may  contain  blood-glob- 
ules ;  in  yery  active  forms  of  the  disease,  the  casts  may  be  entirely  composed 
of  coagulated  blood,  called  hlood  casts;  casts  of  this  form  and  composition  are 
found  in  no  other  form  of  Bright's  disease,  unless  it  is  complicated  by  acute 
tubular  inflammation.  In  addition  to  epithelial  and  blood  casts,  small  and 
large  hyaline  casts  may  be  found.  The  small  hyaline  casts  are  formed  in  tubes 
the  epithelium  of  which  has  not  been  removed.  In  addition  to  the  casts,  free 
epithelial  cells  and  blood -globules  may  be  seen.  Hyaline  and  epithelial 
casts  are  sometimes  found  independent  of  Bright's  disease,  and  saccharine 
urine  may  be  loaded  with  them. '  Distinctly  formed  cell  elements  in  a  cast 
point  to  an  origin  in  the  straight  or  collecting  tubes. 

Dropsy  occurs  early  ;  there  have  been  several  theories  advanced  as  to  its 
cause,  but  none  are  perfectly  satisfactory.  One  theory  is,  that  it  is  due  to 
the  sudden  removal  from  the  body  of  a  large  amount  of  albumen  ;  whereas 
in  the  most  rapidly  developed  dropsies  no  albumen  is  carried  out  of  the 
body,  for  the  reason  that  the  patient  passes  little  or  no  urine. '^  Another 
cause  assigned  for  the  dropsy  is,  that  the  kidneys  fail  to  eliminate  the 
watery  portion  of  the  blood  in  the  form  of  urine,  and  that  the  dropsy  occurs 
as  the  result  of  the  retention  of  the  watery  elements  ;  yet  very  extensive 
dropsies  occur  while  the  patient  is  passing  more  than  the  normal  quantity 
of  urine.  ^  Again,  it  is  said  that  dropsy  occurs  in  consequence  of  the 
anaemic  condition  of  the  patient.  The  anaemic  condition  undoubtedly  con- 
tributes to  the  ease  with  which  the  transudation  of  fluid  through  the  walls 
of  the  vessels  takes  place ;  but  a  patient  may  be  exceedingly  anaemic  and 
yet  no  dropsy  be  present,  and  dropsy  very  often  occurs  before  the  patient 
shows  any  evidence  that  he  is  in  an  ansemic  condition. 

1  regard  dropsy  as  a  necessary  symptom  of  acute  Bright's,  but  the  exact 
cause  of  its  occurrence  in  many  cases  cannot  be  satisfactorily  determined. 

Nervous  symptoms  are  of  great  importance  and  prominence.  Undoubt- 
edly these  are  due  to  the  presence  of  some  irritating  poison  in  the  circula- 
tion, which  acts  directly  upon  the  nerve  centres."  Usually  the  nervous 
symptoms  first  manifest  themselves  by  headache  ;  therefore  headache  is  a 
symptom  which  must  not  be  lightly  regarded,  for  it  is  often  the  precursor 
of  more  dangerous  symptoms.  If  persistent  and  severe,  and  permitted  to 
pass  unrelieved,  it  may  be  followed  by  convulsions.      The  larger  proportion 

1  Southey  regards  it  as  an  error  to  suppose  that  the  larger  casts  are  derived  from  the  larger  tortuous 
lubes.  Nothing  but  cellular  elements  cau  pass  through  Henle's  loops  (diameter  1-1200  to  1-1000  in.);  "  when," 
he  says,  "  a  cast  is  assumed  to  come  from  the  profounder  renal  tissue  and  to  be  of  grave  significance,  an 
error  is  committed,  based  on  ignorance  of  anatom3^"    Hyaline  casts  probably  form  in  Henle's  loops. 

2  Cohnheim,  in  his  work  on  pathology,  regards  inflammatory  changes  in  the  walls  of  the  cutaneous  and 
subcutaneous  vessels — whose  causes  are  the  same  as  those  of  acute  Bright's— to  be  the  reason  of  anasarca 
in  many  instances, — the  vessels  being  rendered  more  permeable. 

3  Cohnheim  {Virchow''s  Archiv.  1877,  96,  p.  106),  after  most  elaborate  experimentation,  regards  oedema  as 
the  result,  not  of  dilution  of  the  blood  or  of  increase  in  the  relative  amount  of  water,  but  of  hydrcemit 
plethoi'a,  i.  e.,  increase  in  the  absolute  amount  of  water.  This  fact,  with  changes  in  the  walls  of  the  ves- 
sels, is  accepted  by  most  authorities  as  the  most  plausible  and  probable  cause  of  oedema  in  acute 
Bright's. 

■»  The  different  theories  in  regard  to  the  causation  I  have  considered  under  the  head  of  acute  iircemia. 


ACUTE    BRIGHTS    DISEASE.  559 

of  cases  in  acute  Bright's  will  suffer  from  more  or  less  severe  headache, 
without  any  subsequent  convulsions  ;  but  the  fact  that  convulsions  do  fol- 
low it  is  sufficient  to  cause  one  to  watch  for  the  indications  of  their  occur- 
rence. If  the  poisoning  goes  on  gradually  the  patient  will  first  become 
drowsy,  the  drowsiness  passing  into  stupor,  and  frequently  into  coma.  A 
large  number  of  patients  with  acute  Bright's  unquestionably  die  from  the 
direct  effect  of  urea  and  its  allies  upon  the  nervous  centres  ;  but  a  still 
larger  number  die  from  complications. 

DiiFerential  Diagnosis. — If  a  patient  has  headache,  some  fever,  more  or 
less  oedema,  nausea,  and  perhaps  vomiting,  with  scanty,  high-colored 
urine  of  high  specific  gravity,  containing  epithelial,  small  hyaline,  or  blood 
sasts,  it  is  certain  that  acute  Bright's  disease  exists.  There  may  be  other 
pathological  conditions  existing  in  the  kidneys  at  the  same  time,  but  this 
train  of  phenomena  gives  unmistakable  evidence  that  some  of  the  urinifer- 
ous  tubes  are  the  seat  of  acute  inflammation  ; — the  acute  may  be  ingrafted 
upon  the  chronic.  In  every  case  which  presents  this  train  of  symptoms 
frequent  examinations  of  the  urine  should  be  made.  The  general  symptoms 
and  the  changes  in  the  urine  in  acute  Bright's  disease  are  so  obvious 
that  it  can  scarcely  be  overlooked  or  mistaken  for  any  other  disease. 
The  only  circumstances  under  which  it  is  possible  for  this  affection  to  pass 
unrecognized  are  those  in  which  dropsy  is  not  a  prominent  symptom,  and 
when  a  careful  examination  of  the  urine  has  not  been  made. 

It  is  not  always  easy  to  determine  whether  acute  Bright's  is  primary  or 
secondary — that  is,  whether  it  has  occurred  in  kidneys  that  were  healthy 
previous  to  its  occurrence,  or  in  those  that  were  already  the  seat  of  chronic 
Bright's.  The  previous  history  of  the  patient,  and  the  presence  or  absence 
of  cardiac  hypertrophy,  are  the  only  means  to  guide  one  under  such  cir- 
cumstances. 

The  points  of  differential  diagnosis  between  congestion  of  tlie  hidneys 
and  acute  Bright's  disease  have  already  been  given. 

Acute  Bright's  is  distinguished  from  paroxysmal  hcematuria  and  albu- 
minuria by  the  abrupt  commencement  and  brief  duration  of  these  affec- 
tions, by  the  marked  nervous  and  gastric  symptoms,  the  slight  jaundice, 
and  the  absence  of  dropsy.  Granular  pigment  in  hsematuria,  and  a 
very  great  quantity  of  albumen  and  tube  casts  in  paroxysmal  albuminuria 
are  characteristic  urinary  symptoms.  Haematuria,  with  a  tendency  to  sup- 
pression, has  few  tube  casts. 

Prognosis.— The  tendency  of  acute  Bright's  disease  is  to  recovery,  but 
the  chances  of  recovery  are  much  better  in  the  young  than  in  those  past 
middle  life.  In  those  cases  which  terminate  in  recovery  the  characteristic 
symptoms  of  the  disease  disappear  within  two  or  three  months  from  the 
commencement  of  the  attack.  So  long  as  albumen  continues  in  the  urine, 
however  small  in  quantity,  recovery  cannot  be  regarded  as  complete.  The 
indications  of  a  fatal  termination  are  very  scanty  urine,  frequent  and  dis- 
tressing vomiting,  extensive  anasarca,  severe  and  persistent  headache, 
convulsions,  coma,  tjrphoid  symptoms,  and  the  occurrence  of  complica- 
tions. 


560  DISEASES    OP   THE    KIDKETS. 

The  pulmonary  complications  which  render  the  prognosis  imfavoraDle, 
are  oedema,  pneumonia,  and  capillary  bronchitis.  The  great  danger  in 
pneumonia  which  complicates  acute  Bright's  disease  is  the  sudden  develop- 
ment of  pulmonary  oedema  in  portions  of  the  lung  not  involved  by  the 
pneumonia.  Another  dangerous  complication  is  inflammation  of  the  se- 
rous surfaces,  especially  endocarditis  and  pericarditis.  Acute  meningitis  is 
a  rare,  but  always  a  fatal  complication.  There  may  be  complete  loss  of 
sight  ; — this  form  of  amaurosis  is  usually  temporary,  and  is  unattended  by 
any  change  in  the  retina  recognizable  by  the  ophthalmoscope  ;  it  is  probably 
due  to  the  direct  effect  of  the  urea  upon  the  retina.  Subacute  gastritis, 
functional  hepatic  derangement,  and  oedema  glottidis  are  also  complicating 
conditions  which  render  the  prognosis  unfavorable. 

In  a  small  proportion  of  cases  patients  pass  rapidly  from  acute  into 
chronic  Bright's  disease.'  The  passage  from  acute  into  chronic  is  indicated 
by  a  copious  secretion  of  paler  urine  containing  few  casts.  The  droj^sy 
diminishes,  but  does  not  entirely  disappear.  The  individual  may  be  able 
to  resume  his  ordinary  avocations,  but  the  oedema  of  the  feet  and  ankles 
does  not  entirely  disappear  and  the  urine  remains  albuminous. 

Treatment. — Formerly,  general  and  local  blood-letting  was  practised  in 
the  treatment  of  acute  Bright's  disease.  At  the  present  time  general  blood- 
letting is  never  resorted  to,  unless  in  the  very  acute  form  which  is  at- 
tended by  violent  cerebral  symptoms.  As  soon  as  its  pathology  was  better 
understood,  a  plan  of  treatment  was  adopted,  based  on  the  proposition  that 
the  first  essential  in  the  treatment  of  an  inflamed  organ  was  rest.  It  was 
proposed  to  treat  an  inflamed  kidney  upon  the  same  principle  as  an  inflamed 
eye  or  an  inflamed  joint  would  be  treated  :  that  is,  give  the  kidneys  perfect 
rest.  With  this  end  in  view  it  was  proposed  to  supplant  the  function  of 
the  kidneys  as  far  as  possible  by  increasing  the  function  of  the  skin,  so  that 
it  should  perform  the  work  of  the  kidneys.  The  so-called  diaphoretic  plan 
of  treatment,  as  well  as  the  free  administration  of  hydragogue  cathartics,  is 
based  on  this  principle. 

The  object  of  these  two  plans  is  to  eliminate  the  i-etained  excrementitious 
materials,  allowing  the  inflamed  kidneys  to  rest.  The  usual  method  of 
producing  profuse  diaphoresis  is  to  place  the  patient  in  bed  and  cover  him 
with  flannel  blankets,  and  then  by  means  of  the  hot-air  apparatus  in- 
troduce a  constant  current  of  hot  air  beneath  the  bed-clothes,  until  pro- 
fuse perspiration  is  induced  and  the  excretory  power  of  the  skin  is  taxed 
to  its  utmost.  The  bath  should  be  continued  from  half  an  hour  to  an 
hour;  then  the  patient  should  be  allowed  to  gradually  become  cool,  and 
when  so,  to  resume  his  clothing  and  walk  about  the  room  or  ward,  the 
temperature  of  which  should  be  above  70°  F.  These  baths  may  be  re- 
peated once  or  twice  each  day,  or  every  other  day,  as  the  condition  of  the 
patient  may  demand.  The  effect  usually  produced  by  these  baths  is  a 
rapid  subsidence  of  the  oedema.  It  may  not  require  more  than  half  a 
dozen   baths    to   entirely   remove    the    dropsy  from    a    "  water-logged " 

^  Of  forty-one  hospital  cast-s,  twenty-one  terminated  in  complete  recovery,  twelve  died,  and  seven 
passed  into  chronic  Bright's  ;  in  private  practice  the  rate  of  mortality  is  usually  less. 


ACUTE   BRTGHT'S   DISEASE.  561 

patient,  and  as  far  as  that  one  symptom  is  concerned  to  give  complete 
relief ; — but  the  relief  is  only  temporary.  Soon  the  patient  becomes 
anaemic,  loses  his  strength,  and  after  a  time  a  point  is  reached  at  which 
the  oedema  returns,  although  the  hot-air  baths  are  continued,  and  the 
toxic  effects  of  urea  steadily  increase.  I  have  seen  patients  pass  into  con- 
vulsions while  in  a  hot-air  bath. 

In  addition  to  the  baths,  it  is  customary  to  administer  hydragogue  ca- 
thartics in  sufficiently  large  doses  to  produce  daily  three  or  four  watery 
discharges  from  the  bowels ;  under  the  conjoined  action  of  these  two 
plans,  this  class  of  patients  for  a  time  will  appear  very  much  relieved  ;  but 
after  a  few  active  purgations,  and  a  few  hot-air  baths,  they  will  begin  to 
complain  of  extreme  weakness,  and  very  soon  reach  a  point  at  Avhich  the 
combined  action  of  these  agents  fails  even  to  relieve  the  distressing  symp- 
toms, and  their  condition  is  then  worse  than  before  their  administration  was 
commenced. 

Several  years  ago  I  became  convinced  that  this  depurative  plan  of  treat- 
ment was  wrong,  and  that  it  was  wrong  because  it  rapidly  depleted 
patients  who  could  not  bear  depletion.  Exhaustion  can  as  certainly  be 
produced  by  diaphoresis  and  hydragogue  cathartics  as  by  repeated  general 
bleedings.  Besides,  the  repeated  use  of  hydragogue  cathartics  interferes 
with  the  processes  of  digestion  and  assimilation. 

In  the  treatment  of  acute  Bright's  disease,  there  are  three  important 
things  to  be  accomplished.  First :  the  elimination  of  urea  and  its  allies. 
Second :  the  removal,  as  rapidly  as  possible,  of  the  inflammatory  products 
which  obstruct  the  uriniferous  tubules.  Third :  to  counteract  the  effect  of 
urea  and  waste  j)roducts  upon  the  nervous  system. 

Th9  question  arises  :  How  shall  we  meet  these  indications  ?  The  main 
thing  to  be  done  is  to  remove  the  exudation  which  obstructs  the  urinifer- 
ous tubules.  This  exudation  not  only  interferes  with  the  elimination  of 
urea  and  its  allies,  by  preventing  the  kidneys  from  performing  their  nor- 
mal eliminative  function,  but  if  it  remains  in  the  tubules  it  induces  de- 
generative processes.  If  the  excretory  power  of  the  kidneys  can  be  so  in- 
creased that  they  will  pour  out  fluid  in  sufficient  quantity  to  carry  off  this 
material,  the  desired  result  will  be  reached. 

Digitalis  is  the  drug  which  will  accomplish  this  result,  as  it  increases 
the  urinary  secretion  without  stimulating  the  kidneys  ;  it  overcomes  the 
obstruction  in  the  renal  circulation,  and  thus  causes  an  increased  flow  of 
the  watery  portion  of  the  urine  through  the  Malpighian  tufts  into  the 
upper  portion  of  the  uriniferous  tubules.  Thus  the  obstruction  in  the 
tubes  is  washed  out,  and  at  the  same  time  the  eliminative  function  of  the 
kidneys  is  increased,  so  that  urea  is  carried  out  of  the  system  much  more 
rapidly  and  completely  than  it  can  be  by  the  skin  or  bowels.  If  diluent 
drinks  are  given  water  is  the  test.  Spirits  of  nitrous  ether,  acetate  of 
potash,  tincture  of  the  perchloride  of  iron,  or  squills  may  often  be  ad- 
vantageously combined  with  digitalis. 

In  connection  with  the  administration  of  digitalis,  I  would  recommend 
the  application  of  dry  cups  over  the  region  of  the  kidneys.     In  order  that 


562  DISEASES   OF   THE   KIDNEYS. 

the  dry  cupping  may  be  more  effective,  each  cup  should  he  removed  as  soon 
as  the  vessels  beneath  are  well  filled.  The  object  is  to  draw  the  blood 
from  the  arteries  into  the  capillaries,  but  not  with  sufficient  force  to  cause 
extravasation.  The  object  of  dry  cupping  is  not  to  irritate  the  surface,  but 
to  rapidly  draw  the  blood  from  the  arteries  and  as  rapidly  carry  it  through 
the  capillaries  to  the  veins  in  its  backward  course  to  the  heart.  After  dry 
cupping,  warm  poultices  over  the  kidneys  may  be  applied  with  benefit ; 
digitalis  leaves  may  be  used  for  a  poultice,  and  thus  applied  they  will 
increase  the  diuretic  effect  of  the  drug  administered  internally.  After  the 
free  administration  of  digitalis  and  the  application  of  dry  cups,  if  the 
ursemic  symptoms  are  still  urgent,  hot-air  baths  and  hydragogue  cathartics 
may  temporarily  be  resorted  to,  to  aid  in  carrying  the  patient  over  the 
period  of  greatest  danger  ;  but  their  use  should  not  be  continued  after  free 
diuresis  is  established. 

The  next  object  to  be  accomplished  is  to  relieve  the  nervous  symptoms ; 
the  means  to  be  employed  to  accomplish  this  are  the  same  as  in  the  treat- 
ment of  acute  uraemia.  For  the  successful  management  of  acute  Bright's 
disease,  whatever  may  have  been  its  exciting  cause,  the  patient  must  be 
kept  in  bed,  in  a  large,  well-ventilated  apartment,  with  a  temperature  of 
75°  F.  Milk  should  be  the  only  article  of  diet.  Skimmed  milk  is  advo- 
cated highly  ;  besides  being  nourishing,  it  is  a  good  diuretic.  Dry  cups 
should  be  applied  over  the  kidneys,  and  the  infusion  of  digitalis  should  be 
freely  administered.  If  this  plan  is  systematically  carried  out  from  the  very 
commencement,  the  urine  soon  becomes  copious,  the  albumen  gradually 
diminishes,  and  the  dropsy  passes  away.  As  soon  as  the  flow  of  urine  com- 
mences, the  administration  of  digitalis  must  be  discontinued,  and  diluent 
driuKS  are  to  be  given.  If  the  renal  secretion  be  not  re-established  in 
twenty- four  hours,  hot-air  baths,  hydragogue  cathartics  or  pilocarpin  hypo- 
dermically  in  one-eighth  or  one-tenth  grain  doses  are  to  be  used.  For 
the  relief  of  convulsions  or  coma,  hypodermics  of  morphine  should  be 
^given. 

CHEONIC  BEIGHT'S  DISEASE, 
dhronic  Bright's  disease  will  be  described  under  the  following  heads  : — 

I.   Chronic  Parenchymatous  Nephritis. 
II.  Interstitial  Nephritis  ;  or,  "  Cirrhotic  Kidney." 
III.  Amyloid  Degeneration  ;  or,  "  Waxy  Kidney." 

CHRONIC    PARENCHYMATOUS     NEPHRITIS. 

As  already  stated,  chronic  parenchymatous  nephritis  may  be  a  sequela 
of  the  acute  form,  but  it  is  oftener  a  chronic  degenerative  process  from  its 
onset.  Under  this  head  may  be  included  the  large  fatty  hidney,  the  large 
white  hidney,  and  the  small,  granular,  fatty  hidney. 

Morbid  Anatomy. — Chronic  parenchymatous  nephritis  is  almost  always  a 
legitimate  consequence  of  depraved  cell-development,  and  it  may  make  its 
appearance  in  any  form  of  renal  lesion  in  which  there  is  a  protracted  inter- 


CHRONIC    PARENCHYMATOUS   NEPHRITIS. 


563 


ference  with  the  normal  nutrition  of  the  tubes.  In  the  large  fatty  kidney, 
but  few  of  the  epithelial  cells  of  the  urinifcrous  tubes  at  first  undergo 
change,  but  as  the  transformation  becomes  general,  the  entire  contents  of 
the  affected  tubules  become  loaded  with  minute  oil  globules.  The  mucous 
membrane  of  the  pelvis  and  calicos  is  thickened,  opaque,  and  anaemic,  or  it 
presents  a  vai-icose  dilatation  of  its  veins.  The  kidneys  are  enlarged,  their 
capsules  are  non-adherent,  and  their  surface  smooth  ;  their  color  is  paler 
than  normal,  presenting  a  more  or  less  yellow  appearance  ;  sometimes  they 
are  mottled. 

On  sectifm,  the  enlargement  of  the  organ  will  be  found  to  be  due  chiefly 
to  an  increase  in  the  size  of  its  cortical  substance,  which  is  of  a  pale  yel- 
loAvish  color.  There  is  but  little  change  in  the  medullary  portion.  The 
Malj)ighian  tufts  do  not  stand  out  prominently,  for  there  is  more  or  less 
fatty  material  in  the  dilated  portion  of  the  uriniferous  tubes  around  the 
Malpighian  tufts,  which  gives  them  a  somewhat  pale  appearance.  The  vas- 
cularity of  the  whole  kidney  seems  to  be  very  much  diminished  ;  but  here 
and  there  spots  of  hemorrhage  or  congestion  are  seen.  The  principal 
changes  take  place  in  the  convoluted  tubes  of  the  cortical  portion,  esjae- 
cially  in  those  which  surround  the  Malpighian  tufts. 

These  sections  of  the  cortical  substance  in  this  form  of  degeneration 
are  very  opaque  ;  under  a 
low  power  they  show  little 
more  than  uriniferous  tu- 
bules irregularly  distended 
with  fatty  granules,  and  va- 
ricose. To  the  unaided  eye 
the  tubules  look  like  streaks 
of  sebaceous  matter.  At 
some  points  they  are  greatly 
increased  in  size,  at  others 
they  are  of  normal  calibre. 
In  the  Malpighian  bodies  are 
found  oil-globules  in  vary- 
ing quantities,  but  the  capil- 
laries of  the  tuft  are  un- 
changed. Under  a  high 
power,  fine  fat  granules  are 
seen  about  the  nuclei  in 
the  protoplasm  of  the  epi- 
thelial cells,  and  also  in 
the  cells  of  the  external  coat 
of  the  small  vessels.  Gran- 
ulo-fatty  material  covers  a 
homogeneous  vitreous  sub- 
stance in  Henle's  tubules. 
The  lacunae  and  cells  of  the 
intertubular  connective-tissue  are  also  filled  with  fine  fat  granules. 


Fig.  13f 

Chronic  Parenchymatous  Nephritis. 
Section  from  the  Cortex  of  a  Kidney. 

A.  Slightly  thickened  capsule  of  the  glomerulus. 

B.  Vascular  tuft,  nearly  normal.     A  small  ammmt  of  gran- 

ular matter  is  seen  beneath  the  capsule. 

C.  C,  C.  Convoluted  i/ulmles— epithelium  nearly  destroyed.  Some 

of  the  tubes  are  entirely  filled  with  fatty  granules.     The 
nuclei  of  the  epithelia  are  yet  plainly  seen. 

D.  Longitudinal  section  of  Henle's  looped  tube— ascending  por* 

Hon.  ' 

E.  A  small  artery.        v.  350. 


564  DISEASES    OF   THE   KIDJS'ETS. 

Large  Wliite  Kidney. — In  this  variety  of  parencliyinatous  nephritis, 
the  kidneys  may  be  twice  their  normal  size,  of  an  ' '  ivory-white "  color, 
their  surface  smooth,  and  their  capsule  non-adherent. 

On  section,  the  enlargement  is  found  to  be  due  to  an  increase  in  the 
volume  of  the  cortical  substance.  The  medullary  portion  shows  no  appre- 
ciable alteration.  The  microscope  will  show  that  the  morbid  changes  are 
confined  almost  exclusively  to  the  epithelium  of  the  convoluted  tubules  and 
that  lining  the  Malpighian  bodies.  The  epithelium  is  granular,  and  so 
much  swollen  that  the  lumen  of  the  tubes  is  obstructed  and  may  be  dis- 
tended with  a  hyaline  material.  There  is  a  dilated  and  varicose  condi- 
tion of  the  tubes,  with  some  thickening  of  their  walls.  In  some  cases 
Henle's  loops  present  alterations  similar  to  those  that  occur  in  the  convo- 
luted tubes. 

Small  Granular  Fatty  Kidney. — The  atrophic  alterations  in  the  kidney 
in  this  variety  (or  stage)  of  parenchymatous  nephritis  are  entirely  different 
from  those  of  atrophy  produced  by  interstitial  nephritis.  The  epithelium 
which  may  have  been  the  seat  of  fatty  or  granular  change,  disintegrates, 
liquefies,  and  is  absorbed  or  passes  off  in  the  urine.  The  tubes,  deprived  of 
their  epithelium,  collapse.  Some  claim  that  renal  atrophy  and  granular 
degeneration  of  the  kidney  are  the  same.  That  these  processes  are  asso- 
ciated is  very  evident.  During  the  process  of  atrophy,  developments  occur 
in  the  walls  of  the  tubes  and  in  the  intertubular  tissue,  which  lead  to, 
or  are  followed  by,  thickening  of  the  tubules  and  blood-vessels.  The 
processes  of  inflammatory  atrophy  are  always  slowly  progressive.  An 
atrophied  white  kidney  is  markedly  diminished  in  size,  its  surface  is 
uneven  and  more  or  less  nodular ;  its  capsule  is  adherent  and  slightly 
thickened,  and  when  removed  portions  of  kidney  tissue  may  be  removed 
with  it  ;  the  denuded  surface  is  more  or  less  granular,  its  color  varies, 
it  may  be  white,  have  a  stellate  vascularity,  or  present  a  mottled  appear- 
ance. 

On  section,  it  will  be  found  that  the  diminution  in  the  size  of  the  kid- 
ney is  mainly  due  to  atrophy  of  its  cortical  substance  ;  the  medullary  por- 
tion retains  very  nearly  its  normal  dimensions  ;  the  cortical  substance  be- 
tween the  pyramids  will  be  somewhat  atrophied.  The  kidney  is  firm  and 
jtough.  The  granulations  on  its  surface  and  in  its  substance  are  the  pyra- 
mids of  Ferrein.  Under  low  power  a  section  of  the  cortical  substance  will 
show  an  increase  in  the  stroma  of  the  organ,  the  walls  of  the  vessels  will  be 
thickened  and  the  Malpighian  tufts  will  have  lost  their  distinctness.  The 
uriniferous  tubules  will  be  denuded  of  their  epithelium,  in  some  places  filled 
with  granular  or  fatty  material,  and  distended  ;  in  others  they  will  be  en- 
tirely obliterated,  atrophied,  and  more  or  less  shrivelled.  This  form  of 
kidney  degeneration  may  be  distinguished  from  the  contracted  kidney  of 
interstitial  nephritis  by  the  larger  size  of  the  organ,  its  less  firm  consis- 
tency, its  more  uneven  surface,  its  pale  yellow  and  large  granulations  not 
only  on  its  surface  but  throughout  its  substance,  evidently  formed  by  the 
accumulation  of  fat  in  the  tubules,  and  by  the  absence  of  cysts  either  on  ibs 
surface  or  in  its  substance.     It  is  not  necessary  that  the  small  atrophic 


CHRONIC   PABENCHYMATOUS  KEPHEITIS.  565 

Mdney  of  chronic  parenchymatous  Lephritis  should  have  been  preceded  by 
an  enlarged  fatty  or  granular  kidney. 

Etiology. — Chronic  parenchymatous  nephritis  may  be  the  sequela  of 
acute.  It  is  more  common  in  males  than  in  females,  it  occurs  in  early 
adult  life  rather  than  past  middle  life.  Exposure,  moderate  alcoholism, 
bad  hygiene,  phthisis,  diabetes,  arthritis  deformans,  emphysema,  and 
chronic  cardiac  diseases  predispose  to  its  development.  The  cause  is 
sometimes  undiscoverable. 

Symptoms. — This  form  of  chronic  Bright's  disease  may  be  ushered  in  by 
acute  symptoms  or  come  on  insidiously ;  in  either  case,  when  once  fully 
developed,  the  symptoms  are  identical.  There  are  two  symptoms  which 
are  always  present,  viz. :  albuminuria  and  dropsy.  If  its  advent  is  marked 
by  acute  symptoms,  its  development  is  attended  by  the  phenomena  of  acute 
Bright's  ;  the  patient  rapidly  reaches  a  condition  of  general  anasarca ;  his 
countenance  assumes  a  pallid  appearance  ;  the  pallor  is  not  like  the  clear 
pallor  of  phthisis,  nor  the  dingy  pallor  of  cancer,  but  is  peculiar  to  the  dis- 
ease. When  he  has  reached  an  apparently  hopeless  condition  his  urine 
becomes  gradually  increased  in  quantity.  His  appetite  returns,  nausea 
disappears,  he  suffers  less  from  restlessness,  the  anasarca  gradually  dimin- 
ishes, the  sleep  becomes  refreshing — in  short,  there  is  a  gradual  improve- 
ment in  all  his  symptoms.  The  improvement  may  be  continued  or 
relapses  may  occur,  but  after  a  few  weeks  or  perhaps  months  he  may  reach 
a  condition  of  comparative  health  ;  this  class  of  patients  never  so  far 
recover  that  no  traces  of  the  disease  remain.  There  will  always  be  some 
cedema  along  the  line  of  the  tibia  and  over  the  internal  malleolus,  and  the 
albumen  will  never  entirely  disappear  from  the  urine.  Patients  in  such  a 
condition  are  always  inspired  with  the  hope  that  they  will  reach  com- 
plete recovery  ;  but  they  are  liable  at  any  time  to  a  sudden  return  of 
their  dropsy. 

When  the  disease  comes  on  gradually  without  any  acute  symptoms  one 
of  its  earliest  indications  is  increased  frequency  of  micturition  ;  the  oedema 
may  not  be  very  extensive,  but  it  is  always  present ;  perhaps  there  is  at  no 
time  pain  in  the  back  or  loins  ;  but  there  is  a  time,  early  in  the  history  of 
the  disease,  when  the  urine  is  scanty  and  high  colored  ;  afterward  it  be- 
comes copious,  of  a  pale  color  and  low  specific  gravity.  The  gastric  and 
nervous  symptoms,  so  prominent  in  acute  Bright's,  are  never  severe  ;  there 
is  gradual  loss  of  energy  with  progressive  emaciation  ;  the  skin  becomes 
dry  and  harsh,  the  surface  assumes  a  peculiar  pale,  sallow  appearance,  there 
is  often  great  thirst,  very  troublesome  dyspeptic  symptoms,  and  often  marked 
signs  of  anaemia.  The  pulse  becomes  feeble  and  irregular  in  force,  and  the 
patient  grows  old  rapidly. 

The  urine  after  a  time  becomes  more  abundant  than  normal,  of  low  spe- 
cific gravity,  sometimes  as  low  as  1.010,  and  the  quantity  of  albumen  is  in- 
creased. Fatty  and  hyaline  casts  are  present  ;  when  the  stage  of  atrophy 
is  reached  the  urine  sometimes  becomes  very  abundant,  and,  although  the 
albumen  at  times  may  be  small  in  quantity,  it  never  entirely  disappears, 
and  large  hyaline  and  fine  granular  casts  are  always  present.     As  the  elim- 


566  DISEASES   OF   THE   KIDJSTEYS. 

ination  of  urea  is  steadily  diminislied,  it  is  important  to  subject  the  urine 
to  frequent  quantitative  analyses.  Cardiac  lijrpertrophy  develops,  and  albu- 
minous retinitis  is  of  frequent  occurrence. 

It  is  to  be  remembered  that  the  symptoms  and  course  of  this  form  of 
Bright's  disease  are  not  continuous  ;  there  will  be  remissions,  periods  when 
these  patients  seem  to  be  recovering,  and  suddenly  the  urgent  symptoms 
of  chronic  ansemia  will  develop,  and  the  patient  passes  into  a  state  of  list- 
lessness,  stupor,  or  coma,  and  death  rapidly  ensues. 

Differential  Biagnosis. — "When  the  urine  is  abundant,  of  a  pale  color,  low 
specific  gravity,  highly  albuminous,  and  contains  fatty,  granular  and  hyaline 
casts,  accompanied  by  oedema  of  the  lower  extremities,  one  readily  makes  a 
diagnosis  of  chronic  parenchymatous  nephritis,  especially  if  a  careful  analy- 
sis of  the  history  of  the  patient  corresponds  to  the  usual  course  of  its  de- 
velopments. A  state  of  uraemic  stupor,  with  a  dry  tongue  and  sordes  on 
the  teeth,  may  be  mistaken  for  typhoid  fever,  yet  the  history  of  the  case, 
and  a  careful  examination  of  the  urine  will  soon  remove  all  doubts. 

If  the  urine  is  carefully  examined  it  is  hardly  possible  for  one  to  con- 
found the  anmmia  and  cachexia  which  sometimes  attend  the  stage  of 
atrophy  of  chronic  parenchymatous  nephritis  with  the  cachexia  of  other 
clironic  diseases.  The  mistakes  that  are  made  in  diagnosis,  or  rather  the 
failures  to  recognize  its  existence,  are  usually  due  to  the  fact  that  a  careful 
examination  of  the  urine  has  not  been  made.  In  every  case  of  persistent 
dyspepsia  careful  examination  of  the  urine  should  be  made. 

Prognosis. — One  of  the  most  constant  attendants  of  the  advanced  stage  of 
this  form  of  Bright's  disease  is  the  development  of  cardiac  hypertrophy. 
It  is  probably  due  to  interference  with  the  systemic  capillary  circulation, 
and  it  is  an  evidence  that  the  renal  disease  has  existed  for  a  long  time  ;  it 
suggests  the  possible  occurrence  of  cerebral  hemorrhage,  and  therefore 
renders  the  prognosis  unfavorable  ;  visceral  inflammations,  especially  pneu- 
monia and  bronchitis,  are  liable  to  occur,  and  often  are  the  direct  causes  of 
death. 

The  most  frequent  serous  inflammations  in  this  connection  are  pleurisy, 
pericarditis,  and  meningitis.  They  are  usually  insidious  in  their  develop- 
ment, and  always  render  the  prognosis  unfavorable.  Another  complication 
which  may  render  the  prognosis  unfavorable  is  subacute  inflammation  of 
the  mucous  membrane  of  the  stomach.  Patients  never  entirely  recover 
from  the  structural  changes  which  occur  under  such  circumstances. 
Amaurosis  is  first  indicated  by  the  patient's  inability  to  see  distinctly ;  sub- 
sequently he  has  more  or  less  difficulty  in  reading  print  which  formerly  he 
had  read  with  ease  ;  lenses  do  not  improve  his  vision  ;  after  a  time  the 
sight  may  be  entirely  lost.  This  amaurosis  is  due  to  a  neuro-retinitis  ;  it 
is  present  to  a  greater  or  less  degree  in  a  large  number  of  these  patients. 
The  structural  changes  in  the  kidneys  in  the  advanced  stage  of  this  form 
of  Bright's  disease  are  such  that  they  do  not  admit  of  repair.  All  j)ortions 
of  the  kidney,  however,  are  not  equally  involved  ;  consequently  the  de- 
purative  function  of  the  organ  is  not  suspended,  but  only  imperfectly 
carried  on.     So  long  as  the  degenerative  process  is  not  progressive  this  class 


CHRON"IC    PARENCHYMATOUS   NEPHRITIS.  667 

of  patients  may  get  on  quite  comfortably,  but  its  tendency  is  to  progress 
until  it  reaches  a  point  beyond  which  life  cannot  be  sustained.  In  a  large 
number  of  cases,  long  before  this  limit  is  reached,  some  one  of  the  com- 
plications to  which  reference  has  been  made  will  cause  death. 

In  the  advanced  stage,  the  most  trustworthy  jorognostic  indications  are 
to  be  obtained  by  comparing  the  evidences  furnished  by  examinations  of 
the  urine  with  the  general  symptoms ;  one  must  always  be  cautious  in 
giving  a  prognosis,  for  the  uraemic  symptoms  may  suddenly  be  greatly 
aggravated  by  exposure  to  cold  or  errors  in  diet,  and  the  j)atient  quickly 
passes  from  a  condition  of  comparative  good  health  into  ursemic  coma.  Al- 
though in  all  advanced  cases  the  prognosis  is  unfavorable,  still  there  is 
reason  to  hope  that  by  judicious  management,  even  in  the  most  unprom- 
ising, relief  may  be  obtained  from  many  of  the  more  distressing  symptoms 
and  life  be  prolonged. 

Treatment. — At  one  time  mercurials  were  extensively  employed  in  the 
treatment  of  this  form  of  Bright's  disease,  with  the  idea  of  keeping  up  its 
constitutional  effects  for  months.  This  plan  is  now  abandoned  ;  there 
are  some,  however,  who  claim  that  the  bichloride  may  be  employed  with 
benefit.  I  shall,  in  considering  the  cirrhotic  kidney,  refer  to  a  class  of 
cases  in  which  the  administration  of  this  form  of  mercury  is  admissible.  It 
is  important  that  the  diuretic  plan  of  treatment  should  be  continued  when 
a  patient  passes  from  acute  into  chronic  parenchymatous  nej)hritis.  Digi- 
talis in  moderate  doses,  or  at  intervals,  is  always  indicated  ;  it  is  imj)ortant 
that  the  accumulations  in  the  uriniferous  tubules  should  be  removed  the 
same  as  in  the  acute  stage. 

There  is  another  element  which  enters  into  the  treatment.  The  most 
important  thing  to  be  accomplished  in  the  treatment  of  this  form  of  Bright's 
is  the  establishmenfof  healthy  nutrition  ;  the  nutrition  of  the  kidneys  is 
always  imperfectly  performed,  and  these  patients  are  always  more  or  less 
ansemic.  For  this  reason  it  is  important  that  the  nutritive  processes  be 
carried  to  their  highest  point ;  that  after  the  degenerated  material  is  re- 
moved from  the  uriniferous  tubes,  the  degenerative  inflammatory  processes 
maybe  arrested  and  the  epithelial  lining  of  the  tubes  restored.  Digitalis 
combined  with  iron  should  be  given  in  sufficient  quantity  to  produce  mod- 
erate diuresis.  In  most  instances  milk  is  the  best  article  of  diet.  Adults 
will  often  take  three  or  four  quarts  in  twenty-four  hours  ;  when  taken 
freely  it  supplies  an  abundance  of  liquid,  which  acts  to  some  extent  as  a 
diuretic.  In  most  cases  a  moderate  amount  of  stimulants  will  be  of  ser- 
vice.    Wines  are  to  be  preferred,  and  they  should  be  taken  with  the  food. 

The  patient  must  be  placed  under  the  best  hygienic  conditions,  in  a  uni- 
form temperature,  and  the  surface  of  the  body  must  be  covered  with  flan- 
nel ;  over-indulgence  of  every  kind,  and  exposure  of  the  surface  to  cold  must 
be  carefully  avoided  ;  a  residence  in  a  uniformly  dry  climate  is  of  the  utmost 
importance.  The  urinary  secretion  must  be  carefully  watched  both  as  to 
its  quantity  and  quality.  In  the  stage  of  atrophy  there  will  be  no  necessity 
for  the  administration  of  diuretics,  for  the  urinary  secretion  is  abundant. 
The  disease  is  attended  by  great  feebleness,  and  on  account  of  their  feeble 


568  DISEASES   OF   THE   KIDNEYS. 

digestive  power  this  class  of  patients  will  be  compelled  to  take  food  in  small 
quantities  and  at  short  intervals  ;  they  will  generally  be  greatly  benefited 
by  cod-liver  oil,  combined  with  iron.  Wines  are  always  indicated  in 
moderation.  Whenever  the  urine  becomes  scanty,  two  or  three  full 
doses  of  digitalis  should  be  administered  and  dry  cups  applied  over  the 
kidneys. 

The  urgent  symptoms,  such  as  dropsy,  etc.,  must  be  relieved  by  an  oc- 
casional hot-air  bath,  hydragogue  cathartics  or  stimulating  diuretics,  and 
at  the  same  time  great  care  must  be  exercised  lest  the  depletion  be  carried 
too  far.  Jaborandi  or  the  hydrochlorate  of  pilocarpin  may  be  cautiously 
used  in  very  urgent  cases  ;  they  are  prompt  and  efficacious,  but  sometimes 
dangerous.  Iron  and  cod-liver  oil  are  the  two  great  remedial  agents  in  this 
disease,  and  should  be  daily  administered,  unless  the  condition  of  the  stom- 
ach of  the  patient  shall  contraindicate  their  use.  Milk  should  be  the  prin- 
cipal article  of  diet.  By  living  in  a  warm  climate,  by  constant  watchfulness, 
and  by  following  the  rules  given  in  acute  Bright's,  a  fatal  termination  may 
be  long  delayed,  although  complete  recovery  cannot  be  hoped  for. 

Let  me  impress  this  fact : — that  no  depleting  remedies  should  be  em- 
ployed, except  in  times  of  emergency,  when  from  some  sudden  renal  con- 
gestion the  function  of  that  portion  of  the  kidney  structure  which  is  still 
performing  the  work  of  elimination  becomes  suddenly  arrested  or  impaired, 
and  acute  uraemic  symptoms  are  developed. 


CIREHOTIC    BEIGHT  S   DISEASE. 

In  the  cirrhotic  form  of  Bright's  disease  the  morbid  processes  do  not  pass 
through  distinct  stages.  The  changes  consist  essentially  in  an  increase  of 
the  intertubular  structure,  and  a  consequent  atrophy  of  all  the  other  struc- 
tures. As  has  been  stated,  it  has  been  called  interstitial  nephritis,  the 
gouty,  hob-nailed  or  small  red  kidney. 

Morbid  Anatomy.— Kidneys  that  are  the  seat  of  interstitial  nephritis  are 
at  no  time  very  much  increased  in  size.  The  changes  are  characterized  by 
a  gradual  increase  in  the  connective-tissue  of  the  kidneys  and  by  atrophy  of 
the  tubules.  In  its  early  stage  the  capsule  is  somewhat  adherent,  its  sur- 
face uneven,  and  the  stroma  of  the  cortical  substance  somewhat  increased. 

In  the  advanced  stage  of  the  process  the  kidneys  are  diminished  in  size, 
sometimes  to  one-fourth  their  normal  bulk  ;  their  capsule  becomes  thick- 
ened and  very  adherent ;  the  thickening  of  the  capsule  is  quite  character- 
istic, and  there  is  more  or  less  prolongation  of  the  connective-tissue  from 
the  capsule  into  the  cortical  substance,  in  consequence  of  which  a  portion 
of  the  kidney  structure  will  be  removed  when  the  capsule  is  torn  off,  leav- 
ing the  surface  of  the  organ  uneven  and  ragged,  having  sometimes  a  finely 
granular  appearance  and  of  a  reddish  color.  Such  kidneys  have  a  dense 
fibrous  feel,  and  dilated  veins  are  sometimes  seen  upon  their  surface. 

Upon  section  it  is  found  that  the  diminution  in  the  size  is  due  to  decrease 
in  the  cortical  substance.     It  is  more  markedly  diminished  in  this  than  in 


CIRREOTIO   BRIGHT'S   DISEASE. 


569 


any  other  form  of  Bright's  disease  ;  it  will  also  be  noticed  that  the  blood- 
vessels are  more  distinctly  visible  than  in  the  normal  kidney.  The  Mal- 
pighian  tufts,  however,  are  not  as  prominent ;  the  medullary  portion  retains 
very  nearly  its  normal  appearance  and  is  not  markedly  diminished  in 
size. 

The  principal  change,  so  far  as  retraction  is  concerned,  takes  place  in 
the  cortical  portion.  This  portion  may  be  reduced  to  one-sixth  its  normal 
thickness.  The  shrinking  is  not  only  apparent  in  the  cortical  substance 
beyond  the  bases  of  the  pyramids,  but  also  in  the  tissue  between  the 
pyramids.  Cysts  are  usually  found  m  the  cortical  portion,  especially  near 
its  surface.  These  cysts  are  of  varying  size,  and  may  be  the  result  of  a 
variety  of  changes. 

The  usual  anatomical  changes  which  occur  are  as  follows  : — 
First,  there  is  cellular  infiltration  of  the  intertubular  connective-tissue 
of  the  cortical  substance,  most  abundant  around  the  capsule  of  the  Mal- 
pighian  tufts  ;  this  gradually  develops  into  a  fibrillated  structure  ;  in  this 
stage  of  the  process  the  tubes  and  their  epithelium  are  but  slightly,  if  at 
all,  implicated.  The  Malpighian  tufts 
are  diminished  in  size,  their  capsule 
thickened,  and  around  the  tufts  are 
laminated,  concentric  zones  of  connec- 
tive-tissue, between  whose  lamellae  are 
flat,  stellate,  or  small  round  cells.  The 
intertubular  growth,  by  its  pressure 
and  contraction,  causes  atrophy  of  the 
tubes,  which  in  some  ]3laces  are  obliter- 
ated, in  others  irregularly  distended, 
and  they  contain  degenerated  epithelial 
products  ;  as  the  atrophy  proceeds  the 
intertubular  tissue  becomes  filled  with 
granular  and  fatty  debris.  Tlie  walls 
of  the  small  arteries  '  become  thickened 
by  hypertrophy  of  all  their  coats,  espe- 
cially the  middle,  but  they  have  an  ir- 
regular outline.  The  firm,  dense  mass 
of  connective-tissue  between  the  Mal- 
pighian tufts  completely  obliterates  the 
expanded  uriniferous  tubules,  bringing 
the  tufts  much  nearer  to  each  other 
than  in  the  normal  kidney,  but  it  does 
not  as  a  rule  obliterate  them.  The 
shrinking  and  even  total  disappearance 
of  the  convoluted  tubes  near  the  tufts,  cause  the  tufts  to  almost  touch 
one  another.     The  Malpighian  tufts  are  sometimes  obliterated,  but  their 

'  Johnson  regards  induration  of  the  arterial  walls  as  due  to  an  hypertrophy  of  the  muscular  coat :  Gull 
and  Sutton  regard  it  as  a  deposit  of  a  hyal in-fibroid,  or  hyaline-granular  mass  infiltrating  the  walls  of  the 
arterioles  and  capillaries.  Cornil  and  Ranvier  say  it  is  neither  :  it  is  but  a  chronic  arteritis  to  them,  both 
intima  and  adventitia  being  involved,  i.  e.,  endarteritis  and  periarteritis. 


Fig  139. 

Cirrhotic  Bright"*  Disease.    Early. 

Section  from  the  Cortex  of  a  Kidney  in  Cir- 
rhosis. 

A.  Capsule  of  a  Malpighian  body  thickened  with 

concentric  layers  of  connective-tissue,  con- 
taining Jlat  and  round  cells. 

B.  Vascular  tuft  of  the  glomerulus  diminished  in 

size. 

C.  Aferent  and  efferent  ressds  of  tvft. 

D  and  E.  Convoluted  tubes  in  transverse  and 
longitudinal  section — Epithelium,  nearly 
normal. 

F.  Small  artery  in  longitudinal  section,     x  350. 


570 


DISEASES    OF   THE    KID1S"BYS. 


obliteration  is  usually  due  to  the  development  of  cysts.     The  cysts  are  often 
"colloid  cysts."  ' 
Sometimes  connective-tissue  formations  extend  into  the  medullary  por- 


FiG.  140. 

Cirrhotic  Blight's  Disease. 

Section  from  tJie  Cortex  of  a  Kidney  in  advanced  Cirrhosis. 

A,  A,  A.  Malpighian  bodies  with  shrunken  tufts  and  thickened  capsules  which  fuse 

with  the  intertubular  connective-tissue. 

B,  B.  Nearly  obliterated  convolvted  tubes. 

C,  Small  Arteries  with  thickened  walls. 

B.  Convoluted  tvbes  containing  colloid  material,     x  60. 

tion,  and  more  or  less  shrinking  of  the  pyramids  occurs  as  a  result.  It  is 
usually,  however,  confined  to  the  cortical  portion.  Those  tubes  that  retain 
their  normal  diameter  are  filled  with  fatty,  granular  or  colloid  cells  ; 
and  their  lumen  contains  hyaline  or  colloid  casts.  Blood  pigment  often 
stains  the  cells  of  the  tubules.  The  tubules  in  an  uncomplicated  cirrhotic 
kidney  contain  coagulated  fibrin,  which  will  be  indicated  by  the  presence 
of  hyaline  casts  in  the  urine  :  all  the  tubular  changes  are  secondary. 

The  pelvis  and  calices  are  congested  ;  the  submucous  tissue  is  dense  and 
thickened  ;  sometimes  the  pelvis  and  calices  are  dilated.  In  the  advanced 
stage  of  this  form  of  kidney  degeneration  the  organs  are  very  greatly  dimin- 
ished in  size — their  capsules  exceedingly  thickened,  their  surface  finely 
granular,  and  the  vessels  on  the  surface  varicosed  and  much  enlarged.     The 

1  Concerning  colloid  casts,  Cornil  and  Ranvier  state  that  "  after  inflammatory  destruction  of  the  nor- 
mal cells  of  the  convoluted  tubules  there  are  developed  cells — not  having  the  character  of  secreting  cells — 
but  assuming  the  cubical  or  flat  form  ;  these  cells  undergo  colloid  transformation  and  fuse  into  a  colloid 
mass,  which  is  increased  by  the  deposit  of  successive  layers,  while  at  the  same  time  new  cells  at  the  perlph' 
ery  become  colloid." 


CIRRHOTIC    BRIGHT'S    DISEASE.  571 

cortical  substance  is  tough  and  fibrous ;  the  kidneys  are  of  a  red  or  buff  color, 
and  usually  a  number  of  small  cysts  are  scattered  through  their  substance. 

Etiology. — The  two  most  common  causes  of  this  form  of  kidney  degenera- 
tion are  gout  and  rheumatism.  One  of  these  causes  is  so  frequently  associ- 
ated with  its  development  that  it  has  given  the  name  of  "  gouty  kidney  " 
to  it.  The  constant  and  continued  use  of  alcohol  may  be  regarded  as  an- 
other cause  of  cirrhotic  kidney,  for  we  not  infrequently  find  this  condition 
of  the  kidney  associated  with  cirrhosis  of  the  liver  ;  and  the  same  steady 
and  prolouged  indulgence  in  the  use  of  alcoholic  drinks  which  produces 
cirrhosis  of  the  liver,  may  produce  cirrhotic  kidney.  These  are  its  three 
principal  causes. 

It  is  occasionally  met  with  in  connection  with  lead  poisoning.  It  has  been 
claimed  that  the  passive  hyperaemia  of  the  kidneys  which  occurs  in  con- 
nection with  some  forms  of  heart  disease  leads  to  the  development  of  cir- 
rhotic kidney.  Cold,  especially  in  a  variable  climate,  exposure,  poverty,  and 
bad  hygiene  are  strong  predisposing  causes.  It  is  met  with  most  often  in 
and  after  middle  life.  Active  brain  workers  are  more  liable  to  it  than 
those  who  are  indolent  and  lihlegmatic. 

Symptoms. — The  early  symptoms  of  the  cirrhotic  form  of  Bright's  disease 
are  always  obscure.  It  is  so  insidious  in  its  development  that  its  commence- 
ment can  rarely  be  determined  One  of  its  earliest  and  most  constant  signs 
is  a  frequent  desire  to  pass  urine,  which  may  contain  neither  albumen  nor 
casts.  Dropsy  may  be  absent,  and  there  may  be  none  of  the  symptoms 
which  usually  mark  the  presence  of  kidney  disease.  Tiiere  may  be  only 
ill-defined  nervous  symptoms  during  life,  and  yet  at  the  autopsy  extensive 
cirrhotic  degeneration  of  the  kidneys  may  be  found. 

Usually  the  disease  is  developed  in  the  following  manner  :  an  individual 
notices  that  he  is  growing  feeble  without  any  apparent  cause  ;  he  is  suffering 
from  dyspeptic  symptoms  ;  he  notices  that  he  is  passing  a  larger  quantity 
of  urine  than  normal,  and  perhaps  at  the  same  time  there  will  be  a  slight 
swelling  of  the  lower  extremities  after  prolonged  exertion,  such  as  stand- 
ing or  walking.  This  oedema  comes  and  goes,  is  more  marked  at  night  on 
retiring,  and  disapjDears  in  the  morning  on  rising.  The  complexion  assumes 
a  dingy  hue.  His  disposition  changes,  he  is  morose,  fretful,  and  his  mem- 
ory is  treacherous.  Insomnia  and  headache  are  tormenting,  and  there 
may  be  sudden  loss  of  sight.  The  appetite  is  lost  or  is  capricious.  It  is 
for  the  relief  of  their  dyspeptic  symptoms  that  this  class  of  patients  usu- 
ally consult  a  physician,  and  a  plan  of  treatment  is  adopted  for  their 
relief,  with  the  assurance  that  they  will  be  better  as  soon  as  they  can  leave 
off  work  and  take  rest.  A  single  or  repeated  examinations  of  the  urine 
may  fail  to  detect  either  albumen  or  casts,  and  the  promises  of  speedy  re- 
covery become  more  positive.  The  case  goes  on  ;  the  patient  becomes 
more  and  more  feeble,  he  has  a  careworn  look,  the  complexion  is  altered, 
the  eye  has  a  peculiar  expression  on  account  of  the  oedema  of  the  conjunc- 
tiva, nervousness  and  restlessness  increase,  and  insomnia  becomes  con- 
stant ;  suddenly  under  great  excitement  convulsions  occur  and  the  indi- 
vidual passes  into  coma,  remains  insensible  for  twenty  four  hours  and  dies. 


672  DISEASES    OF   THE   KIDNEYS. 

Perhaps  the  urine  was  examined  the  day  before  the  convulsion  and  no  al- 
bumen was  found  ;  but  if  it  is  examined  at  the  time  of  the  seizure  both 
albumen  and  casts  are  present. 

The  three  prominent  symptoms  of  this  form  of  Bright's  disease  are 
changes  in  the  urine,  the  dropsy  and  the  nervous  phenomena. 

The  urme  is  increased  in  quantity  and  of  low  specific  gravity.  It  is 
characteristic  of  the  urine  in  this  form  of  Bright's  disease  that  albumen  is 
sometimes  present  and  sometimes  absent.  In  the  other  forms,  albumen  is 
always  found  in  greater  or  less  quantities.  It  may  be  necessary  to  examine 
several  specimens  before  casts  will  be  found,  but  when  found,  they  usu- 
ally are  of  the  large  hyaline  variety ;  granular  casts  are  infrequent  ;  often 
several  examinations  of  the  urine  are  necessary  before  any  satisfactory  evi- 
dence of  the  disease  can  be  obtained. 

Dropsy  is  never  very  marked.  Slight  oedema  of  the  feet  and  ankles  after 
exertion  is  present  in  most  cases.  When  oedema  of  the  feet  and  ankles  is 
constant,  and  is  associated  with  the  general  symptoms  and  conditions  of  the 
urine  which  have  been  described,  the  diagnosis  is  readily  made.  When  as- 
cites is  present,  it  is  due  to  changes  which  have  taken  place  in  the  liver 
rather  than  to  those  in  the  kidney. 

Its  most  prominent  symptoms  are  associated  with  its  nervous  phenomena  : 
they  come  and  go  in  a  manner  not  well  understood.  The  earliest  and 
most  constant  is  headache,  which  is  often  violent ;  occurring  as  it  very 
commonly  does  with  gout  and  rheumatism,  it  is  very  apt  to  be  regarded  as 
gouty  or  rheumatic  in  character.  With  these  headaches  there  is  more  or 
less  disturbance  of  nerve  function,  such  as  vertigo,  temporary  inability  to 
speak,  loss  of  sight  and  hearing,  diplopia,  myopia,  presbyopia — numbness, 
neuralgic  pains,  muscular  cramps,  chorea,  temporary  and  partial  paraly- 
sis in  one  arm  or  leg,  hemiplegia  or  paraplegia.  Nervous  dyspnoea  is  not 
uncommon,  and  it  may  be  accompanied  by  "  Oheyne-Stokes'  respira- 
tion." There  may  be  confusion  of  thought  or  impairment  of  memory;  con- 
iBrmed  mania  may  be  developed.  TJraBmic  vomiting  inducing  great  prostra- 
tion, and  angemia — unaccompanied  by  dropsy — are  alarming  symptoms. 
There  may  be  excessive  itching  of  the  surface.  These  patients  are  al- 
ways liable  to  convulsions  after  severe  mental  or  physical  exertion  ;  from 
the  convulsions  they  may  pass  directly  into  coma,  or  become  delirious, 
with  a  brown,  dry  tongue,  dilated  pupils,  and  thus  gradually  become 
comatose. 

It  is  always  important  to  remember  the  dangers  to  which  these  patients 
are  constantly  exposed.  Cardiac  hypertrophy  is  present  in  a  greater  or  less 
degree  in  the  advanced  stage.  The  hypertrophy  is  usully  confined  to  the 
left  ventricle.  The  presence  of  left  ventricular  hypertrophy  without  val- 
vular insufficiency  is  sufficient  to  direct  attention  to  the  kidneys.  If,  in 
connection  with  the  cardiac  hypertrophy  the  urine  is  abundant  and  of 
low  sijecific  gravity,  containing  only  a  trace  of  albumen,  the  evidences  of 
contracted  kidney  are  almost  positive.  Many  theories  have  been  advanced 
to  explain  the  connection  between  cardiac  hypertrophy  and  the  cirrhotic 
kidney  ;  some  regard  it  as  purely  mechanical,  produced  by  '*the  obstruc- 


CIRRHOTIC    BRIGHT'S   DISEASE.  573 

tion  to  the  renal  circulation  and  the  consequent  increased  pressure  in  the 
aorta;"  but  there  is  no  conditio /i  ot  renal  obstruction  that  will  explain 
the  hypertrophy.  Otliers  claim  that  the  walls  of  the  renal  and  of  all 
the  other  arteries  progressively  hypertrophy  from  the  altered  condition  of 
the  blood  and  the  retained  urinary  excretion,  until  the  heart  becomes 
hypertrophied  as  "a  result  of  the  antagonism  of  forces."  The  order  of 
its  occurrence  seems  to  be,  first,  capillary  resistance  ;  second,  high  arterial 
tension  ;  third,  cardiac  and  arteriole  hypertrophy.' 

Amaurosis  is  a  frequent  attendant  of  cirrhotic  kidney  ;  the  loss  of  sight 
comes  on  gradually  ;  one  eye  only  may  be  affected,  but  usually  both  eyes 
are  equally  involved  ;  the  cause  of  the  loss  of  sight  is  a  true  neuro-retini- 
tis,  which  can  readily  be  recognized  by  an  ophthalmoscopic  examination. 
The  optic  papilla  is  cloudy  and  swollen  ;  the  retinal  veins  are  distended 
and  tortuous,  and  there  are  white  patches  on  the  retina.  White  dots  and 
streaks  in  the  perimeter  of  the  macula  lutea,  are  thought  to  be  character- 
istic. 

Differential  Diagnosis. — This  variety  of  Bright's  disease  may  be  mistaken 
for  diabetes.  The  thirst,  the  large  quantity  of  urine  passed,  the  dyspeptic 
symptoms,  the  progressive  emaciation,  the  absence  of  casts  and  albumen 
lead  toward  diabetes ;  but  the  low  specific  gravity  of  the  urine  and  the 
absence  of  sugar  soon  settle  the  question.  The  presence  of  a  gouty  or 
rheumatic  diathesis,  the  insidious  development  of  the  disease,  the  large 
quantity  of  urine,  its  low  specific  gravity,  with  little  or  no  albumen  and 
only  occasional  casts,  are  sufficient  to  distinguish  this  from  the  other  forms 
of  Bright's  disease. 

Prognosis. — When  the  anatomical  changes  which  characterize  this  form 
of  renal  disease  are  once  established,  their  tendency  is  to  progress ;  and 
although  a  long  period  may  elapse  between  their  commencement  and  the 
fatal  termination,  yet  whenever  there  is  reason  to  believe  that  the  morbid 
processes  are  advanced  the  patient  is  constantly  in  danger  from  complica- 
tions. Serous  inflammations  are  not  as  liable  to  occur  as  in  other  varie- 
ties of  Bright's  diseases,  but  mucous  inflammations  are  more  frequently 
met  with,  especially  bronchitis,  which  assumes  a  chronic  type. 

Its  complications  are  pericarditis,  pneumonia,  acute  and  chronic  bron- 
chitis, pleurisy,  chronic  gastric  and  intestinal  catarrh,  cirrhosis  of  the 
liver,  atheroma  and  sclerosis  of  arteries,  eczema,  and  psoriasis.  In  its 
advanced  stage  hemorrhages  from  mucous  and  serous  surfaces,  as  well  as 
into  the  substance  of  organs,  are  liable  to  occur.  The  most  serious  of 
these  hemorrhages  are  the  cerebral.  It  is  more  frequently  associated  with 
cerebral  apoplexy  than  any  other  form  of  kidney  disease.  Hemorrhages 
in  the  retina  are  common.^  It  must  be  remembered  that  inflammation  of 
the  uriniferous  tubes  may  be  ingrafted  upon  cirrhotic  kidney,  and  that 
the  three  forms  of  degeneration  may  be  present  in  the  same  kidney. 

'  Dickenson  regards  the  vascular  lesion?  as  partly  hypertrophy,  and  partly  fibroid. 

2  In  100  cases  reported  by  Mahomed  seventeen  died  of  heart  disease  and  fifteen  of  apoplexy,  i.  e., 
thirty-two  per  cent,  of  cardio-vas-cular  changes.  Of  thirteen  who  died  of  surgical  diseases,  he  says  many 
died  indirectly  from  failing  heart.  Eighteen  died  of  lung  diseases  (eleven  from  severe  bronchitis  and 
emphysema,  and  seven  from  pleurisy  and  pneumonia). 


57-±  DISEASES  OF  THE   KIDNEYS. 

Treatment. — In  this  form  of  kidney  disease  no  special  plan  of  treatment 

can  be  adopted.  It  has  been  claimed  that  the  long-continued  administra- 
tion of  mercury  in  small  doses  has  the  power  to  arrest  or  prevent  connec- 
tive-tissne  dcTelopment,  but  there  is  no  evidence  that  it  has  such  power ; 
besides,  in  most  instances,  cirrhotic  kidney  is  developed  in  connection  with 
a  gouty  or  rheumatic  diathesis  which  most  positively  contraindicates  the 
prolonged  use  of  mercurials.  When  it  is  developed  in  connection  with  lead- 
poisoning,  mercurials  are  most  decidedly  contraindicated.  Mercurials  can 
be  employed  with  possible  advantage  only  in  those  cases  in  which  cirrhotic 
kidney  is  developed  in  connection  with  a  cirrhotic  liver.  The  bichloride 
is  the  preparation  -usually  employed  in  such  conditions.  If  the  disease  de- 
velops in  connection  with  gouty  or  rheumatic  manifestations,  the  same 
means  which  are  employed  to  relieve  gouty  or  rheumatic  articular  manifes- 
tations will  afford  relief. 

Many  of  these  patients  will  derive  great  benefit  from  residing  for  a  time  in 
those  localities  where  they  may  constantly  use  water  from  alkaline  springs. 
The  Germans  and  French  recommend  very  extensively  the  use  of  alkaline 
waters  in  the  treatment  of  this  class  of  diseases.  Milk,  skimmed  milk,  and  but- 
ter-milk have  all  been  vaunted  as  possessing  curative  pro23erties  ;  hence  the 
once  famous  "milk  cure."  Although  these  patients  appear  anaemic,  their 
nervous  symptoms  are  aggravated  rather  than  relieved  by  the  use  of  iron. 
In  a  certain  proportion  of  cases  cod-liver  oil  will  be  found  of  service,  espe- 
cially when  combined  with  the  hypophosphite  of  soda ;  diuretics  are  not 
indicated,  but  when  a  marked  diminution  in  the  urinary  secretion  occurs, 
their  temporary  employment  may  be  of  service.  When  the  disease  is  devel- 
oped in  connection  with  cirrhosis  of  the  liver,  an  occasional  hydragogue 
cathartic  may  be  attended  with  benefit.  It  is  of  the  utmost  importance 
that  this  class  of  patients  should  make  a  permanent  residence  in  a  warm 
climate,  and  that  all  the  exciting  causes  of  cirrhotic  development  should 
be  carefully  avoided.  Although  a  cure  cannot  be  hoped  for,  the  progress 
of  its  development  may  be  delayed,  and  by  carefully  watching  the  condition 
of  the  nervous  system,  and  by  timely  interference,  the  development  of  the 
graver  forms  of  nervous  disturbance  may  be  delayed  or  prevented,  and  the 
life  of  the  patient  prolonged.  For  symptoms  or  complications  that  demand 
a  narcotic  or  anodyne,  opium  is  to  be  used  in  preference  to  all  others.  In 
its  advanced  stages,  inhalation  of  oxygen  has  caused  disappearance  of  albu- 
men. ' 

Whenever  there  is  extensive  general  anasarca,  and  the  respiration  be- 
comes impeded  by  cedema  of  the  chest-walls,  or  by  an  oedematous  condition 
of  the  lungs,  and  all  other  means  have  failed  to  relieve  the  drojjsy,  prompt 
and  sometimes  permanent  relief  may  be  afforded  by  making  free  incisions 
through  the  skin  into  the  areolar  tissue  above  the  ankles,  or  by  pricking 
the  parts  with  needles  in  many  places.^  Those  dyspeptic  and  gastric  symp- 
toms which  are  so  obstinate  and  distressing  can  usually  only  be  relieved  by 
a  carefully  regulated  diet. 

1  Dajardin-Beaumetz. 

*  See  London  Lancet,  1877,  i.  649.    Southey  uses  drainage  tubes  in  anasarca. 


WAXY    KIDNEY. 


575 


WAXY    KIDNEY. 


("  Amyloid  Form  "  of  Bright' s  Disease.) 

Amyloid  degeneration  is  always  chronic  ;  it  has  no  acute  stage,  and 
usually  invades  several  organs  of  the  body  simultaneously  ;  when  the  kid- 
ney is  the  seat  of  this  degeneration  its  tissues  become  infiltrated  with  amy- 
loid material.  Cornil  and  Ranvier  found  that  waxy  degeneration  in  the 
kidneys  was  invariably  associated  with  chronic  parenchymatous  nephri- 
tis ;  they  are,  moreover,  convinced  that  the  latter  condition  always  pre- 
cedes amyloid  degeneration. 

Morbid  Anatomy. — The  primary  waxy  changes  take  place  in  the  walls 
of  the  minute  arteries ;  secondarily  the  secreting  tubes  and  cells  are  in- 
volved. At  first,  when  the  walls  of  the  vessels  are  principally  involved,  there 
is  little  change  in  the  appearance  of  the  kidneys.  They  may  be  slightly 
increased  in  size,  firmer,  and  of  a  paler  color  than  normal. 

Upon  section  the  Malpighian  tufts  appear  more  prominent  than  normal, 
and  present  the  appearance  of  gray  translucent  points,  which  reflect  light 
better  than  the  surrounding  tissue.  Usually  both  the  cortical  and  medul- 
lary portions  are  simultaneously,  but  unequally,  involved  ;  by  the  "  iodine 
test "  the  amyloid  change,  however  slight,  will  become  very  distinct,  and  a 
section  under  the  microscope  will  show  the  change  to  be  most  marked  in 
the  vessels  in  the  Malpighian 
tufts,  the  vasa  recta  and  in  the 
middle  coats  of  the  small  arteries. 

In  a  more  advanced  stage  of 
the  process  the  kidneys  will  be 
increased  in  size,  their  capsules 
be  non-adherent,  their  surfaces 
smooth  and  of  a  pale  color  with 
stellate  vascularity. 

On  section  the  increase  in  the 
size  will  be  found  to  be  due  to  an 
increase  in  the  cortical  substance, 
which  is  denser  than  normal. 
The  medullary  substance  is  but 
slightly  increased.  The  normal 
anatomical  outline  of  the  cortical 
and  medullary  portion  is  lost,  the 
Malpighian  tufts  are  indistinct, 
looking  like  little  grains  of  boiled 
sago,  and  the  whole  cortical  sub- 
stance has  a  peculiar  waxy  ap- 
pearance. Under  the  microscope 
an  entire  section  will  present  a 
shining  yellow  appearance,  as  if  all  the  tissues  of  the  organ  were  infiltrated 
with  amyloid  material.     The  glomeruli,  most  of  the  arterioles,  the  small 


Fig.  14  . 

Waxy  Kidney, 

Section  from  the  Cortex  of  a  Kidney  in  commencing  Amy 

laid  Degeneration. 

A.  Malpighian  body.     The  lower  part  of  the  vasovlar 

tvfi  i,i  the  seat  of  the  amyloid  change. 

B,  B.  Conholuted  tubes  'containing  hyaline  and  granulO' 

fatty  matter. 

C,  C.  Arteries,  with  coats  shmving  waxy  degeneration. 
Z>,  D.  EjAthelium  of  convoluted  'tvbes  containing  granu- 
lar and  fatty  matter.    X  300. 


576 


DISEASES   OF   THE   KIDKETS. 


veins  and  the  basement  membrane  of  the  tubules  will  be  infiltrated. 
The  epithelial  cells  of  the  convoluted  tubes  are  not  infrequently  flattened. 
The  contents  of  the  tubes  may  be  made  up  of  broken-down  epithelium  and 
fatty  granules,  mingled  with  a  material  which  is  fibrinous  in  its  nature  ; 
this  material  will  not,  however,  give  the  characteristic  reaction  of  amyloid 
matter.  Fatty,  granulo-fatty,  and  hyaline  materials  are  found  in  all 
cases  in  addition  to  the  above.  Usually  the  kidneys  atrophy  and  become 
very  much  diminished  in  size,  sometimes  less  than  one-half  their  normal 
size;  their  capsules  are  adherent,  their  surfaces  uneven,  granular,  and  of 
a  pale  color. 

On  microscopical  examination  it  will  be  seen  that  the  diminiition 
in  size  is  due  to  decrease  of  both  the  medullary  and  cortical  portions. 
The  Malpighian  tufts  are  large  and  prominent,  and  are  grouped 
together ;  the  small  arteries  are  enlarged  and  at  points  are  imper- 
vious.    On  examination  of  sections  from  different  portions  of  the  kidney, 

the  tubules  will  be  found  at  all  points 
more  or  less  atrophied  and  their  walls 
collapsed  ;  some  are  obliterated  ;  the 
blood-vessels  will  appear  thickened,  and 
their  outline  will  be  more  or  less  irregu- 
lar. Iodine  upon  the  degenerated  Mal- 
pighian tufts  will  give  the  characteristic 
amyloid  reaction.  The  degree  of  atrophy 
may  vary,  but  however  extensive  it  may 
be,  by  dipping  a  section  in  the  iodine 
solution,  and  microscopically  examining 
it  with  a  low  power,  one  will  always 
find  abundant  evidence  of  amyloid  ma- 
terial in  the  degenerated  vessels  and 
tubes. 

Etiology. — The  primary  cause  of  amy- 
loid degeneration  is  still  a  vexed  ques- 
tion. It  never  occurs  in  those  who 
are  in  perfect  health,  and  the  circum- 
stances under  which  it  almost  uniformly 
occurs  determine  to  a  certain  extent  its 
causation.  It  is  most  frequently  met 
with  in  syphilitic  subjects.  Another 
frequent  cause  is  prolonged  suppura- 
tion, especially  when  associated  with 
diseases  of  bone.  A  long-continued  empyema  may  give  as  a  result  an  amy- 
loid kidney.  It  is  not  infrequently  met  with  in  those  who  die  of  pulmonary 
phthisis,  consequently  chronic  suppurative  diseases  of  the  lungs  must  be 
ranked  among  its  causes.  Caries  of  bone,  ulcers  of  the  intestines,  cancer, 
and  chronic  rheumatism  may  induce  it. 

Symptoms. — The  symptoms  which  attend  the  development  of  amyloid  de- 
generation of  the  kidney  are  never  well  marked.     The  usual  manner  of  its 


Fig.  142 

Waxy  Kidney. 

Vertical  Section  from  the  Medullary  Portion  of 

a  Kidney  in  advanced  Waxy  Degeneration. 
A,  A.  Collecting  tubules  containing  fatty  gran^ 

ules,  B,  and  colloid  matter,  C. 
D,  D.  Wall  of  tubules  showing  thickening  and 
irregularity,  the  result  of  waxy  change. 
Transverse  and  F  longitudinal  sec- 
tion of  blood-vessels  with  lumen  nearly 
obliterated  by  amyloid  degeneration 
of  the  coats.  G.  Ascending  limb  of 
Henle^s  loop,     x  350. 


E. 


WAXY    KIDNEY.  577 

development  is  as  follows  :  an  individual  who  is  suffering  from  tertiary 
syphilis  or  some  exhausting  form  of  disease,  notices  that  he  is  •  losing 
strength,  that  he  is  becoming  more  feeble  than  usual,  and  that  he  has  less 
mental  and  physical  vigor  than  he  is  accustomed  to  have  ;  that  he  is  trou- 
bled with  shortness  of  breath  on  exertion  ;  that  he  has  an  unusually  pallid 
countenance,  and  that  there  is  a  great  increase  in  the  quantity  of  urine 
passed.  He  is  obliged  to  rise  two  or  three  times  during  the  night  to  pass 
urine,  and  at  times  he  passes  large  quantities.  He  also  notices  a  fulness 
of  the  abdomen  which  he  has  never  before  observed,  and  sometimes  there 
is  a  sense  of  weight  in  its  upper  portion.  He  may  have  detected  a  tumor 
in  the  right  and  perhaps  in  the  left  hypochondrium.  When  he  assumes 
the  recumbent  posture,  he  must  have  the  upper  portion  of  the  body  ele- 
vated to  prevent  dyspnoea.  Doubtless  the  dysj^noea  is  partially  due  to  the 
anaemia  and  partially  to  the  pressure  caused  by  an  enlarged  liver  and  spleen. 
Perhaps  there  is  slight  oedema  about  the  ankles,  especially  at  night.  The 
patient  does  not  perspire  readily,  but  when  he  does  the  perspiration  has  a 
urinous  odor.  Certain  articles  of  food,  especially  fatty  substances,  which 
never  before  have  disagreed  with  him,  now  give  rise  to  dyspeptic  symptoms 
and  he  may  have  occasional  vomitings. 

This  train  of  symptoms  coming  on  in  one  who  has  been  the  subject  of 
any  of  the  forms  of  disease  to  which  I  have  referred,  leads  to  the  suspicion 
that  amyloid  degeneration  of  the  kidney  is  taking  place.  If,  upon  further 
examination,  a  marked  enlargement  of  the  liver  and  spleen  is  found,  and 
the  surface  of  the  liver  is  smooth  and  its  edges  sharp,  it  is  almost  certain 
that  the  amyloid  form  of  Bright's  disease  exists.  With  these  symp- 
toms there  will  also  be  more  or  less  fluid  found  in  the  abdominal  cavity, 
but  its  presence  will  be  due  to  changes  which  have  occurred  in  the  liver  and 
not  to  changes  in  the  kidneys.  The  blood  is  slightly  altered ;  the  white 
corpuscles  are  somewhat  increased  in  number,  and  the  red  are  diminished 
and  ill-defined  ;  in  a  large  proportion  of  cases  there  is  a  peculiar  cachexia 
present  which  is  almost  characteristic.  The  patient  has  a  pale,  waxy  com- 
plexion, with  little  pigmentary  deposits  in  the  skin,  particularly  about  the 
eyelids.     This  cachexia  is  usually  most  marked  in  syphilitic  subjects. 

As  in  the  other  forms  of  kidney  disease,  there  are  three  important  symp- 
toms to  be  considered.  First,  abnormal  changes  in  the  urine  ;  second, 
dropsy ;  third,  nervous  phenomena. 

The  urine  is  increased  in  quantity,  the  patient  perhaps  passing  as  much 
as  one  hundred  ounces  in  twenty-four  hours.  It  is  light  colored,  looking 
very  much  like  clear  water,  or  it  may  have  a  slight  amber  color.  It  is  of 
low  specific  gravity,  sometimes  as  low  as  1.005.  When  tested  for  albumen 
it  will  be  found  always  to  contain  an  appreciable  quantity,  never  a  large 
quantity.  The  amount  of  urea  excreted  is  but  little  if  at  all  diminished  ; 
the  urine  will  always  contain  casts,  either  large  hyaline  or  fine  granular,  or 
both,  but  tlie  hyaline  predominate.  Casts  of  eitiier  variety  usually  are 
not  abundant,  and  several  examinations  may  be  required  before  their  pres- 
ence or  absence  can  be  positively  determined.  Epithelial  and  fatty  casts 
are  sometimes  found. 
37 


578  DISEASES   OF   THE    KIDNEYS. 

Dropsy  is  never  very  marked  in  this  form  of  Bright's  disease.  The  gen- 
eral anasarca  which  is  so  frequently  met  with  in  connection  with  paren- 
chymatous nephritis,  is  never  present.  There  may  be  slight  oedema  of  the 
feet,  especially  at  night,  and  there  may  be  fluid  in  the  abdominal  cavity. 
The  nervous  symptoms  are  never  very  prominent.  This  class  of  patients 
do  not  usually  sufl:er  very  much  from  headache,  and  rarely  have  convulsions 
or  pass  into  coma.  They  usually  die  from  exhaustion,  or  from  some  com- 
plication, or,  in  other  words,  die  from  amyloid  degeneration  of  other  organs, 
diarrhoea,  the  result  of  amyloid  changes  in  the  mucous  membrane  of  the 
intestine,  or  ascites. 

Differential  Diagnosis. — The  diagnosis  of  this  form  of  Bright's  disease  is 
not  difficult  when  it  occurs  as  a  late  manifestation  of  syphilis.  A  copious 
secretion  of  urine  of  low  specific  gravity  containing  little  albumen  and  few 
casts,  in  one  who  has  a  syphilitic  history  with  an  enlarged  liver  and  spleen, 
leaves  little  doubt  as  to  the  character  of  the  kidney  change.  It  is  hardly 
possible  to  confound  the  cachexia  which  attends  this  form  of  Bright's 
disease  with  that  of  any  other  chronic  disease,  for  a  urinary  examination 
will  give  positive  evidence  of  the  renal  disease,  and  it  only  remains  to  de- 
termine its  character,  which  is  usually  readily  reached  by  the  history  of 
the  case.  The  large  quantity  of  urine  passed  often  causes  the  patient  to 
consult  the  physician  with  the  idea  that  he  has  diabetes,  but  the  urinary 
examination  soon  settles  this  question. 

Prognosis. — The  duration  of  this  form  of  Bright's  disease  is  uncertain  ; 
it  undoubtedly  takes  many  years  for  the  anatomical  changes  in  the  kidney 
to  reach  the  stage  of  atrophy,  yet  when  waxy  changes  are  once  established 
recovery  is  impossible.  Eesulting  as  it  does  from  a  grave  constitutional 
cachexia,  the  causes  which  produce  it  are  so  often  continuous  that  they  are 
only  in  a  slight  degree  influenced  by  treatment. 

The  progress  of  the  disease  may  sometimes  be  temporarily  arrested,  but 
its  usual  course  is  steadily  progressive  to  a  fatal  termination.  Amyloid 
degeneration  of  the  kidneys  may  exist  for  many  years,  and  yet  the  patient 
enjoy  a  comparatively  good  degree  of  health.  I  now  have  the  care  of  a 
medical  gentleman  in  whom  the  disease  has  existed  certainly  eight  years, 
yet  he  is  in  such  good  health  as  to  be  able  to  discharge  the  duties  incum- 
bent upon  a  large  country  practice.'  An  exhausting  diarrhoea  or  an  ab- 
dominal dropsy  is  often  the  direct  cause  of  death.  Most  of  the  com- 
plications which  occur  are  degenerative  in  character.  Patients  are  not 
especially  liable  to  have  pneumonia,  bronchitis  or  pericarditis,  or  any  of 
the  acute  inflammations  which  occur  in  connection  with  other  forms  of 
kidney  disease^  Cardiac  hypertrophy  is  rarely  present  in  any  stage  of  the 
amyloid  kidney.  Its  early  symptoms  are  so  obscure  that  it  is  difficult  to 
determine  its  average  duration. 

Treatment. — This  is  an  incurable  disease  ;  there  are  no  known  means  for 
arresting  it  or  preventing  its  development.  The  same  general  principles  are 
to  govern  its  treatment  as  govern  the  treatment  of  waxy  degeneration  in 
other  organs.     First,  if  possible  remove  its  cause,  as  diseased  bones,  pro- 

1  Bartholow  records  a  case  where  there  was  complete  recovery  from  the  waxy  kidney. 


PYELITIS.  579 

longed  suppuration,  or  purulent  accumulations.  If  it  occurs  with  syphilis 
anti  syphilitic  remedies  are  indicated,  always  remembering  that  waxy  de- 
generation occurs  only  as  a  tertiary  manifestation  of  syphilis,  and  that  all 
measures  which  have  a  tendency  to  debilitate  the  patient  must  be  avoided. 
Iodide  of  potassium  and  mercury  are  the  most  reliable  remedial  agents. 
Both  of  these  agents  have  gained  some  favor  as  remedies  in  the  treatment 
of  Bright's  disease,  and  there  are  those  who  employ  indiscriminately  one  or 
the  other  or  both  of  them.  The  benefit  derived  in  certain  cases  from  their 
use  is  undoubtedly  due  to  their  power  over  syphilitic  manife.stations.  In 
such  cases,  the  long-continued  use  of  small  doses  of  mercurials  will  gen- 
erally be  followed  by  marked  improvement,  but  care  should  be  exercised 
that  their  use  be  not  continued  until  the  specific  effect  of  the  drug  is 
produced. 

When  these  patients  are  in  a  debilitated  condition  iodide  of  potassium 
with  cod-liver  oil  will  be  of  greater  service.  The  form  of  iodine  which  I 
have  found  most  serviceable  to  this  class  of  patients  is  pil.  ferri  iodidi. 
One  of  these  pills  given  three  times  a  day,  at  the  time  of  taking  food,  is 
often  followed  by  the  most  beneficial  results.  Diuretics  and  hydragogue 
cathartics  will  rarely  be  required.  The  tincture  of  the  perchloride  of  iron, 
quinine,  nux  vomica,  and  sirups  of  the  phosphates  are  often  beneficial. 

PYELITIS. 

Pyelitis  is  an  inflammation  of  the  mucous  membrane  of  the  pelvis  and 
calices  of  the  kidney,  and  may  run  an  acute  or  chronic  course.  It  may  in- 
volve the  pelvis  and  infundibula  of  one  or  of  both  kidneys.  Some  describe 
an  acute  catarrhal,  pseudo-membranous,  and  calculous  pyelitis  and  a 
chronic  purulent  pyelitis  that  may  or  may  not  result  in  pyonephrosis. 

Morbid  Anatomy. — In  acute  pyelitis  the  mucous  membrane  of  the  pelvis 
of  the  kidney  is  at  first  more  or  less  reddened.  When  very  hypergemic  the 
surface  will  be  dotted  here  and  there  with  little  dark-red  spots  which  are 
minute  ecchymoses ;  the  epithelium  of  the  mucous  surface  is  more  or  less 
removed ;  sometimes  it  is  entirely  removed,  at  others  it  is  removed  in 
patches.  The  peculiar  "  tailed"  cells  of  the  pelvis  are  thrown  off  in  great 
quantity.  As  the  inflammation  progresses  the  mucous  surface  becomes 
covered  with  more  or  less  muco-pus.  The  urine  in  the  |)elvis  will  contain 
numerous  desquamated  epithelial  and  lymph  cells. 

In  some  cases  a  membranous  exudation  may  be  developed  upon  the 
mucous  membrane  of  the  pelvis,  called  ^' pseudo-membranous"  pyelitis. 
It  is  a  diphtheritic  exudation  occurring  in  connection  with  diphtheritic 
exudations  in  other  parts  of  the  body,  and  should  be  called  diphtheritic 
pyelitis.  This  diphtheritic  membranous  exudation  is  liable  to  become  de- 
tached and  block  up  the  ureter.  Sloughs  may  form,  and  after  their  re- 
moval an  ulcerated  surface  may  be  left. 

In  chronic  pyelitis  the  mucous  membrane  of  the  pelvis  of  the  kidney  is 
congested  and  thickened,  and  its  surface  presents  small  vascular  granula- 
tions.    It  assumes  a  grayish  white  or  slate  color  and  is  traversed  by  dilated 


580  DISEASES    OF   THE    KIDI^EYS. 

yeins  ;  the  pelvis  and  infundibula  and  ureter  are  dilated  and  more  or  less 
thickened.  Pus  is  more  or  less  abundantly  formed,  and  if  there  is  no  ob- 
struction it  passes  off  with  the  urine.  Calculi  or  fragments  of  calculi  may 
be  found  mingled  with  the  pus. 

Should  there  be  an  impediment  to  its  escape  it  accumulates  in  the  pelvis, 
which  it  distends  more  and  more,  and  at  last  gives  rise  to  a  condition 
known  as  pyonephrosis.  This  dilatation  as  it  progresses  encroaches  first 
upon  the  papillae,  which  become  flattened  and  obliterated,  next  on  the 
pyramids,  and  finally,  by  the  pressure  it  causes,  the  cortical  portion  of  the 
kidney  disappears.  The  apices  of  the  pyramids  may  suppurate  and  ulcer- 
ate. In  such  cases  only  a  sacculated  pouch  remams  containing  from  one 
to  several  ounces  of  fluid,  which  may  be  mixed  with  inspissated  pus,  broken 
down  calcareous  matter,  ammoniacal  products  and  calculi. 

If  a  renal  calculus  is  present,  and  the  cause  of  the  pyelitis,  more  or  less 
extensive  ulcerations  may  be  established.  These  ulcerations  may  cause 
perforation  of  the  pelvis,  and  give  rise  to  extravasation  of  urine  into  the 
adjacent  tissues.  In  this  (so-called)  calculous  pyelitis  the  kidneys  are  al- 
ways the  seat  of  interstitial  nephritis,  cysts,  marked  atrophy,  etc.  The 
ureter  of  the  kidney  which  is  the  seat  of  the  pyelitis  may  be  completely  ob- 
structed, and  pus,  blood,  and  urinous  material  may  accumulate  behind  the 
obstruction.  If  these  obstructions  are  permanent  an  opening  may  be  made 
through  the  dilated  ureter  and  the  contents  of  the  sac  discharged  into  the 
adjacent  tissues,  into  some  hollow  viscus  or  into  the  abdominal  cavity,  or 
by  an  adhesive  inflammation  reach  the  surface  and  be  discharged  externally. 

When  the  obstructions  are  temporary  the  contents  of  the  sac  are  dis- 
charged into  the  bladder  through  the  ureter  when  they  give  way,  and  such 
obstructions  or  accumulations  may  occur  repeatedly.  Sometimes  these  re- 
tained accumulations  undergo  entire  absorption,  and  there  remains  a  thick 
cicatricial  tissue,  with  the  normal  kidney  tissue  entirely  obliterated,  and 
the  ureter  becomes  transformed  into  a  tendinous  cord.  Under  such  cir- 
cumstances if  the  fellow  kidney  is  healthy  it  becomes  increased  in  size  and 
performs  in  a  very  satisfactory  manner  the  function  of  both  kidneys,  and 
the  patient  may  live  for  many  years.  Again,  in  certain  cases,  the  accumu- 
lation in  the  kidney  is  changed  into  a  cheesy  material,  and  presents  an  ap- 
pearance resembling  what  is  known  as  tubercular  kidney.  Mingled  with 
this  cheesy  mass  may  be  found  the  urine-salts  which  cause  it  to  have  a 
sandy  feel  The  kidney  may  be  changed  into  a  fibrous  shell  containing 
pus  and  debris. 

Etiology. — Pyelitis  is  seldom,  if  ever,  a  primary  disease.  Its  most  fre- 
quent cause  is  the  presence  of  calculi  or  some  foreign  substance  in  the 
pelvis  of  the  kidney,  and  the  pyelitis  is  then  secondary  to  mechanical  irri- 
tation. Pyelitis  may  result  from  extension  of  inflammation  from  the 
bladder  or  ureter,  or  from  acute  interstitial  nephritis,  rarely  from  perine- 
phritic  abscess.  It  may  result  from  the  irritation  produced  by  the  decom- 
position of  urine  retained  in  the  pelvis  of  the  kidney,  as  a  consequence  of 
some  obstruction  to  its  normal  outlet.  For  instance,  an  enlarged  prostate 
gland,  a  tumor  pressing  on  the  ureter,  paralysis  of  the  bladder,  or  an 


PYELITIS.  581 

urethral  stricture  which  causes  obstruction  to  the  passage  of  urine  from 
the  bladder.  As  a  result  of  retention  of  urine  in  the  bladder,  cystitis  is 
developed,  and  the  inflammation  of  the  mucous  surface  of  the  bladder  may- 
extend  to  the  ureters,  and  from  the  thickening  of  their  mucous  lining  and 
the  diminution  of  their  calibre,  the  passage  of  urine  from  the  kidneys  to 
the  bladder  is  obstructed,  and  there  is  not  only  retention  of  urine  in  the 
bladder  but  also  in  the  pelvis  of  the  kidneys.  As  a  result  of  such  retention 
the  urine  undergoes  decomposition,  the  urea  is  changed  into  carbonate  of 
ammonia  and  vs^ater,  the  carbonate  of  ammonia  acts  as  an  irritant  and  ex- 
cites inflammation  of  the  lining  membrane  of  the  pelvis,  and  thus  pyelitis 
is  developed. 

The  absorption  of  the  ammonia  resulting  from  the  decomposition  of  the 
urea  may  be  sufficient  to  give  rise  to  a  condition  which  has  received  the 
name  of  ammonmmia.  This  condition  is  not  infrequently  mistaken  for 
uraemia,  yet  they  differ  widely  in  their  manifestations  and  the  dangers 
which  attend  their  development.  In  ammonsemia  the  urine  when  voided 
isammoniacal,  as  are  also  the  breath  and  perspiration.  The  mucous  mem- 
brane of  the  mouth  is  dry  and  shining;  the  complexion  is  sallow  and  there 
is  increasing  emaciation ;  no  dropsical  accumulations  are  present.  Con- 
vulsions and  vomiting  are  rare ;  chills  are  frequent.  Death  is  usually  pre- 
ceded by  coma.  The  development  of  the  train  of  symptoms  indicative  of 
ammonsemia,  accompanied  by  the  evidence  of  obstruction  to  the  normal 
outlet  of  the  urine,  should  cause  one  to  hesitate  before  performing  any 
operation,  especially  an  operation  for  relief  of  stricture  of  the  urethra. 

Pyelitis  not  infrequently  occurs  in  connection  with  that  class  of  diseases 
which  depend  upon  blood  poisoning — pyaemia,  diphtheria,  and  typhus 
fever.  In  this  connection  it  is  generally  a  complication  of  acute  Bright's 
disease,  which  is  not  severe  in  character,  but  which  causes  bloody  urine. 
It  is  an  almost  diagnostic  complicating  symptom  of  myelitis.  Pyelitis 
occasionally  occurs  in  consequence  of  over-doses,  or  the  prolonged  use,  of 
certain  irritating  drugs,  as  turpentine,  cantharides,  and  other  stimulating 
diuretics.  In  very  rare  instances  it  seems  to  come  on  idiopathically  from 
exposure  to  cold  and  wet,  or  from  some  unknown  cause. 

Symptoms. — In  the  majority  of  cases  the  development  of  pyelitis  is  pre- 
ceded or  accompanied  by  symptoms  due  to  the  causes  which  produce  it, 
such  as  renal  calculi,  diseases  of  the  bladder,  etc'  Prominent  among  those 
symptoms  which  directly  attend  its  development  is  pain  in  the  back.  This 
is  present  in  the  mild  as  well  as  in  the  severe  cases.  This  pain  may  have 
its  point  of  maximum  intensity  over  one  or  both  lumbar  regions.  It  is 
often  of  an  aching  character,  and  shoots  down  along  the  course  of  the 
ureters.  This  pain  is  usually  accompanied  by  frequent  micturition,  and 
when  it  is  very  intense  the  voiding  of  urine  is  almost  incessant  and  is 
attended  by  severe  pain.  The  commencement  of  acute  pyelitis  is  usually 
marked  by  rigors,  and  in  that  chronic  form  in  which  temporary  obstruc- 
tion of  the  ureter  occurs,  rigors  are  frequent. 

1  It  is  said  (Klebs)  that  bacteria  may  be  carried  into  the  bladder  on  unclean  catheters  or  other  instrut 
mente,  and  that  these,  making  their  way  into  the  pelvis,  cause  pyelitis. 


582  DISEASES    OF   THE    KIDNEYS. 

Symptoms  of  hectic  fever  may  also  mark  the  occurrence  of  permanent  ob- 
struction of  the  ureter  and  the  development  of  that  condition  termed />yo- 
neplirosis.  There  is  usually  considerable  lassitude  attending  the  progress 
of  pyelitis,  and  when  the  disease  is  due  to  the  presence  of  a  calculus,  the 
patient  ordinarily  sufEers  more  or  less  pain  on  motion. 

All  of  these  symptoms  are  accompanied  by  changes  in  the  urine,  and 
these  changes  are  its  most  reliable  signs  ; — in  its  early  stage  the  urine  con- 
tains blood  mixed  with  mucus  and  epithelial  cells  from  the  pelvis  and  in- 
fundibula  :  the  presence  of  these  epithelial  cells,  which  are  readily  distin- 
guished from  epithelium  of  any  other  portion  of  the  urinary  tract  by  their 
characteristic  shape  and  appearance,is  its  most  certain  diagnostic  indication. 
The  specific  gravity  of  the  urine  ranges  from  1.025  to  1.030,  and  it  usually 
retains  its  acid  reaction.  In  the  more  advanced  stages  the  characteristic 
epithelium  is  to  a  great  extent  replaced  by  an  abundance  of  pus  cells,  but 
the  urine  retains  its  acid  character.  If  sacculation  of  the  kidneys  is  devel- 
oped, the  urine  will  become  ammoniacal.  More  pain  and  hemorrhage  at- 
tend calculous  pyelitis  than  the  other  forms.  Albumen  is  present  in  pro- 
portion to  the  amount  of  pus  and  blood.  In  the  advanced  stage  of  pyelitis, 
if  the  urinary  channels  remain  free  the  discharge  of  pus  is  constant.  If  the 
ureter  becomes  blocked,  for  a  time  the  urine  may  be  quite  normal,  but  the 
removal  of  the  obstruction  is  followed  by  a  copious  flow  of  purulent  urine. 
This  may  be  repeated  from  time  to  time,  at  intervals  varying  from  a  few 
days  to  a  few  months.  If  the  pelves  of  both  kidneys  are  affected,  and  there 
is  partial  or  complete  obstruction  of  one  side,  the  accumulation  of  pus  in  the 
urine  is  diminished,  but  not  entirely  prevented.  If  the  obstruction  is  long 
continued  or  becomes  permanent,  a  tumor  develops  in  the  lumbar  region. 

The  development  of  d^pyonephrotic  tumor  indicates  complete  obstruction 
of  the  ureter.  The  existence  of  the  tumor  is  determined  by  the  presence  of 
bulging  between  the  crest  of  the  ilium  and  the  false  ribs  on  the  right  or  left 
side,  according  as  the  right  or  left  kidney  is  involved.  As  a  consequence 
the  outline  of  the  abdomen  is  rendered  unsymmetrical.  On  palpation,  deep- 
seated  fluctuation  is  felt  over  the  tumor,  which  usually  is  tender  on  press- 
ure. The  area  of  percussion  dulness  will  correspond  to  the  outline  of  the 
tumor,  except  where  it  is  crossed  by  the  colon.  With  these  physical  signs 
present,  and  a  history  of  pyelitis,  one  will  be  justified  in  resorting  to  the 
exploring  trocar  to  complete  the  diagnosis. 

Differential  Diagnosis. — The  diagnosis  of  pyelitis  in  its  first  or  acute  stage 
rests  almost  exclusively  on  the  presence  in  the  urine  of  the  characteristic 
epithelium  of  the  pelvis  and  infundibula  mixed  with  blood  globules  and 
mucus.  If  the  urine  contains  pus  cells  mixed  with  these  epithelial  cells  it 
indicates  a  more  advanced  stage  of  the  disease.  The  presence  of  pus  and 
acid  urine,  with  pain  in  the  lumbar  region,  accompanied  by  the  develop- 
ment of  a  tumor  at  the  seat  of  pain,  which  tumor  gradually  increases  in 
size  and  suddenly  disappears  at  the  same  time  that  a  copious  discharge  of 
pus  takes  place  from  the  bladder,  which  discharge  is  attended  by  a  sense  of 
great  relief  to  the  patient,  renders  the  diagnosis  of  pyonephrosis  very  cer- 
tain.    If  the  ureter  of  the  affected  kidney  is  permanently  obstructed,  the 


PYELITIS.  583 

lumbar  tumor  is  liable  to  be  mistaken  for  Jiydronephrosis,  an  hydatid  cyst, 
or  Q.  perinepJiritic  abscess. 

In perinephritic  abscess  neither  pus,  blood,  mucus,  epithelia  nor  albu- 
men will  be  found  in  the  urine  ;  in  pyonephrosis  they  are  common  and 
constant.  Pain  on  motion,  the  occurrence  of  slight  oedema  over  the  tumor, 
the  delayed  appearance  of  fluctuation — these  are  in  contrast  to  the  symp- 
toms of  pyonephrosis.  The  mass  of  tumor  in  perinephritic  abscess  may  be 
tilted  forwards  by  pressure  in  the  renal  region,  which  is  never  the  case  with 
pyonephrosis.'  Fever  is  a  marked  symptom  in  abscess,  and  slight  or  absent 
in  pyoDephrosis.  In  women  a  pyonephrotic  tumor  has  been  confounded 
with  an  ovarian  cyst.  The  exploring  trocar  will  very  quickly  remove  all 
doubts. 

Pyelitis  is  distinguished  from  cystitis  by  absence  of  vesical  pain  and  fre- 
quent micturition,  by  lumbar  pain,  and  by  the  intimate  admixture  of  for- 
eign materials  in  the  urine.  Pelvic  epithelial  cells  are  not  found  in  the 
urine  of  uncomplicated  cystitis.  In  pyelitis  the  urine  is  acid  ;  in  cystitis 
it  is  alkaline.  When  pyelitis  occurs  as  a  complication  of  chronic  cystitis, 
an  enlarged  prostate  gland,  or  urethral  stricture,  it  is  often  impossible  to 
diagnosticate  its  existence  if  there  is  no  tumor  in  the  lumbar  region.  Under 
these  circumstancesthe  character  of  the  urinary  constituents  is  not  of  much 
assistance.  If,  however,  the  quantity  of  pus  is  large,  the  urine  slightly 
acid,  the  loins  painful  on  pressure,  and  the  febrile  movement  constant, 
with  rapid  loss  of  flesh  and  strength,  there  is  good  reason  to  believe  that 
chronic  pyelitis  has  been  added  to  disease  of  the  bladder  and  urethra. 

Prognosis. — The  prognosis  in  pyelitis  depends  upon  the  nature  of  its  ex- 
citing cause.  In  simple  catarrhal  pyelitis,  not  connected  with  extensive 
disease  of  other  portions  of  the  urinary  ajjparatus,  the  prognosis  is  good, 
unless  the  disease  affects  both  kidneys  and  has  reached  the  purulent  stage; 
then,  whatever  may  have  been  its  cause,  the  prognosis  is  bad.  When  the 
disease  is  confined  to  one  side,  recovery  is  possible,  although  one  kidney 
may  be  completely  destroyed.  We  suspect  unilateral  layelitis  with  calculi 
and  with  tumors  that  compress  an  ureter ;  but  following  a  cystitis,  ure- 
thritis, prostatitis,  etc.,  the  affection  is  usually  bilateral,  and  the  prognosis 
is  unfavorable. 

Pyelitis  may  be  regarded  as  a  hopeless  disease  when  it  is  secondary  to  an  en- 
larged prostate  gland,  extensive  chronic  cystitis,  urethral  stricture,  creancer 
of  the  kidney.  It  is  exceedingly  grave  when  it  depends  upon  renal  calculi  or 
hydatids,  although  it  is  not  necessarily  fatal.  The  issues  of  a  pyonephrosis 
are  uncertain  ;  the  various  directions  in  which  a  sac  may  burst  determine 
to  a  great  extent  its  termination.  Eupture  into  the  peritoneal  or  thoracic 
cavity  is  speedily  fatal.  Kecovery  is  possible  if  the  rupture  takes  place 
externally  or  into  the  intestine.  Sometimes,  when  the  sac  does  not  rupture, 
patients  die  from  the  exhaustion  caused  by  the  long-continued  discharge. 
Eecovery  may  be  reached  by  a  gradual  diminution  of  the  discharge  and  a 
final  contraction  and  obliteration  of  the  sac,  provided  the  other  kidney  is 
unaffected.     Death  may  occur  from  uremia  or  ammonsemia. 

1  London  Lancet,  January,  February,  March,  1879. 


584  DISEASES    OF   THE    KIDNEYS. 

Treatment. — The  first  thing  in  the  treatment  of  pyelitis  is,  if  possible, 
to  remove  its  cause.  If  the  attack  is  an  acute  one,  and  at  the  onset  of  the 
disease  the  fever  is  considerable,  the  pain  in  the  lumbar  region  severe,  and 
the  urine  bloody,  wet  cups  should  be  freely  applied  to  the  loins,  followed 
by  a  hot  bath,  and  a  suflBciently  large  hypodermic  of  morphine  to  entirely 
relieve  pain.  The  patient  should  drink  freely  of  alkaline  fluids  and  should 
be  l\ept  in  bed. 

In  chronic  pyelitis,  when  the  secretion  of  pus  is  abundant,  astringents 
may  be  employed  to  diminish  the  purulent  secretion.  Balsams  are  here 
indicated.!  Attention  should  be  paid  to  the  general  health  of  the  patient. 
Cod-liver  oil  and  quinine  should  be  administered  with  a  nutritious  and 
non-stimulating  diet.  A  residence  at,  and  prolonged  use  of  the  waters  of 
some  alkaline  spring  will  often  be  found  of  great  service.  Diluent  alkaline 
drinks  and  milk  should  be  the  sole  articles  of  diet  in  the  acute  stage. 

When  a  tumor  exists  and  can  readily  be  reached  through  the  integument, 
aspiration  may  be  performed,  after  which  the  question  of  a  free  permanent 
external  opening  will  present  itself,  and  must  be  decided  by  the  peculiarities 
of  the  case. 

ARTEEIO-CAPILLAET    FIBROSIS,    WITH    CONTRACTED    KIDNEYS. 

Dr.  Bright  himself  and  most  pathologists  since  his  time  noticed  that 
the  granular  contracted  kidney,  the  ''small  red  kidney"  of  the  English 
writers,  was  usually  associated  with  morbid  changes  in  other  organs,  and 
it  was  generally  held  that,  under  these  circumstances,  the  kidney  was  the 
organ  primarily  affected,  and  that  tbe  other  changes  were  the  result  of  the 
cachexia  produced  thereby. 

In  1872,  Sir  Wm.  W.  Gull  and  Wm.  Henry  Sutton'^  denied  the  correct- 
ness of  this  latter  opinion,  and  claimed  that  all  the  morbid  changes, 
those  found  in  the  kidney,  as  well  as  those  of  the  other  organs,  were 
equally  dependent  upon  a  fibroid  degeneration  of  the  walls  of  the  smaller 
arterioles  and  capillaries.  To  this  degeneration  they  gave  the  name 
arterio-capillary  fibrosis,  and  while  admitting  that  it  commonly  began  in 
the  kidneys,  they  claimed  that  there  was  evidence  of  its  primary  appear- 
ance in  other  organs,  and  also  of  its  occasional  localization  elsewhere, 
to  the  entire  exclusion  of  the  kidney.  The  theory  then  advanced  has 
been  very  thoroughly  worked  out  by  subsequent  writers,  whose  arguments 
and  proofs  are  very  strong,  although,  perhaps,  not  yet  entirely  demon- 
strated. The  supporters  of  this  theory  maintain  the  existence  of  a  general 
fibroid  degeneration  usually  occurring  during,  or  after  middle  life,  but 
sometimes  also  at  earlier  periods,  and  deserving  to  be  classified  with  the 
other  recognized  degenerations,  the  fatty,  amyloid,  etc.^  The  morbid 
changes  peculiar  to  this  degeneration  have  long  been  recognized  by  patholo- 
gists, as  have  also  the  corresponding  clinical  facts,  but  the  connection  be- 

1  TJva  ursi,  buchu,  copaiba,  pareira  brava,  and  sandal-wood  oil  are  regarded  as  beneficial,  and  are  to  be 
given  with  allialine  waters. 

^  Medico-Chirurg.  Transactions,  1872. 

3  Mahomed,  London  Lancet,  August,  1877. 


ARTERIO-CAPILLARY   FIBROSIS,    WITH   CONTRACTED    KIDNEYS. 


585 


tween  them  was  not  understood.  It  is  this  connection,  this  grouping  to- 
gether, with  a  more  detailed  knowledge  of  the  minute  changes,  that  con- 
stitutes the  theory. 

The  cause  of  the  degeneration  is  attributed  to  some  form  of  blood- 
poisoning,  either  temporary  or  chronic,  such  as  gout,  alcoholism,  preg- 
nancy, scarlet  fever,  lead  poisoning,  and  certain  forms  of  dyspepsia,  mal- 
assimilation  and  functional  disorders  of  the  liver,  which  act  by  producing 
first  a  functional  and  then  an  organic  increase  of  the  arterial  tension. 

The  pathological  changes  consist  in  a  general  increase  in  the  amount  of 
fibroid  tissue  throughout  the  body,  especially  marked  in  the  excretory 
organs,  together  with  hypertrophy  of  the  left  and  dilatation  of  the  right 
ventricle.  The  increase  of  fibrous  tissue  usually  begins  in  the  outer  coat 
of  the  smallest  arteries,  and  spreads  thence  through  the  connective-tissue 
stroma  of  the  organ  involved.  It  is  seen  under  the  microscope  as  a  more 
or  less  thick  granular  and  generally  structureless  ("  hyalin-fibroid  ")  border 
on  the  outside  of  the  vessel  staining  deeply  with  carmine.  The  inner  coat 
is  also  sometimes  much  swollen,  granular  and  thickened.  In  the  capillaries 
the  new  tissue  is  granular  and  without  any  fibroid  appearance.  According 
to  Gull  and  Sutton  the  muscular  coat  of  the  artery  is  atrophied.  The  re- 
sult of  these  changes  is  to  diminish  the  calibre  and  destroy  the  elasticity 
of  the  vessels.  This  alteration  in  the  vessels  is  the  primary  and  essential 
morbid  process  ;  by  its  reaction  upon  the  heart  and  by  its  spreading  to 
the  adjoining  tissues,  it  produces  the  following  secondary  changes.  By 
the  formation  and  retraction  of 
new  connective-tissue,  especially 
in  the  kidneys,  gastro-intestinal 
tract,  and  skin,  these  organs  di- 
minish in  size  and  lose  more  or 
less  of  their  granular  epithelial 
elements. 

The  lungs  are  firm  with  promi- 
nent bronchi  and  often  show  well- 
marked  vesicular  emphysema. 
There  is  atheroma  of  the  aorta 
and  of  the  cardiac  valves,  opacity 
of  the  arachnoid,  and  increase 
in  the  amount  of  the  sub-arach- 
noid liquid. 

The  kidneys  are  small,  red, 
and  granular  with  adherent  cap- 
sules, and  with  small  cysts  scat- 
tered through  them.  This  con- 
dition of  the  kidney  must  be 
distinguished  from  the  mixed 
or  yellrnv granular  kidney,  which, 
according  to  this  theory,  is  either 
a  large  white  kidney  that  has  shrunk  and  become  granular,  or  else  is  the 


Fig.  143. 

Arterio-Capillary  Fibrosis. 

Section  from  the  Cortex  of  a  contracted  Kidney,  showing 
two  Glomeruli. 

A.  Capsule  of  a  Malpighian  body  thicTcened  with  lamin- 

ated connective  tissue. 

B.  Vascvlar  tuft  deqenerated  into  a  fibrous  nodule. 

C.  Capsule  of  another  Malpighian  body,  ivith  fibrous 

tMclcfning,  smaller  in  amount  than  at  A. 

D.  Vascular  tuft,  adherent  to  capsule,  with  round  cell 

infiltration.  _ 

E.  Nucleated  fibrous  tissue  surrounding  the  atrophied 

glomeruli,     x  300. 


586  DISEASES    OF   THE    KIDISTEYS. 

consequence  of  an  attack  of  acute  parenchymatous  nephritis  supervening 
upon  the  chronic  interstitial  change.  The  microscopical  appearance  of  the 
kidney  is  such  as  has  been  described  in  interstitial  nephritis.  There  is 
increase  of  intertubular  connective-tissue,  especially  around  the  Malpighian 
bodies,  and  in  and  around  the  walls  of  the  minute  arteries.  The  urinif- 
erous  tubules  present  all  the  degrees  or  changes  between  an  almost  com- 
plete destruction  and  the  normal  condition.  The  changes  when  found  seem 
due  to  a  fibroid  thickening  of  the  wall  of  the  tubule,  with  destruction  of 
the  epithelium  and  diminution  of  the  lumen  of  the  tube,  although  some- 
times the  tubes  are  irregularly  dilated.  The  importance  of  the  granular 
condition  of  the  epithelium  is  claimed  by  Gull  and  Sutton  to  have  been 
greatly  exaggerated,  and  they  attribute  this  appearance  either  to  post-mor- 
tem change,  or  to  a  simple  venous  congestion  preceding  death.  The  in- 
crease in  the  amount  of  intertubular  connective-tissue  and  the  thickening 
of  the  walls  of  the  minute  arteries  have  been  long  recognized,  but  the 
interpretation  given  to  the  latter  change  has  been  explained  differently 
heretofore,  and  its  general  distribution  has  not  been  known.  It  was  sup- 
posed to  be  due  to  an  increase  of  the  muscular  coat,  and  to  indicate  an  in- 
creased ability  on  the  part  of  the  vessels  to  propel  the  blood  through  them. 
According  to  the  present  view,  the  change  is  entirely  different,  and  the 
flow  of  blood  is  impeded  by  the  diminution  of  the  lumen  and  the  lack  of 
elasticity  in  the  wall  of  the  vessel.  The  hypertrophy  of  the  heart,  which 
is  found  so  constantly  in  connection  with  the  small  red  kidney,  is  readily 
explained  on  this  theory.  The  heart  is  called  upon  for  greater  effort,  in 
order  to  overcome  the  obstruction  to  the  blood-current  created  by  the  change 
in  the  arterioles  and  capillaries,  and,  as  in  the  case  of  other  muscles,  the 
heart  increases  in  size  and  strength  to  meet  the  additional  calls  made  upon 
it.  The  increase  of  arterial  pressure  is  also  felt  within  the  heart,  and  ulti- 
mately produces  the  other  changes  seen  upon  the  valves,  changes  which  are 
found  at  the  points  subjected  to  great  pressure. 

This  explanation  is  in  harmony  with  the  following  facts  observed  by  Gull 
and  Sutton  :  hypertrophy  of  the  left  ventricle  existed  in  all  cases  in  which 
the  vessels  were  generally  thickened  by  the  hyalin-fibroid  change,  and  its 
degree  varied  directly  with  the  degree  or  the  extent  of  the  change.  They 
argue  that  it  is  due  not  to  renal  disease,  but  to  the  morbid  changes  in  the 
vessels,  because  (1)  it  is  often  absent  in  cases  of  large  white  kidney,  in 
lardaceous  disease,  and  in  scrofulous  pyelitis  with  almost  complete  destruc- 
tion of  the  organ  ;  (2)  whenever  hy23ertro23hy  of  the  heart  coexisted  with 
large  white  kidney  the  hyalin-fibroid  change  was  also  present ;  and  (3) 
hypertrophy  is  found  at  a  very  early  period  of  the  kidney  affection  when 
the  excretory  function  is  not  greatly  altered. 

Symptoms. — The  symptoms  vary  with  the  organ  chiefly  affected  and  the 
period  of  the  disease.  The  first  in  order  of  time,  and  the  one  upon  which 
Mahomed  places  the  most  reliance  as  a  means  of  diagnosis  is  the  in- 
crease of  arterial  tension,  recognized  by  the  pulse,  or  better  by  the  sphyg- 
mograph.  During  this  stage,  if  the  pressure  has  increased  rapidly,  dropsy 
and  albuminuria  may  be  present,  but  ordinarily  these  two  symptoms  denota 


AKTERIO-CAPILLARY    FIBROSIS,    WITH    CONTRACTED    KIDNEYS.        587 

accompanying  epithelial  change  in  the  kidney  or  an  exaccrljation  in  the 
progress  of  the  disease.  Albuminuria  is  not  itself  a  symptom  of  arterio- 
capillary  fibrosis  with  contracted  kidney ;  on  the  contrary,  the  affection 
may  run  its  course  without  the  aj)pearance  of  this  symj)tom.  In  such 
cases  the  vascular  changes  have  involved  other  organs,  and  have  left  the 
kidney  unchanged  or  but  slightly  affected  ;  such  patients  die  with  symp- 
toms of  pulmonary  or  gastro-intestinal  troubles  or  of  cerebral  hemorrhage 
or  aneurism. 

The  condition  begins  as  a  diathesis  in  early  life,  gaining  ground  every 
year,  and  betraying  itself  by  the  pulse,  pulmonary  emjDhysema,  or  dyspep- 
sia, and  if  at  any  time  a  serious  exacerbation  occurs  death  may  be  caused 
with  symjDtoms  referable  more  directly  to  the  kidneys. 

Diagnosis. — The  diagnosis,  therefore,  is  to  be  made  mainly  by  a  considera- 
tion of  the  character  of  the  pulse,  and  it  is  claimed  that  heretofore,  in  the 
majority  of  cases,  the  disease  has  passed  unrecognized,'  the  diagnosis  being 
made  only  when  the  kidneys  were  sufficiently  involved  to  give  rise  to 
albuminuria.  The  important  point,  therefore,  is  to  recognize  the  condition 
of  high  arterial  tension.  The  sphygmograph  alone  can  always  do  this 
with  certainty,  but  careful  examination  of  the  heart  and  pulse  will  usually 
suffice.  The  pulse  of  high  pressure  has  been  variously  described  as  hard, 
cord-like,  persistent,  long  or  slow.  The  most  constant  and  characteristic 
quality  is  that  designated  as  persistent  or  slow  (not  infrequent).  The 
artery  feels  full  under  the  finger  during  diastole  as  well  as  systole  of  the 
heart,  and  its  systolic  expansion  is  prolonged, — the  so-called  pulsus  tardus, 
shown  on  the  sphygmograph  by  a  prolongation  of  the  elevation  of  the  trace. 
The  heart  signs  of  high  arterial  pressure  are,  according  to  Mahomed,  a. 
long  or  reduplicated  first  sound  heard  over  the  inter-veutricular  septum, 
and  an  accentuated  second  sound. 

The  following  conclusions,  taken  from  Grull  and  Sutton's  first  paper  and 
Mahomed's  last  upon  the  subject,  present  the  points  in  convenient  form. 
There  is  a  disease  characterized  byhyalin-fibroid  formation  in  the  arterioles 
and  capillaries,  attended  with  atrophy  of  the  adjacent  tissues.  This  morbid 
change  in  the  vessels  is  the  primary  and  essential  condition  of  the  morbid 
state  called  arterio-capillary  fibrosis  with  contracted  kidney.  The  kidneys, 
however,  may  be  little  if  at  all  affected,  while  the  morbid  change  is  far 
advanced  in  other  organs.  The  blood  condition  which  produces  the  high 
arterial  pressure  is  the  primary  condition,  and  is  not  secondary  to  deficient 
renal  excretion  as  heretofore  held.  The  cardio-vascular  changes,  when 
found  alone,  may  be  taken  as  evidence  of  the  existence  of  the  disease.  The 
condition  of  high  pressure  is  almost  constantly  present  in  old  age,  and  in 
one  form  or  another  brings  about  a  large  proportion  of  the  deaths  of  those 
over  fifty  years.  Tlie  existence  of  high  arterial  tension  in  the  pulse  of 
young  persons  indicates  a  diathesis,  and  is  of  grave  importance.     The  same 

1  Mahomed  says:  "How  often  patients  are  allowed  to  die— nay,  more,  even  killed— when  their 
hearts  are  failing  from  the  terrible  arterial  pressure  they  can  no  longer  overcome.  Their  flagging,  over- 
taxed ventricles  dilate  ;  the  wretched,  feeble,  laboring  pulse  is  thought  to  mean  weakness  which  requires 
stimulation,  its  persistence  (indicating  over-distention)  is  passed  unnoticed,  and  the  struggling  heart, 
failing  at  last  in  its  work,  stops  and  the  patient  dies  for  want  of  a  lancet  or  purge." 


688  DISEASES    OF   THE    KIDNEYS. 

condition  being  of  frequent  occurrence  after  the  age  of  fifty  is  not  of  such 
great  importance,  unless  present  in  an  excessive  degree.  It  then  produces 
serious  symptoms  and  calls  for  active  treatment. 

ACUTE   SUPPUEATIVE    INTERSTITIAL   NEPHRITIS. 

{Surgical  Kidney.) 

Morbid  Anatomy. — The  kidney  is  intensely  hypersemic,  softer  than  nor- 
mal, and  the  fat  about  it  is  oedematous.  When  the  thickened  and  opaque 
capsule  is  stripped  off,  pus  often  flows  from  beneath  it.  The  surface  shows 
arborescent  injection. 

On  section,  several  purulent  foci  are  seen  in  the  cortex  and  pyramids, 
about  the  size  of  a  pea  ;  these,  coalescing,  may  form  a  large  abscess.  When 
pygemia  is  its  cause,  the  abscesses  are  wedge-shaped,  and  colonies  of  bacteria 
are  found  surrounding  the  shreddy  necrotic  tissue,  and  in  the  centre  of 
the  suppurating  mass  the  epithelium  is  cloudy  and  desquamated.  Cell- 
infiltration  takes  place  in  the  adjacent  connective-tissue,  and  secondary 
thrombi  are  found  in  the  small  veins.  Micrococci  are  found  in  the  arteri- 
oles.' When  the  abscesses  are  wedge-shaped  they  are  called  "^  metastatic;^' 
but  when  circular  they  are  merely  spots  of  "suppuration  in  foci." 

In  cJironic  suppurative  nephritis,  decomposing  pus,  calcareous  salts,  and 
a  serous,  fetid  fluid  are  contained  in  a  sac  whose  wall  is  connective-tissue. 
With  these  (so-called)  chronic  abscesses,  cysts  and  renal  atrophy  are  present. 
In  large  pysemic  or  non-pygemic  abscess  ulceration  may  take  place  at  the 
tips  of  the  pyramids,  and  the  abscess  may  open  into  the  pelvis,  the  intestine, 
externally,  or  into  the  peritoneum.  The  liver  has  been  involved  from  the 
breaking  of  a  renal  abscess  into  its  softened  parenchyma  (Rayer). 

Diffuse  purulent  infiltration "  is  of  rare  occurrence  ;  then  the  whole  kid- 
ney seems  to  be  a  mass  of  pus  ;  the  surface  and  cut  section  are  homogene- 
ous looking.  Pus  is  readily  scraped  off,  and  ecchymoses  are  seen  studding 
its  surface.' 

Etiology. — Any  of  the  causes  of  pyelitis  may  be,  secondarily,  causes  of 
surgical  kidney.  Pyaemia,  ulcerative  endocarditis,  typhoid  fever,  and  puer- 
peral fever  may  be  complicated  by  it.  Wounds,  blows,  and  severe  contu- 
sions cause  it.  Eeflex  irritation  and  some,  as  yet  unknown,  nervous  con- 
ditions are  supposed  by  many  to  be  the  cause.  Certain  spinal  diseases  are 
attended  by  it, — perhaps  from  disturbance  of  "trophic  influences." 

Symptoms. — There  is  lumbar  pain,  tenderness  on  pressure  over  the  kid- 
ney, recurring  chills,  fever,  languor,  anorexia,  emaciation,  perhaps  diar- 
rhcBa,  nausea  and  vomiting  ;  the  mouth  and  skin  become  clammy,  sordes 
may  collect  on  the  teeth,  the  breath  becomes  offensive,  and  there  is  drowsi- 

'  This  is  Kleb's  parasitic  nephritis  ;  the  infecting  particles  or  spores  ascend  ("presumably  from  the  blad- 
der) to  the  pelvis  thence  up  the  tubules.  Hyaline  casts  in  "  parasitic  nephritis  "  have  spores  and  algse  on 
their  periphery.    Coriiil  and  Ranvier  think  they  may  be  formed  in  the  kidney  during  life. 

2  Full  descriptions  are  given  in  Ei'ichsen's  Surgery,  p.  712,  etseq.,  vol.  ii. 

3  Marcus  Beck  (in  "  Qiiain's  Diet,  of  Med.,"  pp.  1563-5)  describes  acute  interstitial  nephritis  without  eup- 
pnration  as  one  variety  of  the  surgical  kidney  ;  infiltration  of  small  round  cells  in  the  intertubular  struc- 
ture and  about  the  Malpighian  tufts  being  the  chief  pathological  event.  An  acute  or  sub-acute  interstitial 
(non-suppurative)  nephritis  I  have  already  described. 


HYDRONEPHROSIS.  589 

ness  whicli  rarely  passes  into  coma.'  These  symptoms  (especially  the  chills 
and  febrile  movement)  are  often  severe,  and  then  the  disease  is  of  short 
duration.  The  patient  passes  rapidly  into  a  state  of  stupor  without  con- 
vulsions and  with  a  subnormal  temperature.  The  urine  may  be  in  excess 
of  the  normal  quantity  or  be  scanty  ;  albumen  is  present  in  varying  quan- 
tities ;  hyaline  and  pus  casts  and  renal  epithelia  are  also  present  in  A^arying 
amounts.  Blood  is  always  found  in  the  acute  cases.  The  specific  gravity 
is  never  very  high.  The  urine  is  in  many  cases  ammoniacal.  Should  a 
tumor  be  felt,  it  will  fluctuate  ;  but  rarely  is  there  a  distinct  tumor. 

Differential  Diagnosis. — From  pymmia  it  is  distinguished  by  the  absence 
of  recurring  chills  and  sweats  ;  by  its  lower  temperature  ;  by  absence  of 
joint  and  lung  symptoms,  and  by  the  purulent  bloody  urine.  It  is  often 
diflScult  to  distinguish  it  from  septiccemia. 

A  perinephritic  abscess  is  distinguished  from  suppurative  nephritis  by  its 
tumor,  and  by  the  fact  that  in  uncomplicated  perinephritis  urinary  symp- 
toms are  absent. 

Pyelitis  has  the  characteristic  angular  "■  tailed  "  cells  from  the  mucous 
membrane  of  the  pelvis  in  the  urine,  and  the  constitutional  symptoms  are 
insignificant  compared  with  those  of  suppurative  nephritis. 

Prognosis.— The  prognosis  is  always  grave.  The  free  discharge  of  a  large 
abscess  may  prolong  life,  and,  if  unilateral,  be  followed  by  recovery.  Death 
from  complications  is  its  frequent  termination.  In  the  aged  it  is  almost 
necessarily  fatal.     Asthenia,  ursemia,  and  complications  cause  death. 

Treatment. — The  treatment  is  for  the  most  part  surgical.  Tonics,  stim- 
ulants, and  condensed  nutriment  are  indicated  from  its  onset.  A  pure  milk 
diet  is  advantageous.  Dry  cupping,  fomentations  and  poultices  or  leech- 
ing over  the  loins  are  of  service.  The  bladder  is  to  be  washed  out  with 
quinine,  Condy's  fluid  and  sulphuric  acid,  or  thymol  water.  Benzoic  acid 
or  benzoate  of  ammonia  may  be  given  to  relieve  the  offensiveness  of  the 
urine. 

HYDRONEPHEOSIS . 

Hydronephrosis  is  a  chronic,  non-inflammatory  affection  of  the  pelvis 
of  the  kidneys.  Whenever  the  flow  of  urine  through  the  ureters  into  the 
bladder  is  permanently  obstructed,  the  urine  collects  in  the  pelvis  and  in- 
fundibula,  compressing  the  renal  substance,  which  becomes  partially  or 
completely  atrophied,  so  that  after  a  time  the  kidney  is  converted  into  a 
sac  or  pouch.  This  condition  has  received  the  name  of  hydronephrosis, 
or  dropsy  of  the  kidney.  The  dilatation  may  affect  the  ureter  and  pel- 
vis, or  only  the  pelvis. 

Morbid  Anatomy.— In  a  kidney  that  is  the  seat  of  moderate  hydronephro- 
sis following  simple  dilatation  of  the  pelvis,  the  papillse  will  become  flat- 
tened, hardened  and  shrunken,  and  gradually  disappear.  The  remaining 
portion  of  the  renal  substance  gradually  diminishes  from  the  pressure  and 
becomes  more  or  less  tough  and  resistant.  In  extreme  cases  the  kidney 
substance  finally  entirely  disappears  and  the  kidney  is  converted  into  a  large 

1  There  is  a  frequent  desire  to  micturate.    Suppression  of  urine  may  occur. 


590  DISEASES   OF   THE   KIDNEYS. 

multilocular  cyst  ;  sometimes  it  is  unilocular.  At  times  sucli  a  cyst  at- 
tains a  size  as  large  as  a  child's  head  ;  there  is  a  case  recorded  where  the 
whole  abdominal  cavity  was  occupied  by  an  enormous  tumor  containing 
sixty  pounds  of  fluid.  Some  healthy  kidney  substance  will  nearly  always 
be  found  in  its  walls.  That  portion  of  the  ureter  which  is  the  seat  of  dila- 
tation may  reach  the  size  of  a  small  intestine,  has  a  blue-white  color,  its 
walls  become  greatly  thickened,  and  it  may  become  convoluted. 

The  fluid  contained  in  hydronephrotic  cysts  is  generally  altered  urine. 
It  is  much  more  watery  than  normal  urine,  containing  more  or  less  of  the 
urinary  salts ;  it  may  also  contain  blood,  pus,  epithelium  and  some  albu- 
men. Sometimes  it  is  perfectly  clear ;  it  is  usually  alkaline.  Adhesions 
frequently  form  between  the  enlarged  kidney  and  neighboring  organs. 

Etiology.— Closure  of  a  ureter  which  gives  rise  to  hydronephrosis  may 
be  due  to  compression  by  a  tumor  external  to  its  walls,  especially  rectal  or 
uterine,  or  to  the  impaction  of  a  calculus,  blood-clot,  or  mass  of  echi- 
nococci  within  it,  or  to  inflammation  which  has  caused  adhesion  of  its 
walls  and  complete  obliteration  of  its  lumen.  A  moderate  degree  of  dila- 
tation of  the  ureter  sometimes  results  from  obstruction  to  the  free  dis- 
charge of  urine  from  the  bladder  ;  when  this  is  the  case  the  pelvic  dilata- 
tion is  bilateral,  and  can  never  become  very  extensive  without  destroying 
life,  for  when  the  pressure  becomes  equal  to  that  within  the  blood-vessels 
the  urinary  secretion  is  entirely  suppressed.  Congenital  defects  often 
cause  it. 

Symptoms. — The  symptoms  of  hydronephrosis  depend  upon  the  nature 
of  its  cause  and  the  extent  of  dilatation.  If  the  sac  is  small  and  the  op- 
posite kidney  healthy,  there  may  be  no  symptoms  to  indicate  its  existence  ; 
there  will  be  no  diminution  in  the  urinary  secretion,  as  the  healthy  (usu- 
ally hypertrophied)  kidney  performs  the  work  of  its  diseased  fellow. 
There  may  be  pain  in  the  lumbar  region. 

As  soon,  however,  as  the  tumor  attains  suflficient  size  to  be  readily  felt, 
the  existence  of  hydronephrosis  may  be  determined  by  it.  This  tumor 
causes  no  pain  or  inconvenience  except  by  its  pressure.  "With  double  hy- 
dronephrosis ursemic  symptoms  may  develop  suddenly.  The  nephritic 
tumor  is  fluctuating,  usually  lobulated,  and  gives  a  tympanitic  resonance 
in  front  on  percussion  unless  the  colon  has  been  pushed  aside.  If  the  ob- 
struction to  the  escape  of  urine  from  the  kidney  is  temporarily  removed, 
its  removal  will  be  followed  by  a  sudden  diminution  and  disappearance  of 
the  tumor,  coincident  with  a  sudden  discharge  of  a  large  quantity  of  pale 
urine.  Such  an  occurrence  is  almost  pathognomonic  of  hydronephrosis. 
Constipation,  from  pressure  of  the  tumor  on  some  portion  of  the  intestine, 
is  not  infrequent. 

Differential  Diagnosis. — Hydronephrotic  tumors  may  be  confounded  with 
ovarian  cysts,  ascites,  hydatid  cysts,  and  pyonephrosis. 

They  are  distinguished  from  ovarian  cysts  by  the  presence  of  the  colon 
in  front  of  the  tumors,  by  the  absence  of  tympanitic  percussion  in  the  lum- 
bar region,  and  by  a  vaginal  and  rectal  examination. 

Single  hydronephrosis  is  distinguished  from  ascites  by  the  non-existence 


CYSTIC    KIDNEYS.  591 

of  dulness  in  both  lumbar  regions.  In  ascites,  when  the  position  of  the 
patient  is  changed,  there  is  a  change  in  the  level  of  dulness,  which  never 
occurs  in  hydronephrosis. 

It  is  quite  impossible  to  distinguish  hydronephrosis  from  an  hydatid 
cyst,  unless  the  hydatid  vesicles  are  found  in  the  urine,  or  the  hydatid  fre- 
mitus is  present. 

It  is  distinguished  from  pyonephrosis  by  the  non-purulent  character  of 
the  urine,  aud  by  the  absence  of  constitutional  symptoms.  An  aspirating 
needle  will  generally  decide  the  diagnosis,  for  the  watery  urine  withdrawn 
differs,  chemically  and  microscopically,  from  the  fluid  obtained  from  hy- 
datid or  ovarian  cysts  or  the  pus  of  a  pyonephrosis  or  a  perinephritic  ab- 
scess. 

Prognosis. — The  prognosis  is  more  favorable  in  this  than  in  any  other 
form  of  renal  tumor  ;  yet  it  is  always  serious.  When  only  one  kidney  is 
involved  life  may  be  indefinitely  prolonged,  and  there  is  always  a  possibility 
that  spontaneous  evacuation  of  the  sac  may  occur.  But  cases  are  recorded 
where — one  kidney  only  being  involved — it  caused  death  by  pressure  on 
neighboring  parts.  If  the  healthy  kidney  becomes  the  seat  of  any  form  of 
nephritic  degeneration,  the  prognosis  becomes  unfavorable  ;  complete  sup- 
pression of  the  urine  may  then  occur  at  any  moment;  or  if  the  impedi- 
ment which  has  obstructed  one  ureter  extends  so  as  to  prevent  the  flow  of 
urine  from  both  kidneys,  urgemic  symptoms  will  be  developed,  and  death 
speedily  follow. 

Treatment. — In  hydronephrosis  the  principal  thing  to  be  accomplished  is 
the  evacuation  of  the  tumor.  To  accomplish  this  result  it  should  be  care- 
fully manipulated.  This  can  readily  be  done,  as  the  tumor  generally  causes 
no  pain.  If  this  does  not  cause  its  evacuation,  aspiration  should  be  re- 
sorted to.  I  now  have  a  case  under  observation  in  which  aspiration  has 
twice  been  performed  with  complete  relief  to  the  patient,  and  the  aspira- 
tion has  not  been  followed  by  any  unpleasant  symptoms  ;  nothing  is  to  be 
expected  from  medicinal  treatment. 

CYSTIC    KIDNEYS. 

Oysts  of  the  kidneys  are  very  frequently  met  with  at  autopsies,  but  they 
are  of  very  little  clinical  importance,  for  if  the  cysts  are  of  small  size 
they  give  no  symptoms  during  life.  Cystic  degeneration  may  have  a  con- 
genital origin,  and  both  kidneys  may  be  converted  into  a  mass  of  cysts  of 
sufficient  size  to  entirely  fill  the  abdominal  cavity  ;  such  conditions  are 
usually  associated  with  other  congenital  malformations.  It  is  claimed  that 
cysts  originate  in  the  epithelia  or  even  in  the  fibrous  stroma  of  the  kid- 
ney. They  are  often  found  scattered  through  kidneys  that  are  otherwise 
healthy.  It  is  difficult  to  make  any  practical  distinction  between  the 
cysts  of  a  true  cystic  kidney  and  those  occurring  with  cirrhotic  kidney. 
They  are  usually  situated  in  the  cortical  substance  near  the  surface. 
Colloid  cysts  of  the  glomeruli  are  freqiiently  surrounded  by  laminae  of 
fibrin  from  hemorrhages  within  the  capsule. 


a93 


DISEASES   OF   THE   KIDNEYS. 


The  contents  of  kidney-cysts  vary  in  character  even  in  the  true  cyst. 
They  may  contain  a  clear  albuminous  fluid  ;  sometimes  it  is  gelatinous, 
containing  phosphates,  carbonates,   cholesterin,  and  very  rarely  urea  and 

uric  acid.  The  vascular  tuft  in 
a  glomerulus  that  is  transformed 
into  a  cyst,  is  flattened  against  the 
wall  of  the  thickened  capsule,  and 
the  cyst  may  be  lined  with  pavement 
epithelia. 


Fia.  144. 
Cystic  Kidney. 
Drawing  sliotoing  a  Vertical  Median  Section  of  a 
Kidney  containing  Cysts. 


Fig.  145. 
Cystic  Kidney. 
Section  from  the  Cortex  of  a  Cirrhotic  Kidney,  show- 
ing the  Epithelial  lining  of  a  small  Cyst- 

A.  Cirrhotic  intertubular  tissue. 

B.  A  small  artery  in.  transverse  section  sJiowing  the 

thickened  coats. 

C.  Cavity  of  a  small  cyst. 

D.  EpitJielial  lining  of  the  last,  partly  detached. 

(The  extreme  temiity  of  this  lining  cannot  be 
well  shown  in  a  wood-cut.)     x  300. 


The  origin  of  these  cysts  is  obscure,  although  there  is  reason  to  believe 
that  they  are  the  results  of  dilatation  of  the  kidney  tubules  and  Malpighian 
bodies.  Congenital  cysts  have  their  origin,  as  a  rule,  in  the  Malpighian 
bodies.  Serous  cysts  are  often  found  in  kidneys  that  have  undergone  senile 
atrophy.  They  may  be  developed  in  the  connective-tissue  by  an  enlarge- 
ment of  a  lacunar  lymph-space. 


RENAL    CALCULI. 

Eenal  concretions  vary  greatly  in  shape  and  differ  in  their  composition. 
They  may  be  deposited  in  the  tubes  of  the  pyramids,  in  the  cortical  sub- 
stance, or  in  the  pelvis  of  the  kidney.  Their  development  occurs  at  any 
age  ;  they  are  met  with  in  the  kidney  of  the  foetus  in  utero  and  in  the 
kidneys  of  the  vei-y  aged. 

Morbid  Anatomy. — In  the  kidneys  of  infants  dying  within  forty-eight 
hours  after  birth,  brownish  striae  of  amorphous  urates  will  invariably  be 
found  running  from  the  papillae  to  the  base  of  the  pyramids.  In  adults, 
urate  of  soda,  in  the  form  of   crystals,  may  be  found  deposited  in  the 


RENAL   CALCULI. 


593 


■white  lines  in  the  pyramids  and  cortical  substance,  both  in  the  tubular  and 
intertubular  structure  ;  this  is  always  associated  with  a  gouty  diathesis. 
Carbonate  and  phosphate  of  lime  may  be  found  deposited  in  the  tubes  and 
l^yramids  of  the  kidneys  of  old  people,  or  in  connection  with  diseases  of  the 
bones.  By  far  the  most  frequent  variety  is  uric  acid.  Some  think  that 
oxalate  of  lime  forms  the  starting-point  of  uric  acid  deposits.  Cystine, 
ammonio-magnesian  phosphate,  or  urate  of  ammonia  and  the  mixed  urates 
may  form  nuclei  of  renal  calculi.     Mixed  calculi  are  not  uncommon. 

These  different  varieties  of  urinary  concretions  may  be  permanently  im- 
pacted in  the  uriniferous  tubes,  and  render  them  impervious  and  cause 
cysts  to  be  developed,  or  they 
may  be  washed  down  the  tubes 
by  the  urine,  and  finally  de- 
posit in  the  infundibula  and 
pelvis  of  the  kidney.  They 
vary  in  number  and  size.  A 
kidney  may  contain  one  or  a 
large  number  of  concretions. 
They  usually  vary  in  size  from 
a  pin's  head  to  a  hazel  nut ; 
the  larger  ones  may  fill  the 
whole  pelvis  ;  the  smallest  con- 
stitute "  kidney  gravel.'^  If  a 
concretion  becomes  impacted 
in  the  pelvis,  it  may  attain  a 
very  large  size,  weighing  one 
or  two  ounces.  The  smaller 
calculi  pass  through  the 
ureters  into  the  bladder  and 
are  discharged ;  the  larger 
ones  may  permanently  ob- 
struct the  ureters  and  become 
the  cause  of  pyo-  or  hydro- 
nephrosis. 

The     anatomical 
produced  by  renal  concretions 
vary:  they  may  cause  pyelitis,  pyonephrosis,  hydronephrosis,  or  abscess, 
or  they  may  excite  parenchymatous  nephritis. 

Etiology. — The  causes  of  the  different  concretions  found  in  the  kidneys 
are  very  obscure.  Uric  acid  is  most  frequently  met  with  in  infants.  The 
deposits  of  lime  and  triple  phosphates  are  most  frequently  met  with  in 
adults.  They  are  caused  by  the  precipitation  (in  the  nascent  state)  of  uric 
acid  or  oxalate  of  lime  due  to  renal  excess  of  insoluble  uric  acid,  or  to  de- 
ficiency in  water  of  the  urine.  A  colloid  material  composed  of  mucus  or 
blood  globules  or  other  animal  base  exists  in  all.  They  increase  by  accre- 
tion. Certain  constitutional  conditions  are  supposed  to  be  favorable  to  their 
development,  but  the  exact  nature  of  the  urinary  changes  has  not  as  yet 


Fig.  146. 
Renal  Calculi. 


changes   Drawing  showing  an  Impcmted  Eenal  {Mulberiif)  Calculus,  A. 
=>  B.   'Cysts. 


594  DISEASES    OE   THE    KIDNEYS. 

been  determined.  In  most  cases,  calculi  that  develop  in  the  pelyis  of  the 
kidney  have  some  foreign  substance  as  a  nucleus.  These  nuclei  may  be 
pus,  blood,  epithelium,  or  grains  of  pigment.  The  composition  of  the  re- 
maining portions  of  the  calculi  depends  upon  the  varying  conditions  of  the 
urine  which  attend  their  development. 

Symptoms. — The  symptoms  which  indicate  the  presence  of  renal  calculi 
vary.  In  some  instances  they  are  well  marked,  in  others  very  obscure. 
Usually,  the  existence  of  renal  calculi  is  indicated  by  an  aching  pain  in  the 
lumbar  region  and  loins,  which  frequently  shoots  into  the  testicles  or  labia 
and  down  the  thighs,— by  an  itching  at  the  end  of  the  penis,  and  by  a  fre- 
quent desire  to  urinate.  The  urine  often  contains  pus,  blood  and  "  tailed  " 
epithelium  from  the  pelvis  of  the  kidney.  These  symptoms  are  usually 
aggravated  by  anything  that  disturbs  the  position  of  the  calculus,  espe- 
cially by  violent  exercise,  or  by  jolting  in  driving  or  horseback  riding. 

The  symptoms  often  assume  the  characteristics  of  ''renal  colic,"  due  to 
the  passage  of  the  calculus  along  the  ureter  to  the  bladder ;  this  may  occur 
after  violent  exercise  or  without  any  assignable  cause.  The  attack  may  be 
sudden,  or  there  may  have  been  uneasiness  in  the  loins  for  some  time.  The 
passage  of  a  calculus  along  the  ureter  into  the  bladder  is  marked  by  sudden 
and  intense  pain  in  the  region  of  the  affected  kidney.  This  pain  radiates 
in  various  directions,  but  mainly  toward  thehypogastrium,  testis,  inside  of 
the  thigh  and  end  of  the  penis.  There  is  a  constant  desire  to  micturate, — 
*' tenesmus  of  the  bladder," — but  the  urine  is  scanty  or  suppressed,  and 
what  is  passed  is  of  a  smoky,  high  color,  often  bloody,  and  is  discharged  in. 
drops,  the  individual  at  the  time  experiencing  a  painful  burning  sensation. 
When  hemorrhage  is  profuse,  elongated  blood  clots  are  not  infrequently 
found  in  the  urine.  The  testicle  of  the  affected  side  is  retracted.  As  the 
pain  increases  in  severity  the  patient  rolls  from  side  to  side  and  shrieks 
with  pain.  His  countenance  becomes  pale  and  the  surface  of  the  body  is 
covered  with  a  cold  perspiration.  The  pulse  is  small  and  the  hands  and 
Jeet  are  cool.  The  severe  paroxysms  of  pain  are  often  attended  by  violent 
and  frequent  vomitings.  There  is  great  anxiety,  and  if  the  patient  is  of  a 
Tery  nervous  temperament  convulsions  may  occur.  If  the  attack  is  pro- 
longed there  is  a  slight  rise  in  the  temperature.  Syncope  is  common  dur- 
ing the  attack. 

The  duration  of  these  attacks  varies.  Sometimes  they  are  only  of  a  few 
hours'  duration,  at  other  times  they  may  be  prolonged  for  days ;  again, 
temporary  remissions  may  occur,  followed  by  violent  exacerbations. 

As  the  calculus  reaches  the  bladder  the  pain  suddenly  subsides,  with  a 
sense  of  relief,  and  the  patient  is  often  conscious  of  its  passage  into  the 
bladder.  After  the  passage  of  a  calculus  into  the  bladder  it  will  soon  be 
found  in  the  urine  voided.  Occasionally  calculi  become  impacted  in  some 
portion  of  the  ureter.  In  such  cases  the  subsidence  of  the  pain  is  more 
gradual  and  less  complete,  and  signs  of  hydronephrosis  follow,  and  a  tumor 
may  be  felt  in  the  region  of  the  kidney.  By  placing  the  patient  on  his 
back  with  his  knees  drawn  up,  the  enlarged  kidney  may  be  pressed  forward, 
and  with  the  other  hand  in  front  it  may  be  pressed  backward  and  below 


RENAL   CALCULI.  595 

the  margin  of  the  ribs.  In  the  young  and  in  those  who  are  thin  this  method 
will  aid  very  much  in  the  diagnosis.  Renal  calculi  may  attain  a  large 
size  and  destroy  extensive  portions  of  the  kidney,  and  yet  not  a  single  symp- 
tom may  be  present  to  indicate  their  existence.  Again,  tlie  signs  of  renal 
calculi  may  exist  for  a  long  time,  and  finally  atrophy  of  the  kidney  occurs, 
or  they  may  become  encysted  and  cease  to  give  any  indication  of  their 
presence. 

Differential  Diagnosis. — Eenal  calculi  may  be  confounded  with  neuralgia  ; 
the  seat  of  pain  is  the  same,  and  the  neuralgic  pains  are  often  severe  and 
paroxysmal ;  but  the  urinary  symptoms  and  an  examination  of  the  urine 
will  make  the  differential  diagnosis. 

The  passage  of  hlood-clots  or  hydatids  through  the  ureter,  causing  renal 
colic,  cannot  be  distinguislied  from  the  passage  of  renal  calculi,  unless  the 
antecedent  history  is  known  and  appreciated,  and  a  subsequent  urinary 
analysis  is  made. 

The  irritation  produced  by  an  impacted  calculus  on  the  right  side  will 
not  long  be  mistaken  for peritypfiUtis,  if  careful  and  repeated  examinations 
of  the  urine  are  made.  Frequently,  the  abnormal  conditions  of  the  urine 
which  indicate  the  presence  of  renal  concretions  are  j)resent  only  after  vio- 
lent exercise. 

Prognosis. — The  prognosis  in  renal  calculus  is  good,  unless  the  calculi 
become  impacted  and  obstruct  the  ureter,  or  are  of  too  large  size  to  pass 
through  the  ureter  to  the  bladder.  In  these  conditions  the  prognosis  is  the 
same  as  in  similar  conditions  in  pyelitis,  pyonephrosis  and  hydronephrosis. 
Should  both  kidneys  be  involved,  the  prognosis  is  exceedingly  unfavorable. 

Treatment. — The  treatment  of  the  general  condition  is  considered  under 
the  head  of  Urinary  Sediments.  The  treatment  during  the  interval  be- 
tween the  paroxysms  which  mark  the  passage  of  renal  calculi  will  depend 
upon  the  changes  which  have  occurred  in  the  kidneys  ;  different  theories 
have  been  advanced  in  regard  to  the  dissolving  of  these  concretions,  but 
none  of  them  are  of  practical  importance.  The  surgical  treatment  of  im- 
pacted calculi  with  extensively  diseased  kidney  is  now  attracting  much  at- 
tention. The  means  to  be  employed  for  the  relief  of  the  kidney  changes 
due  to  irritation  produced  by  calculi,  have  been  considered  under  pyelitis 
and  pyonephrosis. 

The  paroxysms  which  attend  the  passage  of  renal  calculi,  or  so-called 
nephritic  colic,  must  be  relieved  by  the  free  administration  of  mori^hine 
hypodermatically,  warm  baths,  and  the  application  of  hot  poultices  to  the 
loins  and  abdomen.  In  some  instances,  when  the  pain  is  intense  and  the 
vomiting  constant,  inhalation  of  chloroform  will  be  found  to  give  the  most 
speedy  and  sometimes  permanent  relief.  Change  in  the  position  of  the  pa- 
tient, and  manipulation  of  the  abdomen  along  the  course  of  the  ureters, 
may  sometimes  dislodge  a  calculus  and  facilitate  its  passage  into  the  blad- 
der. 


696  DISEASES   OF   THE   KIDNEYS. 


ITOW    GEOWTHS    11^   THE   KIDNTET. 

{Benal  Cancer.) 

Renal  Cancer  may  occur  as  a  primary  or  secondary  affection.  When  seC' 
ondary,  its  developments  usually  are  of  small  size,  and  may  occur  in  both 
kidneys.  "When  primary,  it  is  limited  to  one  kidney,  which  soon  forms  an 
enormous  tumor. 

Morbid  Anatomy. — Both  primary  and  secondary  cancer  of  the  kidney  are 
generally  of  the  medullary  variety,  and  develop  in  the  form  of  circumscribed 
nodules  in  the  cortical  substance,  or  occur  as  a  diffuse  infiltration.  The 
medullary  cancer,  however,  may  be  nearly  as  hard  as  scirrhus.  Colloid  can- 
cer is  rare.  It  develops  from  the  fibrous  stroma  of  the  cortical  substance. 
Sometimes  a  whole  kidney  is  transformed  into  a  cancerous  mass,  which  at- 
tains an  enormous  size,  filling  up  a  large  portion  of  the  abdominal  cavity. 
The  average  weight  of  a  cancerous  kidney  is  over  eight  pounds  ;  it  has 
weighed  thirty-one  pounds  in  children.  Secondary  cancer  (bilateral)  never 
reaches  a  very  large  size.  The  kidney  tissue  is  always  intensely  congested  ; 
it  is  often  associated  with  cancer  of  the  testicle. 

The  pelvis,  ureters,  the  veins,  the  peritoneum,  colon,  and  even  the  skin 
adjacent  to  the  neoplasm  may  be  involved.  The  lymphatics  and  adjacent 
glands  are  always  enlarged.  With  the  growth  of  the  cancer  all  traces  of 
renal  structure  become  obliterated  and  the  diseased  organ  becomes  adher- 
ent to  the  adjacent  tissue.  Hemorrhages  occurring  in  the  mass  at  varying 
points  give  an  appearance  called  "fungus  haematodes."  Sometimes  a  can- 
cerous kidney  is  movable,  no  adhesions  taking  place  with  surrounding 
parts.  The  minute  anatomical  changes  that  take  place  in  cancerous  devel- 
opments in  the  kidney,  are  similar  to  those  which  occur  in  cancerous  devel- 
opments in  the  other  organs  of  the  body. 

Etiology. — The  etiology  of  renal  cancer  is  as  obscure  as  the  general  eti- 
ology of  cancer.  In  a  large  proportion  of  cases  it  depends  either  upon 
hereditary  taint  or  local  infection.  Primary  cancer  occurs  oftenest  iefore 
the  tenth  and  after  the  fiftieth  year  of  life.^  Secondary  cancer  may  occur 
by  continuity  or  from  metastasis;  e.g.,  mamma,  uterus,  liver,  stomach, 
testis  or  supra-renal  capsules.  Males  suffer  oftener  than  females  ;  the  right 
kidney  oftener  than  the  left. 

Symptoms. — Cancer  of  the  kidney  often  remains  latent  for  a  long  time. 
Its  development  is  marked  by  gradual  emaciation,  for  which  no  cause  can 
be  assigned.  It  may  not  be  attended  by  pain  in  the  lumbar  region ;  if 
pain  is  present  it  is  not  characteristic.  There  may  be  no  change  in  the 
renal  secretion  ;  but  as  the  disease  advances  more  or  less  profuse  hemor- 
rhages occur  ;  sometimes  the  blood  appears  in  the  urine  in  clots,  in  which 
elements  of  the  neoplasm  may  be  found. 

As  the  disease  advances,  and  the  cancerous  mass  reaches  a  large  size,  it 
can  be  felt  through  the  abdominal  walls.  The  form  of  the  tumor  and  its 
immobility  will  enable  one  to  distinguish  it  from  enlargements  of  the  liver 

1  Out  of  Rohre's  107  cases  of  primary  renal  carcinoma,  37  were  under  ten  ;  30  were  over  fifty  years  of 
age. 


NEW   GEOWTHS   IN   THE    KIDNEY.  597 

or  spleen.  Very  large  cancers  of  the  right  kidney  may  displace  the  liver 
upward.  The  tumor  is  usually  nodulated  and  firm,  gives  a  dull  or  tym- 
panitic note  on  percussion,  and  can  be  tilted  forward.  The  colon  lies  in 
front  of  it.  Aortic  impulse  may  cause  it  to  pulsate.  When  haematuria  is 
present  it  is  constant.  In  its  advanced  stage  the  countenance  assumes  the 
characteristic  cancerous  cachexia. 

Differential  Diagnosis. — Cancer  of  the  left  kidney  is  distinguished  from 
splenic  tumors  by  its  lower  site,  absence  of  splenic  notch,  absence  of  blood 
changes,  by  its  nodulated  outline,  and  by  haematuria. 

From  perinephritic  abscess  it  is  distinguished  by  absence  of  febrile 
symptoms,  by  its  slow  growth,  and  absence  of  fluctuation. 

Cancer  of  the  right  kidney  may  be  distinguished  from  hepatic  tumors  by 
an  area  of  tympanitic  percussion  between  the  liver  and  the  tumor.  Reli- 
ance is  also  to  be  placed  on  signs  peculiar  either  to  hepatic  or  renal 
lesions. 

Tumors  of  the  liver  or  spleen  are  carried  down  on  full  inspiration  ;  renal 
cancer  is  not.     Faecal  and  ovarian  tumors  have  peculiar  characteristics.' 

Abscess  and  hydatid  tumors  are  distinguished  by  introducing  an  aspirat- 
ing needle,  which  withdraws  either  pus  or  a  saline  fluid  containing  por- 
tions of  the  echinococci. 

An  ovarian  tumor  when  tapped  is  found  to  contain  a  peculiar  ovarian 
fluid  ;  fluid  from  a  hydronephrosis  contains  some  urinary  elements. 

Prognosis. — The  prognosis  is  always  bad.  But  cancer  of  the  kidney  is 
tolerated  longer  than  that  of  any  other  organ.  Death  is  reached  either  by 
the  exhaustion  produced  by  repeated  and  profuse  hemorrhages,  or  as  a  con- 
sequence of  some  intercurrent  disease,  as  parenchymatous  nephritis  in  the 
unaffected  organ.  The  lungs,  retro- peritoneal  glands,  and  liver  may  be 
secondarily  invaded.  A  year  in  children  and  two  years  in  adults  is  its 
average  duration.  Intestinal  fistulas  may  be  formed,  and  the  skin  may  be 
ulcerated,  as  sequelas  to  cancer  of  the  kidney.  Dropsy  may  result  from 
compression  of  the  vena  cava.     The  vertebrae  may  be  eroded. 

Treatment. — Its  treatment  is  palliative.  The  principal  things  to  be  ac- 
complished are  to  relieve  pain  by  hypodermatics  of  morphine  and  to  sustain 
the  patient. 

Of  the  new  growths  met  with  in  the  kidney,  cancer  is  the  only  one  which 
has  any  special  clinical  significance. 

Leukcemic  tumors  are  occasionally  met  with  as  small  whitish  masses,  de- 
veloped in  the  intertubular  tissue.  They  are  composed  of  lymphoid  cells, 
and  are  always  associated  with  similar  growths  in  the  other  viscera.  These 
"  lymphadenomata''^  are  developed  in  connective-tissue  ;  the  liver  is  usually 
simultaneously  involved. 

Syphilitic  gummata  are  also  met  with  in  the  kidneys  in  the  form  of  small 
nodules,  in  connection  with  similar  developments  in  the  other  organs ; 
cicatrices  may  be  left,  usually  in  the  cortex,  but  sometimes  in  the  medulla 
of  the  organ.  Gummata  destroy  the  tubules.  Patches  of  ''fibrous  tissue" 
independent  of  gummata  occur  in  kidneys  of  those  who  are  syphilitic. 

'  See  "  Intestinal  Obstruction.'-' 


598  DISEASES   OF  THE   KIDN"ETS. 

Fibromata  may  appear  in  the  pyramids  of  kidneys  in  the  form  of  small, 
white,  fibrous  nodules.  The  remaining  portion  of  the  kidney  will  be  nor- 
mal, or  the  seat  of  parenchymatous  nephritis. 

Lipomata  include  those  accumulations  of  fatty  tissue  which  are  some- 
times developed  around  the  capsule  of  the  kidney  and  in  the  pelvis  of 
atrophied  kidneys  ;  sometimes  in  the  cortical  substance  beneath  the  cap- 
sule small,  rounded,  fatty  tumors  are  found.  Growths  of  ho7iy,  muscular, 
and  glandular  tissue  have  also  been  met  with  in  a  few  instances. 

Sarcomata  have  been  found  in  young  children. 


TUBEECULAE   DISEASE    OF    THE   KIDISTEY. 

Tubercles  are  developed  in  the  kidneys  as  an  advanced  lesion  of  gen- 
eral tuberculosis.  Primary  tuberculosis  of  the  kidneys  is  occasionally  met 
with  in  young  subjects. 

Morbid  Anatomy. — At  first,  gray  miliary  tubercles  are  found  throughout 
the  affected  kidney,  principally  in  the  pyramids.  The  tubercles  may  origi- 
nate in  the  stroma  or  in  the  cortex,  in  the  arterioles  separating  the  pyra- 
mids of  Ferrein,  or  on  the  surface  of  the  kidney.  Later,  solid,  cheesy,  yel- 
low masses  are  found  in  the  pyramids  and  in  the  cortex.  The  organ  is  en- 
larged and  lobulated.  The  mucous  membrane  of  the  pelvis  and  ureters  is 
thickened,  infiltrated,  and  often  ulcerated.  When  the  ureter  is  involved 
diminution  of  its  lumen  may  result  in  hydro-  or  pyonephrosis.  The  larger 
yellow  masses  are  found  at  the  junction  of  the  cortex  and  medulla  ;  they 
are  usually  softened  at  their  centres,  containing  a  puriform  debris  ;  the  pel- 
vis and  calices  are  also  dilated  and  filled  with  caseous  pus  or  with  a  semi- 
fluid pulp  rich  in  cholesterin.  The  tubules  are  compressed,  and  their  epi- 
thelium undergoes  gi'anular  and  fatty  change.  An  inflammatory  process 
may  coexist  {strumous  nephritis,  of  English  authors),  and  the  entire  mu- 
cous membrane  of  the  genito-urinary  tract  may  be  involved.  Calcareous 
nodules  and  incrustations  are  found  mingled  with  tubercle  granules.  Every 
portion  of  the  genito-urinary  tract,  especially  in  the  male,  may  show  tu- 
bercle granulations. 

Etiology. — Eenal  tuberculosis  generally  occurs  in  the  young.  Men  are 
far  oftener  affected  than  women,  the  right  kidney  oftener  than  the  left.  It 
may  occur  as  a  primary  tuberculosis,  as  part  of  acute  miliary  tuberculosis, 
or  it  may  complicate  chronic  pulmonary  phthisis. 

Symptoms. — The  symptoms  are  essentially  those  of  pyelitis  ;  such  as  pain 
and  tenderness  in  the  loins,  an  irritable  bladder,  and  scalding  urine,  which 
contains  mucus,  pus  and  blood.  As  the  disease  advances  hectic  fever  de- 
velops, with  the  coexistent  symptoms  of  intestinal  or  pulmonary  tubercu- 
losis. The  urine  will  contain  albumen  [no  casts),  and  under  the  microscope 
it  is  found  loaded  with  fatty  granules,  lymph  cells,  blood  corpuscles, 
and  debris  of  connective-tissue  infiltrated  with  small  and  fatty  granular 
cells.  A  flaky,  cloudy  deposit  always  occurs  in  this  urine,  unless  the  ureter 
from  the  affected  side  is  impermeable.    If  masses  of  cheesy  material  are 


HYDATIDS   OF   THE   KIDNEY.  59^ 

found  they  establisli  the  diagnosis.  A  renal  tumor  may  sometimes  be 
detected. 

Differential  Diagnosis. — The  diagnosis  rests  upon  the  hereditary  history, 
the  presence  of  tubercles  in  lungs  or  prostate,  on  lymphatic  enlargements, 
cheesy,  puriform  urinary  debris,  and  the  presence  of  a  painful  renal  tumor. 

Prognosis. — The  prognosis  is  very  unfavorable  ;  the  complications  are 
tubercle  in  any  or  all  of  the  other  organs  of  the  body,  cystitis,  pyelitis, 
pyelo-nephritis,  abscess,  hydro-  and  pyonephrosis,  waxy  kidney,  peritoni- 
tis, and  urinary  suppression. 

The  Treatment  is  altogether  palliative. 

PARASITES    IN   THE   KIDISTET. 

Renal  parasites  are  occasionally  met  with  ;  the  most  frequent  is  the  echi- 
nococcus.  The  cysticercus  cellulosus,  strongylus  gigas,  pentastoma  denti- 
culatum,  distoma  haematobium,'  spiroptera  hominis,  and  dactylus  aculeatus 
are  parasites  of  rare  occurrence.  They  are  sometimes  found  embedded  in 
the  kidney.  The  symptoms  which  attend  their  development,  and  the  man- 
ner in  which  they  gain  entrance  into  the  kidney,  are  obscure. 

HYDATIDS    OF   THE   KIDNEY. 

While  hydatids  of  the  kidney  are  less  common  than  hydatids  of  the 
liver,  the  affection  occurs  under  similar  conditions. 

Morbid  Anatomy. — A  kidney  the  seat  of  hydatids  is  sometimes  enor- 
mously enlarged  ;  as. a  rule,  a  spherical  cyst  projects  from  the  surface  whose 
fibrous  wall  is  derived  from  the  kidney.  The  inner  cyst  wall  may  or  may 
not  be  covered  with  daughter  vesicles  contaiuing  scolices,  but  a  clear  saline 
fluid  always  distends  it ;  the  pressure  of  the  cyst  causes  atrophy  of  the  kid- 
ney structure.  These  cysts  may  suppurate  and  be  changed  into  a  shriv- 
elled cyst  with  caseous  contents  in  which  are  embedded  echinococci  hook- 
lets.  They  may  rupture  into  the  perinephritic  tissue  and  give  rise  to  a 
lumbar  abscess,  or  into  the  lungs,  intestine,  stomach,  peritoneum,  or  pel- 
vis of  the  kidney. 

Symptoms. — A  nephritic  tumor  is  the  first  noticeable  sign.  A  vesicle 
passing  from  the  pelvis  to  the  bladder  gives  rise  to  the  symptoms  of  renal 
colic.  An  examination  of  the  urine  may  reveal  echinococci  booklets.  In 
all  cases  the  exploring  trocar  will  withdraw  a  clear  saline  fluid  containing 
booklets. 

Percussion  may  elicit  the  hydatid  fremitus.  If  pus  or  blood  appears  in 
the  urine  it  results  from  complicating  inflammation  or  suppuration  set  up 
by  the  cyst  or  its  contents. 

Prognosis. — This  is  always  uncertain.  It  is  possible  for  a  cyst  to  grow 
so  rapidly  as  to  cause  death  of  the  echinococci  by  pressure,  or  the  fluid 

1  The  Bilharzia  hsematobia  in  the  nrirary  vessels  is  the  cause  of  tropical  endemic  haematnria.  The  ova 
get  into  the  syntem  through  foul  drinking  water,  and  their  development  often  causes  grave  lesions  of  the 
mucous  membrane  of  the  genito-urinary  tract.    Diarrhcea,  typhoid  and  septic  symptoms  are  developed. 


600  DISEASES   OF   THE   KIDNEYS. 

necessary  to  their  life  may  be  insufficient,  or  it  may  become  so  altered  that 
calcareous  changes  will  occur  and  then  a  calcareous  mass  may  remain  for 
life  and  cause  no  further  harm.  An  echinococcus  may  be  the  nucleus  of 
a  stone  in  the  bladder  or  in  the  pelvis  of  the  kidney. 

Treatment. — Aspiration  should  always  be  practised,  and  if  it  is  not  fol- 
lowed by  adhesive  inflammation,  iodine  should  be  injected  into  the  cyst. 

PEEINEPHEITIS. 

{Perinephritic  Abscess.) 

This  is  an  inflammation  of  the  connective-tissue  surrounding  the  kidney  : 
it  may  terminate  in  suppuration,  or  in  the  formation  of  fibroid  tissue. 

Morbid  Anatomy. — The  cellular  tissue  about  the  kidney  becomes  cede- 
matous  and  the  seat  of  inflammatory  exudation,  causing  the  cellular,  adi- 
pose and  adjacent  retro-peritoneal  tissues  to  become  solid  and  firm.  Sup- 
puration may  commence  at  the  centre  of  the  mass,  leading  to  the  formation 
of  one  large  abscess  ;  or,  if  it  commences  at  numerous  points  and  gradu- 
ally extends,  a  number  of  circumscribed  abscesses  are  formed.  The  tu- 
mor formed  may  become  so  large  as  to  reach  from  the  level  of  the  liver  or 
spleen  to  the  iliac  fossa,  and  may  project  forward  and  cause  bulging  of  the 
abdominal  wall.  The  pus  contained  in  the  abscess  may  be  odorless,  or  thin, 
fetid  and  ichorous,  especially  if  mixed  with  urine.  The  pus  may  have  an 
odop  of  faeces  independent  of  perforation  from  the  'bowel  into  the  abscess 
cavity.  This  process  may  end  in  gangrene.  The  peritoneum  over  the  tu- 
mor is  thickened. 

A  perinephritic  abscess  may  open  into  the  lung,  pleural  cavity,  or  bron- 
chi, by  extending  into  the  retro-peritoneal  tissue  and  then  through  the  dia- 
phragm. The  pus  may  burrow  along  the  psoas  muscle  and  appear  as  a 
psoas  abscess  on  the  thigh,  or  abdomen.  Spontaneous  opening  usually 
occurs,  externally,  in  the  lumbar  region.  The  bladder,  ureter,  pelvis  of  the 
kidney,  peritoneum,  and  colon  have  all  been  perforated  by  perinephritic 
abscesses.  Sometimes  inflammation  of  the  perinephritic  tissue  is  not  fol- 
lowed by  suppuration,  but  at  the  autopsy  a  thick,  tough,  fibrous  mass  is 
found  occupying  the  place  of  the  (so-called)  adipose  capsule  of  the  kid- 
ney. The  same  result  may  follow  discharge  of  the  abscess  and  cicatriza- 
tion. 

Etiology. — Perinephritis  may  be  caused  by  pyelitis,  suppurative  nephri- 
tis, blows,  falls,  strains,  parasites,  or  wounds  of  the  kidney  or  the  tis- 
sue about  it.  It  may  occur  in  pyaemia  or  in  the  course  of  any  of  the  ex- 
anthems  or  specific  fevers.  It  may  also  complicate  pelvic  cellulitis,  psoas 
abscess,  and  perityphlitis.  It  occurs  more  frequently  in  men  than  in 
women. 

Symptoms. — Eecurring  rigors  are  among  the  first  symptoms,  followed  or 
accompanied  by  pain  in  the  lumbar  region — which  is  increased  by  move- 
ment and  firm  pressure — shooting  down  toward  the  testicle.  The  pulse  is 
rapid  and  feeble.  The  temperature  rises  to  100°-105°  F.  The  skin  at  first 
is  dry,  but  later  it  is  covered  with  a  profuse  perspiration.     There  is  ano- 


ELOATIKG   OR    MOVABLE    KIDNEY.  601 

rexia,  great  thirst,  and  constipation.  The  urine  is  usually  slightly  dimin- 
ished in  quantity  ;  otherwise  it  is  normal,  unless  pyelitis  or  nephritis  should 
coexist. 

Physical  Signs. — A  tumor  forms  in,  or  a  little  below,  the  lumbar  region  ; 
it  rapidly  increases  in  size  ;  at  first  it  is  hard  ;  later  it  gives  signs  of  deep 
fluctuation.  The  skin  over  it  is  oedematous  and  pale.  The  tumor  is  im- 
movable and  cannot  be  separated  from  the  kidney,  but  can  readily  be  dis- 
tinguished from  the  spleen  or  liver  enlargements.  An  exploring  trocar 
will  establish  the  diagnosis. 

Differential  Diagnosis. — The  differential  diagnosis  between  perinephritic 
abscess  and  -pyoneplirosis  and  hydronephrosis  has  already  been  given. 

It  is  distinguished  from  suppurative  nephritis  by  the  presence  of  a  tumor, 
and  by  the  absence  of  casts,  albumen,  blood  or  mucus  in  the  urine. 

From  extravasation  of  blood  due  to  rupture  of  an  aneurism,  it  is  distin- 
guished by  fever,  rigors,  ajluctuating  tumor,  and  the  absence  of  the  causes 
and  physical  signs  of  aneurism. 

Prognosis, — A  perinephritic  abscess  is  always  serious.  Its  duration  is 
usually  from  two  to  four  weeks  ;  in  some  cases  several  months  have  elapsed 
before  the  tumor  has  subsided.  Its  discharge  into  the  intestine  or  bladder, 
or  the  establishment  of  an  external  opening,  may  be  regarded  as  favorable. 
With  an  early  diagnosis  and  prompt  surgical  interference  the  prognosis  is 
good.  Some  regard  many  "  cures"  of  hip-joint  disease  without  deformity, 
as  in  reality  cases  of  suppurative  perinephritis. ' 

Treatment. — A  free  opening  should  be  made  as  soon  as  the  diagnosis  is 
established.  Grainger  Stewart  states  that  early  counter-irritation  by  blister- 
ing is  useful,  and  that  iodide  of  potassium  internally  and  iodine  externally 
may  prevent  suppuration  ;  my  experience  does  not  sustain  this  statement. 
Yet  incision  is  safer  than  aspiration ;  after  an  opening  is  made  the  finger 
should  be  introduced  into  the  abscess-cavity  and  any  adhesions  that  may  be 
present  should  be  broken  down.  Then  a  drainage  tube  should  be  intro- 
duced. Antisepsis  should  be  practised  during  the  operation  and  with 
subsequent  dressings.  Stimulants  and  concentrated  fluid  nutrition  should 
be  freely  administered. 

FLOATIlSrG    OE    MOVABLE   KTOISrEY. 

As  a  congenital  peculiarity  one  or  both  kidneys  may  be  movable,  and  in- 
stead of  occupyiiig  their  normal  position  may  lie  upon  the  brim  of  the 
pelvis,  or  be  freely  movable  in  the  loose  retro-peritoneal  connective-tissue 
which  surrounds  them,  and  the  peritoneum  may  be  so  reflected  in  front 
and  behind  them  as  to  allow  their  free  motion.  The  displacement  of  the 
kidney  under  any  one  of  these  conditions  may  follow  parturition  or  a  severe 
shock  from  a  fall.   It  is  met  with  more  frequently  in  females  than  in  males. 

Morbid  Anatomy.— A  congenital  displacement  is  distinguished  from  an 
acquired  displacement  by  the  abnormal  arrangement  of  the  vessels  of  the 
kidney  and  its  peritoneal  coverings.     The  extent  of  the  mobility  in  any 

>  Afner.  Jour.  Med.  Scieiwes,  April,  1877,  and  Oct.,  1878.    V.  P.  Gibney,  M.D. 


602  DISEASES    OF   THE    KIDNEYS. 

case  is  determined  by  the  length  of  the  vessels  which  form  the  pedicle. 
Movable  kidneys  are  almost  always  surrounded  by  connective-tissue  forma- 
tions, and  after  having  been  once  movable  they  may  become  firmly  fixed 
again  in  their  normal  or  in  an  abnormal  position. 

Symptoms. — A  displaced  kidney  is  usually  felt  midway  between  the  free 
border  of  the  ribs  and  the  umbilicus.  If  the  right  kidney  is  displaced  it  is 
apt  to  make  its  appearance  just  below  the  liver  ;  it  may  be  pushed  upward 
and  backward  into  its  normal  position,  but  it  will  return  as  soon  as  the 
support  is  withdrawn. 

If  a  displaced  kidney  can  be  grasped  its  pressure  causes  a  sickening  sen- 
sation. If  it  gets  compressed  or  otherwise  injured,  it  may  become  painful, 
tender,  and  swollen.  Otherwise  it  may  give  rise  to  no  symptoms  and  be 
recognized  only  by  accident. 

Differential  Diagnosis. — Its  diagnosis  rests — 1st,  on  the  shape  and  size  of 
a  tumor  corresponding  to  that  of  a  normal  kidney ;  2d,  when  the  tumor 
can  be  felt  in  front  there  will  be  an  abnormal  tympanitic  resonance  over 
the  normal  position  of  the  kidney  ;  3d,  the  tumor  can  be  pressed  back  into 
the  normal  kidney  region  ;  4th,  the  peculiar  sickening  sensation  produced 
by  its  manipulation. 

Prognosis. — Such  kidneys  are  never  a  cause  of  death.  Many  observers 
have  doubts  in  regard  to  the  probable  occurrence  of  a  floating  kidney. 
There  is  little  post-mortem  evidence  in  its  favor.  I  have  never  made  but 
one  diagnosis  of  this  condition  during  life  that  was  sustained  by  a  post- 
mortem examination. 

Treatment. — When  a  movable  kidney  is  painful,  rest  is  indicated,  and  a 
concave  abdominal  pad  so  adjusted  as  to  fit  the  form  and  position  of  the 
kidney  tumor  should  be  worn. 

HEMATURIA. 

Hgematuria  is  the  passage  of  urine  containing  blood.  The  blood  may 
have  its  origin  at  any  point  from  the  Malpighian  tuft  to  the  orifice  of  the 
urethra.  As  it  is  a  symptom,  it  has  no  morbid  anatomy  ;  its  causes  con- 
stitute its  pathology. 

Etiology. — Local  causes. — (1)  In  the  kidney  the  conditions  which  induce 
hsematuria  are  active  and  passive  hypersemia,  acute  (rarely,  if  ever,  chronic) 
suppurative  nephritis,  or  surgical  kidney,  infarctions  (including  embolism 
and  thrombosis),  tuberculosis,  a  single  or  multiple  pygemic  abscess,  pyeli- 
tis (especially  when  the  pyelitis  is  calculous),  stone  in  the  kidney,  or  in  the 
pelvis  of  the  kidney,  and,  in  a  few  cases,  hydro-  and  pyonephrosis.  Crystals 
in  the  tubules  may  induce  it.  Among  kidney  causes  may  be  included  the 
drugs  which  cause  hsematuria,  e.  g.,  turpentine,  cubebs,  copaiba,  canthar- 
ides,  etc. 

(2)  The  causes  that  have  their  seat  in  the  ureters  are  ureteritis,  cancer, 
polypi,  ulcers,  and  calculi. 

(3)  The  bladder  causes  are  cystitis  (but  only  when  very  acute  and  accom- 
panied by  erosion  and  ulceration),  cancer,  abscesses  in  the  vesical  walls,  poly- 


H^MATUEIA.  603 

pus  of  the  bladder,  stone  in  the  bladder,  rupture  of  the  bladder,  tubercu- 
losis, specific  or  non-specific  ulcers.  Dilatation  and  varicosity  of  the  vesical 
veins  may  cause  it,  called  oftentimes  "hemorrhoids  of  the  bladder." 

(4)  The  urethral  causes  are  many  :  urethritis  (non-specific  and  specific), 
peri-urethral  abscess,  chordee,  cancer,  fracture  of  penis,  rupture  of  prostatic 
abscess,  an  enlarged  prostate,  urethral  polypi  (especially  in  females),  caustic 
injections,  chancre  and  chancroids,  phimosis,  impacted  stone,  and  new- 
growths  in  the  prostate. 

The  general  causes  of  haematuria  are  acute  infectious  diseases,  fevers, 
especially  malarial,  scurvy,  purpura,  the  condition  know^n  as  hgemophilia 
(the  bleeders),  and  certain  central  nervous  diseases  (see  Mj'Clitis).' 

Symptoms. — The  urine  may  be  almost  black  and  loaded  with  clots,  or  it 
may  be  only  slightly  smoky  or  pinkish  in  color.  It  is  albuminous  ;  under 
the  microscope  swollen  or  shrunken  corpuscles  are  found,  the  degree  of  al- 
teration depending  on  the  time  they  have  remained  in  the  urine.  If  equal 
parts  of  tincture  of  guiacum  and  oil  of  turpentine  are  shaken  together  to 
form  an  emulsion,  an  intense  blue  color  will  arise  when  bloody  urine  is 
slowly  added  to  it. 

To  determine  the  source  of  the  hemorrhages  the  following  rules  may  be 
observed  : — urethral  hemorrhages  are  independent  of  micturition,  as  only 
a  residue  of  blood  is  washed  out  at  the  beginning  of  the  flow  of  urine.  The 
history  will  aid  and  inspection  will  probably  reveal  the  true  state  of  affairs  ; 
albumen,  casts  and  epithelial  cells  are  not  often  found  in  urine  when  it 
becomes  bloody  in  the  urethra.  The  Madder  may  be  suspected  as  the  seat 
of  the  hemorrhage  when  blood  flows  only  at  the  time  of  micturition,  and 
follows  the  discharge  of  urine ;  should  the  stream  suddenly  cease,  a  stone 
or  blood-clot  blocks  up  the  opening  of  the  urethra  into  the  bladder,  and 
this  will  be  well-nigh  diagnostic.  Clots  following  the  flow  of  urine  indicate 
cystic  disease.  When  they  precede  the  flow  or  occur  with  it,  urethral  dis- 
ease is  indicated.  Should  blood  globules,  albumen,  casts,  and  blood  moulded 
in  the  form  of  renal  tubules  be  found  in  the  urine,  renal  disease  may  be  re- 
garded as  the  cause  of  the  hsematuria.  In  renal  hemorrhage  blood  is 
mingled  with  the  urine,  and  is  commonly  as  profuse  at  the  commencement 
as  at  the  end  of  micturition. 

Should  liEematuria  be  combined  with  the  symptoms  of  stone  in  the  blad- 
der, of  pyelitis,  or  of  cystitis,  the  source  of  the  hemorrhage  is  then  no  longer 
a  matter  of  doubt.  Sir  Thomas  Watson  states  "that  slender  cylinders  of 
fibrin  in  the  ureter  indicate  renal  disease  or  commencing  inflammation  of 
the  ureter." 

In  "endemic"  haematuria  the  diagnosis  rests  on  discovering  the  trema- 
tode  or  its  ova  in  the  urine  or  faeces ;  it  causes  pain  along  and  over  the 
genito-urinary  tract. 

'  There  is  a  variety  of  haematuria  which  occurs  in  tropical  countries  (Egypt,  Brazil  and  Cape  of  Good! 
Hope  especially)  caused  by  a  fluke  called  Bilharzia  hsematobia,  aparasite  (atrematodchrematozoon),  which 
is  endemic.  Dr.  John  Harley  discovered  this  parasite  in  the  blood  of  a  patient  in  South  America.  It  is^ 
one-half  to  three-quarters  in.  long,  and  is  found  chiefly  in  the  vessels  of  the  portal  system  and  of  the  blad- 
der. The  eggs  are  found  in  the  urine  ;  they  are  1-100  to  1-180  in.  in  length,  and  are  peculiarly  pointed  at 
one  end,  the  whole  contour,  however,  being  ovoid.  This  parasite  causes  thickening,  ulceration,  ecchy- 
moses  and  large  blood  extravasations  iu  the  mucous  membrane  in  whose  vessels  it  is  lodged. 


^04  DISEASES    OF   THE    KIDNEYS. 

In  the  so-called  false  hsematuria  the  urine  contains  only  haemoglobin,, 
the  microscope  failing  to  discover  any  corpuscular  elements  in  the  urine. 
It  is  also  called  limmoglobinuria,  hcBmathmria,  and  (when  occurring  peri- 
odically), intermittent  or  paroxysmal  hmniaturia.  The  haemoglobin  of  the 
blood  is  set  free  in  one  of  two  ways  :  either  the  extravasated  corpuscles  dis- 
integrate or  the  haemoglobin  escapes  without  rupture  of  the  capillary  walls. 
Once  free  in  the  blood  the  kidneys  eliminate  the  haemoglobin.  Fevers, 
poisons,  gases,  and  cold  are  said  to  cause  this  condition. 

When  intermittent  it  is  usually  dependent  on  malaria,  but  a  malarial 
cause  need  not  necessarily  exist  for  the  paroxysm  to  occur.  Chills,  sweat- 
ings, and,  at  times,  a  rise  in  temperature  attend  the  discharge  of  the  red- 
dish urine,  which  soon  shows  a  granular,  brownish  sediment.  Albumen, 
and  hyaline  and  granular  casts  are  very  often  present,  independent  of  renal 
disease.     In  severe  cases  the  patient  becomes  anaemic  and  cachectic. 

Quite  recently  a  disease  has  been  described  called  "melaBnic  fever," 
resembling  somewhat  in  its  constitutional  symptoms  acute  yellow  atrophy 
■of  the  liver  and  yellow  fever.  The  urine  is  brown-black  and  contains  al- 
bumen, casts,  and  a  large  quantity  of  blood  cori)uscles  (not  haemoglobin 
alone).     Suppression  often  occurs,  and  the  case  ends  fatally.' 

Differential  Diagnosis. — The  points  of  differential  diagnosis  have  been  suf- 
ficiently considered  in  its  etiology.  First,  care  must  be  taken  by  micro- 
scopical examination  and  spectrum  analysis  to  positively  determine  that 
blood  corpuscles  or  haemoglobin  are  actually  present  in  the  urine.  Then 
a  study  of  its  causes  and  accompanying  symptoms  renders  the  diagnosis 
comparatively  easy. 

Prognosis. — The  prognosis  in  haematuria  depends  on  its  cause.  Endemic 
haematuria  is  never  the  direct  cause  of  death,  but  it  may  lead  to  extreme 
anaemia.     Paroxysmal  haemoglobinuria  is  rarely  fatal. 

Treatment. — When  the  haematuria  is  slight  and  of  short  duration  no 
special  treatment  is  required ;  if  profuse  or  persistent  the  patient  should 
be  placed  in  a  recumbent  position,  ice-bags  applied  over  the  seat  of  the 
hemorrhage,  and  haemostatic  remedies  used,  such  as  gallic  or  tannic  acid, 
ergot,  acetate  of  lead,  and  astringent  ferric  preparations.  If  the  haema- 
turia is  of  parasitic  origin  prophylaxis  demands  that  the  drinking  water 
be  filtered  and  boiled  ;  to  expel  the  parasites  male-fern  or  chloroform  may 
be  given  internally.  Harley  advises  belladonna  and  henbane.  Quinine  is 
indicated  in  all  forms  of  paroxysmal  haematuria  or  haemoglobinuria.  If 
the  hemorrhage  is  from  the  bladder  persistent  weak  astringent  injections 
may  be  employed. 

CHYLURIA. 

Chyluria  is  characterized  by  the  occasional  or  continuous  discharge  of 
urine  which  resembles  milk  when  passed  and  coagulates  into  a  jelly  mass  on 
standing. 

Morbid  Anatomy  and  Etiology. — The  kidneys  are  usually  found  free  from 

1  Virginia  Med.  Monthly,  February,  1880. 


CHTLURIA.  605 

disease,  and  the  affection  is  attended  by  no  known  constant  pathological 
lesions.  At  one  time  it  was  regarded  as  a  disease  of  defective  assimilation 
which  permitted  the  chyle  to  miugle  with  the  blood;  at  another,  a  fault  of 
the  kidneys  which  allowed  the  unchanged  chyle  to  be  transuded  with  the 
urine.     Neither  of  these  explanations  has  been  sustained  by  observation. 

There  are  at  present  many  theories  in  regard  to  its  causation  :  first,  that 
there  is  a  direct  communication  between  the  chyle-carrying  vessels  and  the 
urinary  tract ;  second,  that  it  is  a  symptom  of  piarrhsemia  due  to  a  de- 
ranged liver  function  ;  third,  that  it  is  caused  by  an  eczema  along  the 
urinary  tract ;  fourth,  that  it  is  due  to  hypertrophy  of  the  lymph  channels 
and  their  subsequent  assumption  of  glandular  functions  ;  fifth,  that  it  is 
due  to  a  parasite,  but  whether  the  action  of  the  entozoon  is  on  the  function 
of  the  liver  or  causes  irritation  and  rupture  of  the  lymph  and  chyle  chan- 
nels is  not  determined. 

Symptoms. — No  disease  pursues  a  more  irregular  course  :  no  two  cases 
exactly  resemble  each  other.  There  may  be  pain  in  the  loins  and  along  the 
gerii to-urinary  tract,  depression  of  spirits,  and  debility,  before  the  urine 
becomes  chylous ;  or,  the  first  sign  may  be  a  sudden  flow  of  milky  urine, 
having  a  whey-like  or  milky  odor,  made  more  perceptible  by  warmth.  It 
soon  coagulates  on  standing,  but  the  trembling.  Jelly-like  clot  breaks  down 
and  the  urine  decomposes  in  a  few  hours.  Bloody  coagula,  usually  shreddy, 
may  also  form.  White  and  red  blood  discs  are  found  in  varying  quantity. 
Clots  may  form  in  the  bladder,  and  during  micturition  the  flow  may  sud- 
denly stop  from  blocking  of  the  urethra.  The  sp.  gr.  of  the  urine  varies, 
(1.007-1.030).  Heat  and  nitric  acid  cause  a  precipitate.  Shaken  with 
ether  the  urine  loses  its  milkiness.    Fat,  albumen,  and  fibrin  are  all  present. 

Blood  analyses  vary  ;  but  when  the  filaria  sanguinis  hominis  is  not  found 
in  chylous  urine  it  is  found  in  a  drop  of  blood  taken  from  the  finger,  and 
vice  versd.  Hoppe-Seyler  says  blood  in  this  disease  resembles  human 
lymph  in  its  composition.  Chylo-serous  discharges  take  place  also  from 
axilla,  groin,  scrotum,  and  surface  of  the  abdomen  or  inner  corner  of  the 
eye.  Chyluria  is  an  intermittent  disease,  but  there  is  no  periodicity  or 
regularity  to  it. 

Prognosis. — The  disease  runs  a  chronic  course.  Men  have  suffered  on  and 
off  for  fifty  years.  Change  of  climate  does  not  seem  to  improve  the  out- 
look when  the  disease  is  once  established.  Sudden  death  may  occur  at  any 
moment,  even  in  those  with  fair  health.  Elephantiasis,  phlebitis,  haema- 
turia,  "lymph-scrotum,"  craw-craw,  leprosy,  and  furuncles  are  not  infre- 
quent complications. 

Treatment— This  has  been  unsatisfactory.  Turpentine  and  gallic  acid 
are  recommended.  Iodide  of  potash  and  perchloride  of  iron  are  claimed  to 
be  highly  beneficial.  Mangrove  and  nigella  sativa  are  used  by  the  natives 
in  places  where  chyluria  prevails;  sometimes  they  effect  a  cure,  oftener  not, 
however.  Prophylaxis  demands  care  in  drinking  water  in  a  tropical  re- 
gion, and  first  boiling  or  filtering  it. 


606  DISEASES    OF   THE   KIDiS'ETS. 


CYSTITIS. 

Cystitis  is  an  inflammation  of  the  mucous  membrane  lining  the  urinary 
bladder.  It  is  acute  or  chronic;  aud  it  may  be  either  catarrhal,  croupous, 
or  diphtheritic.  The  whole  or  part  of  the  bladder  may  be  involved  j 
when  "  partial,"  it  is  limited  to  the  neck  and  bas-fond. 

Morbid  Anatomy. — In  acate  catarrhal  cystitis  the  appearances  are  in  no 
wise  different  from  those  observed  when  any  mucous  surface  is  inflamed. 
The  small  glands  at  the  base  of  the  bladder  are  enlarged  and  filled  with  a 
pearly  secretion.  The  interior  portion  of  the  trigone  is  also  studded  with 
these  pearly  masses.  They  may  form  a  circle  about  the  neck  of  the  blad- 
der. Intense  (acute)  cystitis  may  end  in  suppuration  of  the  submucous 
connective-tissue,  and  ulceration  of  the  mucous  membrane  may  allow 
these  submucous  abscesses  to  empty  into  the  bladder. 

When  cystitis  results  in  paralysis  of  the  bladder,  gangrene  of  the  mu- 
cous membrane  may  occur ;  then  brownish-black,  irregular  patches  are 
seen  mingled  with  debris  and  phosphatic  incrustations  on  the  surface  of 
the  bladder.  When  the  mucous  layer  is  thus  destroyed  by  gangrene,  the 
urine  infiltrates  the  neighboring  tissue,  and  local  or  general  peritonitis  may 
result.  An  acute  cystitis  may  lead  to  a  pyelo-nephritis.  Ulcerating  cys- 
titis occurs  in  typhoid  and  low  eruptive  fevers,  in  diphtheria,  pyasmia, 
etc.  It  is  called  by  some  diphtheritic.  The  lesions  in  this  form  and  in 
croupous  cystitis  are  similar  to  those  which  take  place  in  diphtheritic 
exudations  on  other  mucous  surfaces.     [See  Inflammation.) 

In  chronic  cystitis  the  mucous  membrane  is  thick,  blue-gray  in  color, 
and  very  tough.  Muco-pus  and  viscid  mucus  are  formed  in  large  quanti- 
ties upon  its  surface.  As  the  disease  progresses  a  peri-cystitis  consolidates 
the  bladder  with  the  neighboring  organs  and  parts.  Chronic  catarrhal 
ulcers  may  form,  and  perforation  of  the  bladder  may  result,  and  the 
vagina,  rectum,  or  abdominal  cavity  may  be  entered,  or  an  external  open- 
ing may  be  formed  through  which  pus  is  discharged.  The  muscular  wall 
of  the  bladder  may  sometimes  be  half  an  inch  thick,  and  the  fasciculi 
give  a  ribbed  appearance  to  the  internal  surface,  called  the  "columnar 
bladder."  The  hypertrophy  of  chronic  cystitis  may  be  eccentric  or  con- 
centric. In  some  cases  diverticuli  are  formed,  in  whose  walls  are  dilated 
and  tortuous  veins.  Some  of  these  cysts  are  in  the  form  of  hernial  protru- 
sions.    In  nearly  all  cases  bacteria  are  found  in  abundance. 

Etiology. — Acute  cystitis  is  rarely  idiopathic. 

It  may  result  from  the  presence  of  foreign  bodies,  especially  calculi. 
Blows  may  cause  it.  Protracted  retention  of  urine  has  set  up  a  rapidly 
fatal  cystitis. 

It  may  be  caused  by  some  unknown  blood  condition,  such  as  occurs  in 
scarlet,  typhus,  and  typhoid  fevers,  pyaemia,  septicaemia,  small-pox,  and 
diphtheria  ;  it  is  a  frequent  complication  of  certain  grave  lesions  of  the 
nervous  system,  especially  myelitis. 

Cystitis  may  result  from  the  extension  of  an  urethritis,  a  pyelitis,  or  a 
pelvic  cellulitis. 


CYSTITIS.  607 

Chronic  cystitis  may  be  the  sequela  of  acute  cystitis  or  result  from  the 
retention  of  urine  caused  by  an  enlarged  prostate  or  urethral  stricture. 
Over-distention,  atony  or  paralysis  of  the  bladder,  calculi,  polypi,  and 
neoplasms  of  all  l<;inds  cause  it.  Gout  and  some  forms  of  kidney  disease 
are  accompanied  by  chronic  cystitis. 

Symptoms. — Acute  cystitis  is  always  accompanied  by  frequent  micturi- 
tion, only  a  few  drops  being  voided  at  each  attempt.  After  its  passage 
the  patient  strains  (as  in  the  tenesmus  of  dysentery)  to  pass  what  he 
imagines  is  still  retained  in  the  bladder.  There  are  dull,  aching  pains 
over  the  pubis  ;  sometimes  the  pains  in  the  vesical  region  are  agoniz- 
ing, and  there  is  a  constant  burning  sensation  along  the  urethra.  These 
local  symptoms  are  not  infrequently  accompanied  by  rigors,  and  the  tem- 
perature rises  to  100°-] 01°  F.,  with  loss  of  appetite,  sleeplessness,  and  a 
feeling  of  great  anxiety  or  depression. 

The  urine  is  cloudy,  deposits  mucus  on  standing,  is  alkaline,  and  some- 
times fetid.  Microscopically,  epithelium,  pus  and  red  blood-corpuscles 
are  found.  Membranous  exudations  may  be  found,  especially  in  females. 
JSTiemeyer  states  that  in  the  "  croupous  cystitis  following  cantharides 
poisoning  and  forcible  forceps  deliveries  large  tenacious  false  membranes 
are  discharged  "  with  the  urine. 

Chronic  cystitis  is  often  only  indicated  by  a  frequent  desire  to  pass  urine. 
Usually  there  is  a  constant,  dull,  aching  pain,  or  a  sense  of  weakness  over 
the  bladder.  The  bladder  is  nearly  always  intolerant  of  its  contents,  no 
matter  how  long  the  catarrh  has  persisted.  Hence  only  a  small  amount  of 
urine  will  be  passed  with  each  act.  Distention  and  muscular  hypertrophy 
of  the  bladder  often  give  rise  to  an  abdominal  tumor  reaching  as  high  as 
the  umbilicus  ;  it  may  contain  from  two  to  eight  pints  of  urine ;  as  large 
a  quantity  as  this,  in  some  cases,  may  constantly  remain  in  the  bladder, 
only  so  much  urine  being  passed  as  exceeds  this  amount,  and  then  a  patient 
will  be  passing  very  nearly  a  normal  quantity,  and  the  introduction  of  the 
catheter  may  remove  a  quart  of  stinking,  alkaline  urine,  which,  when  it 
stands,  divides  into  two  parts,  a  lower  thick,  turbid,  gelatinous,  coherent 
and  opaque  mass — the  supernatant  layer  being  clear.  The  "glairy  mucus  " 
so  frequently  described  in  this  connection  is  only  met  with  when  the  urine 
is  ammoniacal  and  also  contains  pus  ;  it  is  formed  by  the  reaction  of  the 
alkali  upon  the  pus.  Chronic  cystitis  accompanied  by  enlargement  and 
atony  of  the  bladder  often  eventuates  in  ammonaemia,  and  then  typhoid 
symptoms  are  developed.  Great  local  pain,  emaciation  and  occasional 
bloody  urine  indicate  ulceration.  Acute  suppurative  inflammation  of  the 
bladder,  accompanied  by  hectic,  rigors,  and  extreme  exhaustion,  may  accom- 
pany acute  suppurative  nephritis. 

DiflFerential  Diagnosis. — Pyelitis  often  resembles  cystitis  closely  in  its  sub- 
jective symptoms ;  there  may  be  the  same  pain  referred  to  the  bladder, 
and  the  same  frequent  desire  to  micturate.  In  pyelitis  the  lumbar  j)ain, 
the  "tailed  "  cells  in  the  urine,  the  even  admixture  of  pus  with  the  urine, 
the  acid  reaction,  and  the  absence  of  ropy,  gelatinous  mucus,  are  symptoms 
in  marked  contrast  to  those  of  cystitis. 


608  DISEASES    OF   THE   KIDNEYS. 

Prognosis. — The  prognosis  depends  upon  the  cause  ;  in  general  it  is  good. 
Chronic  cystitis  may  continue  for  years  ;  the  longer  it  continues  the  less 
chance  there  is  of  recovery.  Acute  cystitis  is  usually  recovered  from  in 
about  a  week. 

Treatment. — In  acute  cystitis  the  patient  must  have  perfect  rest.  Warm 
hip-baths  give  relief.  Leeching  or  cupping  over  the  bladder  is  often  of 
service.  Suppositories  of  opium  and  belladonna  or  rectal  injections  of  the 
same  are  always  indicated,  with  large  poultices  and  very  hot,  peppery  fo- 
mentations over  the  bladder.  The  bowels  should  be  kept  free  with  the 
mildest  cathartics.  An  anodyne  internally  may  be  demanded  for  the 
relief  of  pain;  I  have  found  chlorodyne  the  best.  Twenty  minims  of  liquor 
potassse  in  mucilage  may  be  given  three  times  in  the  twenty-four  hours. 
Half  drachm  doses  of  fluid  extract  of  Indian  hemp  are  highly  recommended. 
The  diet  should  be  nutritious  ;  milk  is  to  be  preferred.  No  form  of  alcohol 
should  be  allowed  ;  the  patient  may  drink  freely  of  flax-seed  or  linseed  tea, 
barley  water,  or  decoction  of  triticum  repens.  In  all  cases  the  cause  should 
be  sought  for  and  if  possible  removed. 

In  chronic  cystitis  the  catheter  is  to  be  regularly  and  persistently  used. 
The  bladder  should  be  washed  out ;  lime  water  and  glycerine,  very  weak 
solutions  of  nitrate  of  silver,  sulphate  of  copper,  either  in  water  or  in 
glycerine,  are  often  of  service.  Very  weak  solutions  of  salicylic  acid,  car- 
bolic acid,  permanganate  of  potash,  and  chloride  of  sodium  are  also  recom- 
mended. The  daily  use  of  a  mineral  water,  like  Vichy,  is  beneficial  in 
many  cases  of  chronic  cystitis,  I  have  found  more  benefit  from  the  daily 
use  (drachm  doses  after  each  meal)  of  the  "  Lafayette  mixture  "  in  chronic 
cystitis  than  from  all  other  remedies.  All  stimulating  drinks  are  forbidden. 
The  injection  of  quinine  into  the  bladder  has  recently  been  very  success- 
fully practised  for  the  cure  of  chronic  cystitis.' 

»  Lmdon  Lancet,  Feb.  23, 1878,  and  June  1, 1878. 


SECTION    ly. 

ACUTE    GEKERAL   DISEASES. 

Under  this  head  I  shall  include  those  acute  infectious  diseases  which  de- 
pend upon  poisons  developed  outside  the  body  of  the  affected  person. 
These  poisons  possess  two  distinctive  characteristics.  First,  each  poison  is 
specific  and  distinct  from  every  other  in  its  action,  and  hence  inferentially 
in  its  nature,  so  that  the  pathological  processes  which  it  incites  are  always 
identical  in  kind  and  associated  with  that  one  etiological  element,  and  with 
no  other.  These  processes  thus  become  the  means  of  differentiating  this 
class  of  poisons.  Second,  all  these  poisons  possess  the  power  of  indefinite 
reproduction  when  jDlaced  under  favorable  circumstances,  and  their  result- 
ing diseases  are  therefore  generally  endemic,  when  permanent  sources  of 
infection  have  become  established,  or  epidemic,  when  the  poison  affects 
large  numbers  at  the  same  time,  rather  than  sporadic.  Such  a  poison  is 
termed  a  virus,  and  has  its  origin  either  in  the  bodies  of  diseased  living 
beings  or  in  decomposing  organic  matter. 

Every  virus  is  more  or  less  diffusible  and  may  be  conveyed  by  air,  fluids, 
or  solids ;  while  in  some  diseases  it  becomes  so  localized  that  it  can  be 
transmitted  by  inoculation.  These  morbific  agents  give  rise  to  distinctive 
diseases  either  by  changes  which  they  produce  in  the  blood  or  by  their  di- 
rect action  upon  the  cellular  elements  of  the  different  organs  and  tissues. 

When  a  virus  originates  and  attains  its  full  development  only  in  a  living 
animal  and  is  excreted  in  an  active  state  it  is  called  a  contagion,  and  the 
disease  which  it  produces  is  contagious. 

"When  the  morbific  agent  is  solely  the  product  of  decomposing  organic 
matter  it  is  termed  a  miasm,  and  the  affection  it  develops  is  a  miasmatic 
or  malarial  disease.  Contagions  may  be  transmitted  mediately  or  imme- 
diately, and  are  reproduced  with  each  infection.  Miasms  are  conveyed  only 
by  diffusion,  generally  through  air  or  water,  and  their  activity  is  limited 
to  a  single  infection. 

A  third  form  of  virus  originates  solely  in  diseased  animal  organisms,  but 
is  excreted  in  a  passive  condition  and  becomes  active  only  in  the  presence 
of  decomposing  organic  matter.  The  diseases  in  whose  development  such 
a  poison  is  the  etiological  factor  are  termed  miasmatic- contagions. 

As  to  the  exact  nature  of  any  infectious  poison,  or  its  element  of  power 
in  the  production  of  disease,  we  have  no  positive  knowledge.  At  present, 
there  are  two  prominent  theories.  The  first  is  based,  upon  chemical  pro- 
cesses ;  the  second,  upon  tlie  multiplication  of  living  organisms.  The 
chemical  theory  maintains  that  after  the  infectious  element  has  been  re- 
39 


610  ACUTE    GENERAL   DISEASES. 

ceived  into  the  blood  it  acts  as  a  ferment,  and  gives  rise  to  certain  morbid 
processes  upon  the  principle  of  catalysis. 

The  theory  of  organisms,  or  the  germ  theory,  maintains  that  the  in- 
fections poisons  are  living  organisms,  which,  being  received  into  the  blood, 
reproduce  themselves  indefinitely,  and  excite  morbid  processes  which  are 
characteristic  of  certain  types  of  disease.  This  theory,  at  the  present  time, 
is  quite  extensively  adopted,  as  it  so  readily  explains  very  many  remarkable 
facts  connected  with  the  development  and  reproduction  of  this  class  of  dis- 
eases. It  is  readily  understood,  and  there  are  so  many  animal  poisons 
which  appear  to  act  in  this  manner,  that  to  one  whose  opinions  are  not 
based  upon  clinical  experience  and  actual  contact  with  disease,  the  argu- 
ments in  its  favor  seem  conclusive.  According  to  this  theory  all  the  dif- 
ferent forms  of  disease  included  under  the  head  of  infections  may  be  re- 
duced to  two  classes  :  first,  infectious  diseases  which  depend  for  their  de- 
velopment upon  a  living  animal  organism.  Second,  those  which  depend 
for  their  production  upon  a  living  vegetable  organism.  At  j^resent  the 
proofs  of  this  theory  have  not  extended  beyond  the  demonstration  of  the 
presence  of  bacteria  in  the  pathological  products  of  some  infectious  dis- 
eases. Observers  are  not  agreed  as  to  the  identity  of  the  individual  germs 
of  any  infectious  disease,  nor  is  their  etiological  relation  to  diseases  estab- 
lished as  yet  even  in  the  most  general  way.  That  bacteria  are  the  exciting 
cause  of  some  diseases  in  animals  has  been  very  conclusively  proven,  but 
thus  far  the  strongest  proofs  of  any  such  relation  to  human  diseases  are  in- 
sufficient to  warrant  our  general  acceptance  of  the  germ  theory. 

I  shall  adopt  the  etiological  classification  of  acute  infectious  diseases. 

I.  Miasmatic  Contagions  Diseases,  due  to  a  virus  originating  in  a  living 
being  and  developed  in  decomposing  organic  matter. 

1.  Typhoid  Fever.  5.  Oerebro-spinal  Meningitis. 

2.  Yellow  Fever.  6.  SepticaBmia. 

3.  Cholera.  7.  Pyaemia. 

4.  Diphtheria.  8.  Erysipelas. 

9.  Acute  Miliary  Tuberculosis. 

II.  Acute  Contagious  Diseases,  due  to  a  virus  originating  and  developed 
solely  in  a  living  being. 

1.  Typhus  Fever.  6.  Measles. 

2.  Eelapsing  Fever.  7.  Grerman  Measles. 

3.  Small-pox.  8.  Miliary  Fever. 

4.  Varicella.  9.  Influenza. 

5.  Scarlet  Fever.  10.  Whooping  Cough. 

11.  Hydrophobia. 

III.  Malarial  Diseases,  due  to  a  virus  originating  and  developed  solely 
in  decomposing  vegetable  organic  matter. 

1.  Intermittent  Fever.  4.  Pernicious  Fever. 

2.  Eemittent  Fever.  5.  Dengue  Fever. 

3.  Continued  Malarial  Fever.  6.  Chronic  Malarial  Infection. 

"^n  their  pathology  and  clinical  histories  the  fevers  of  the  first  class  have 


TYPHOID   FEVER.  611 

many  things  in  common  with  those  of  each  of  the  other  classes,  and  will 
be  first  considered. 

TYPHOID    FEVER. 

This  is  the  most  prevalent  of  all  fevers  except  malarial.  So  far  as  we 
know,  there  is  no  place  where  it  may  not  be  developed  and  spread.  It  more 
frequently  prevails  in  the  temperate  zones  than  in  the  torrid  or  frigid,  but 
it  is  possible  for  it  to  be  developed  in  all  latitudes  and  in  all  countries. 
This  disease,  which  is  essentially  the  same  in  all  countries,  is  designated  by 
different  names.  American  writers  describe  it  under  the  name  of  typhoid 
fever.  The  French  call  it  the  typhoid  ajfect ion,  or  dothinenteria.  English 
writers  describe  the  same  form  of  disease  under  the  head  of  enteric  fever. 
The  Germans  call  it  abdominal  typhus,  or  gastric  fever,  I  prefer  the  name 
typhoid  fever. 

Morbid  Anatomy. — As  soon  as  the  disease  is  fully  established  a  change  in 
the  hlood  occurs.  It  becomes  darker  in  color,  coagulating  imperfectly,  and 
the  serum  is  of  an  unnaturally  yellow  color.  The  question  arises  : — did 
these  changes  take  place  in  the  blood  prior  to  the  occurrence  of  the  fever, 
between  the  exposure  and  the  period  of  attack  ?  It  is  certain  that  as 
soon  as  the  characteristic  symptoms  of  the  disease  are  present,  the  diminu- 
tion in  the  fibrin  of  the  blood  is  in  exact  proportion  to  the  severity  of  the 
fever,  and  the  number  of  white  globules  is  increased  in  a  similar  ratio. 

In  connection  with  these  blood  changes,  a  series  of  changes  take  place  in 
those  organs  and  tissues  of  the  body  in  which  the  jDrocess  of  waste  and  re- 
pair are  most  rapidly  going  on.  They  are  of  the  nature  of  parenchyma- 
tous degeneration,  the  essential  constituents  of  the  affected  organs  and 
tissues  being  involved.  Similar  parenchymatous  changes  are  met  with  to  a 
greater  or  less  extent  in  other  acute  infectious  diseases. 

Spleen. — The  organ  in  which  parenchymatous  degeneration  occurs  ear- 
liest and  most  extensively  is  the  spleen.  We  find  this  organ  undergoing 
three  distinct  changes  : — 

First.  It  is  increased  in  size,  sometimes  enormously.  The  enlargement 
commences  soon  aftpr  the  beginning  of  the  disease,  and  goes  on  rapidly 
until  the  third  week,  after  which  it  ceases,  and  within  a  few  days  begins  to 
diminish.  If  recovery  takes  place,  by  the  time  it  is  reached,  the  spleen  will 
have  returned  to  its  normal  size.  The  splenic  enlargement  is  apparently 
due  to  congestion  and  to  an  increase  of  normal  elements. 

Second.  As  soon  as  the  spleen  reaches  its  maximum  size,  its  consistency 
diminishes,  and  this  softening  is  sometimes  so  marked  that,  if  a  post-mortem 
be  made  at  the  end  of  the  third  week,  it  will  present  the  appearance  of  a 
dark,  jelly-like  mass,  which  is  easily  broken  down. 

Third.  The  organ  becomes  almost  black  in  color,  owing  to  the  intense 
congestion  which  attends  its  enlargement,  and  to  the  deposit  of  a  brown 
pigment  in  its  substance.  These  changes  in  the  spleen  take  place,  in  a 
greater  or  less  degree,  in  ninety-eight  cases  out  of  every  hundred.  At  the 
post-mortem  of  those  who  have  died  of  typhoid  fever  infarctions  are  some- 


612  ACUTE    GENEEAL    DISEASES. 

times  found,  alfhough  there  is  nothing  peculiar  about  them.     In  rare  in- 
stances, rupture  of  the  spleen  occurs  without  infarctions. 

Liver. — Changes  in  the  liver  are  by  no  means  as  common  as  those  in  the 
spleen.  The  liver  may  be  found  presenting  its  normal  appearance,  or  it 
may  be  soft  and  flabby.  When  soft  and  flabby,  a  microscopic  examination 
shows  the  liver  cells  more  or  less  granular  and  fatty  ;  the  nuclei  of  the  cells 
can  no  longer  be  seen,  and  the  degeneration  may  become  so  extensive  that 
the  outline  of  the  hepatic  cells  is  lost,  and  nothing  but  a  mass  of  granules 
remains.  Occasionally  there  will  be  found  in  the  liver  small  grayish  nod- 
ules situated  along  the  course  of  the  small  veins ;  these  bodies  consist  of 
lymphoid  cells.  The  lining  membrane  of  the  gall-bladder  sometimes  pre- 
sents evidences  of  catarrhal  or  diphtheritic  inflammation,  when  there  has 
been  no  evidence  of  its  existence  during  life ;  cases  are  recorded  where  it 
has  been  found  ulcerated. 

Kidneys. — Degenerative  changes  in  the  kidneys  are  of  not  infrequent  oc- 
currence in  the  course  of  typhoid  fever  ;  they  vary  in  extent  with  the  dura- 
tion and  severity  of  the  fever.  When  present,  they  are  more  marked  in 
the  cortical  than  in  the  medullary  portion  of  the  organ.  In  some  cases 
they  are  confined  to  the  epithelial  elements,  while  in  other  cases  degenera- 
tion of  all  the  anatomical  elements  of  the  organs  can  be  found.  Such  ex- 
tensive changes  are  less  liable  to  occur  in  typhoid  than  in  typhus  fever. 
Small  gray  nodules,  similar  to  those  referred  to  as  occurring  in  the  liver,  are 
sometimes  found.  If  the  epithelial  degeneration  of  the  cortical  substance 
is  extensive,  the  cells  finally  break  down  into  a  granular  detritus,  and  the 
cut  surface  assumes  a  yellow  color  and  is  softer  than  normal.  Infarctions 
are  sometimes  met  with  in  the  kidneys  of  those  dying  of  typhoid  fever. 

Heart. — The  parenchymatous  changes  which  take  place  in  the  heart  are 
more  marked  than  those  in  any  other  organ  except  the  spleen.  In  a  large 
proportion  of  cases  it  becomes  soft  and  flabby,  and  is  of  a  grayish  or  brown 
color.  Sometimes  it  is  so  much  changed  that  its  tissue  is  easily  broken 
down  by  moderate  pressure  ;  it  loses  its"  normal  outline,  and  when  removed 
from  the  body  the  walls  of  its  cavities  readily  fall  together.  When  its  mus- 
cular tissue  is  examined  microscopically,  in  many  instances  it  will  be  found 
that  granular  changes,  affecting  the  ultimate  muscular  fibres,  have  oc- 
curred ;  this  granular  muscular  degeneration  may  be  general  or  local.  Oc- 
casionally the  muscular  fibres  are  infiltrated  with  brown  pigment.  If,  as 
is  sometimes  the  case,  the  heart  retains  its  normal  outline,  is  friable,  and 
its  cut  surface  glistens,  the  muscular  fibres  will  be  found  to  have  undergone 
a  change  which  closely  resembles  amyloid  degeneration  ;  they  will  be  filled 
with  a  material  which  presents  the  same  shining  appearance  as  the  amy- 
loid substance,  but  on  applying  the  iodine  test  the  amyloid  reaction  does 
not  take  place.  It  is  a  form  of  degeneration  which  is  not  confined  to  the 
muscular  tissue  of  the  heart,  but  is  found  to  a  greater  or  less  extent  in  the 
voluntary  muscles  throughout  the  body.  Thrombi  are  sometimes  found  in 
the  heart,  and  vegetations  adhering  to  the  valves  and  chordae  tendinese. 
These  may  give  rise  to  infarctions  in  the  different  organs.  The  existence 
of  these  degenerative  changes  in  the  heart  may  be  recognized  during  the 


TYPHOID   FEVEE.  613 

life  of  the  patient,  for  the  heart-sounds  become  feeble  according  to  the  ex- 
tent of  the  degeneration,  and  in  some  cases  the  first  sound  of  the  heart  will 
be  absent. 

Lungs. — The  lungs  undergo  changes  which  have  received  the  name  of 
splenization,  from  the  close  resemblance  which  the  affected  portion  of  lung 
then  bears  to  the  spleen.  The  affected  tissue  is  of  a  darker  color  than  nor- 
mal, and  scattered  through  its  substance  will  be  seen  minute  red  or  yellow- 
ish-white points  ;  these  points  are  scanty  blood  extravasations.  It  is  of  a 
reddish-blue,  brown,  or  black  color  ;  its  consistence  is  firmer  than  normal, 
it  crepitates  less  freely,  has  a  more  homogeneous  appearance  upon  its  cut 
surface,  and  is  less  moist  than  normal  lung-tissue  ;  a  dark  fluid  will  some- 
times ooze  from  its  cut  surface,  but  not  as  freely  as  in  hypersemia,  and  the 
fluid  is  more  watery  in  appearance.  A  microscopical  examination  of  lung- 
tissue  in  this  condition  shows  the  capillary  vessels  filled  with  blood,  and  the 
alveoli  containing  a  variable  number  of  cells.  It  is  a  condition  closely  re- 
sembling that  condition  known  as  static  pneumonia,  but  no  inflammatory 
process  exists  ;  it  is  simply  a  stasis  in  the  capillary  circulation,  accom- 
panied by  a  slight  increase  in  the  cell  elements  in  the  alveoli. 

So  constantly  is  catarrhal  bronchitis  present  in  this  fever,  that  Dr.  Stokes 
proposed  to  call  typhoid  fever  Ironcliial  typhus.  In  most  cases  this  catarrh 
is  not  extensive,  but  affects  only  the  larger  bronchi  ;  it  may,  however,  ex- 
tend to  the  smaller  tubes  and  give  rise  to  capillary  bronchitis  and  broncho- 
pneumonia. Pulmonary  infarctions  are  frequently  found  in  the  lungs  of 
those  who  have  died  of  typhoid  fever.  They  are  sometimes  quite  numerous, 
are  usually  of  small  size,  and  vary  in  appearance  according  to  the  stage  of 
their  development.  When  recent  they  are  of  dark  color,  and  feel  like  con- 
solidated lung-tissue  ;  later,  the  color  changes  to  yellow  ;  they  may  soften 
and  break  down. 

Larynx. — The  larynx,  as  well  as  the  bronchial  tubes,  is  frequently  the 
seat  of  catarrhal  inflammation  ;  less  frequently  it  is  the  seat  of  diphtheritic 
inflammation.  In  connection  with  these  laryngeal  inflammations,  ulcers 
appear  in  the  larynx  ;  these  have  received  the  name  of  "  typhoid  ulcers  of 
the  larynx  : "  sometimes  they  give  rise  to  quite  extensive  hemorrhages. 
In  connection  with,  or  independent  of,  these  laryngeal  ulcers,  ulceration  of 
the  mucous  membrane  of  the  mouth  and  pharynx  may  occur;  at  times  it 
involves  the  epiglottis  in  such  a  manner  as  to  clip  off  its  edges.  These 
ulcers  may  develop  on  the  mucous  membrane  of  the  Eustachian  tubes.  In 
those  cases  where  permanent  deafness  follows  an  attack  of  typhoid  fever, 
it  will  usually  be  due  to  ulceration  of  the  mucous  membrane  of  the  Eus- 
tachian tube. 

Brain  and  Nervous  System. — As  yet  we  have  not  been  able  to  determine 
whether  there  are  any  structural  changes  in  the  brain  or  nervous  system 
so  constant  that  they  may  be  regarded  as  lesions  of  typhoid  fever,  although 
it  is  reasonable  to  infer  that  in  a  disease  where  such  severe  functional  dis- 
turbances of  the  cerebro-spinal  system  exist  there  must  be  constant  and 
definite  parenchymatous  changes.  (Edema  of  the  pia  mater  and  of  the 
brain  substance,  with  occasionally  quite  extensive  adhesions  of  the  dura 


614  ACUTE   GEISTEKAL  DISEASES. 

mater  to  the  cranium,  not  infrequently  exists.  Punctate  extravasations 
into  the  brain  substance  are  found  in  a  certain  number  of  cases,  but  even 
in  severe  cases  they  are  not  always  present. 

Stomach. — The  changes  which  occur  in  the  stomach  are  equally  impor- 
tant with  those  which  occur  in  the  other  internal  organs,  and  are  degenera- 
tive in  their  nature.  Softening  and  degeneration  of  its  glandular  struc- 
ture are  sometimes  so  extensive  that,  if  recovery  from  the  fever  takes  place, 
a  very  long  time  must  elapse  before  the  organ  can  perform  its  normal  func- 
tion. It  is  the  existence  of  these  degenerative  changes  that  gives  rise  to 
the  disturbance  in  digestion  which  is  present  in  so  many  cases,  not  onlj 
during  the  continuance  of  the  fever,  but  during  convalescence. 

Muscles. — Muscular  degeneration  is  of  two  varieties  -.—first,  a  granulai 
degeneration,  which  corresponds  to  ordinary  fatty  degeneration.  Secondly, 
a  waxy  or  vitreous  degeneration,  which  consists  in  the  conversion  of  the 
contractile  substance  of  the  primitive  bundles  into  a  homogeneous,  waxy 
shining  mass.  Often  both  forms  of  degeneration  occur  together,  one  or  the 
other  predominating.  In  both  forms  of  degeneration  the  muscular  fibres 
become  thicker  and  more  brittle  than  normal.  In  the  highest  degree  of  de- 
generation the  muscular  fibres  are  entirely  lost,  and  the  muscle  may  present 
a  yellowish  or  whitish  appearance,  so  that  hardly  any  traces  of  its  normal 
color  remain.  This  muscular  degeneration,  however,  is  not  peculiar  to 
typhoid  fever,  but  is  met  with  in  all  severe  infectious  diseases.  The  want 
of  muscular  power,  which  is  so  prominent  a  symptom  during  the  height 
of  the  fever,  may  depend  on  the  disturbances  of  the  nervous  system,  but 
the  excessive  loss  of  muscular  power  which  is  so  often  present  during  con- 
valescence is  due  almost  entirely  to  the  muscular  changes.  The  physical 
strength  returns  gradually  during  convalescence  as  the  muscles  are  re- 
generated, and  it  may  be  months  before  it  is  fully  re-established.  The 
muscles  of  the  tongue  undergo  degeneration  in  the  same  way  as  the  other 
voluntary  muscles,  which  accounts  in  some  degree  for  the  interference 
with  the  function  of  that  organ,  so  often  a  prominent  phenomenon  of  the 
disease. 

The  salivary  glands  enlarge,  become  firm  and  tense,  and  assume  a  more 
or  less  brown-yellow  color.  They  have  the  consistence  of  cartilage.  Late 
in  the  disease  the  hardness  diminishes,  and  they  assume  a  red  color.  These 
changes  are  due  to  a  parenchymatous  degeneration,  which  has  been  pre- 
ceded by  a  cellular  hyperplasia.  It  accounts  to  a  certain  extent  for  the 
diminution  of  the  salivary  secretion,  which  is  so  marked  and  constant  an 
attendant  of  the  fever.  Similar  cellular  and  parenchymatous  changes  take 
place  in  the  pancreas.  Changes  similar  to  these  occur  in  other  febrile 
diseases,  so  that  they  cannot  be  regarded  as  characteristic  of  typhoid 
fever. 

Intestines. — The  essential  and  characteristic  lesions  of  typhoid  fever  are 
found  in  the  lymph  structures  of  the  intestines.  They  vary  only  in  degree 
and  not  in  character  with  the  duration  of  the  fever  and  their  proximity  to 
the  ileo-csecal  valve.  Although  changes  closely  resembling  them  may  be 
present  in  other  diseases,  there  is  no  other  disease  in  which  they  follow  a 


TYPnOID    FEVEE. 


615 


regular  course  of  development,  with  stages  limited  by  days  and  weeks. 
These  changes  in  typlioid  fever  correspond  very  closely  in  their  different 
stages  with  the  four  weeks  of  the  disease.  During  the  first  week  they  are 
confined  to  a  catarrhal  inflammation  of  the  intestinal  mucous  membrane, 
most  marked  about  the  Peyerian  jiatches,  with  a  medullary  infiltration  of 
these  and  the  solitary  glands,  which  extends  in  some  cases  into  the  adja- 
cent tissues.  Tlie  infiltrated  cells  are  mostly  lymphoid  cells,  though  large, 
round  and  polygonal  cells  with  multiple  nuclei  are  also  present.  These  lat- 
ter are  swollen  epithelial  cells  from  the  reticulated  tissue  of  the  mucous 
membrane  and  lymph  follicles.  As  a  result  of  these  processes,  there  is 
hyperasmia  and  swelling  of  the  mucous  membrane,  and  the  affected  glands 
become  enlarged  and  elevated  from  one  to  two  lines  above  the  mucous  sur- 
face. They  assume  a  dark  red  or  reddish-gray  color  marked  with  fine  white 
striations,  and  present  the  so-called 
"shaven  beard"  aj^pearance.  Their 
consistence  varies  with  the  severity  of 
the  process.  When  moderately  swollen, 
they  are  soft  and  present  a  spongy  ap- 
pearance, but  in  the  severer  types  the 
entire  gland  becomes  hard  and  smooth. 
These  changes  begin  and  are  most  ex- 
tensive in  the  glands  nearest  the  ileo- 
csecal  valve ;  they  are  generally  well 
marked  within  forty-eight  hours  after 
the  commencement  of  the  disease,  but 
are  not  fully  developed  until  the  end  of 
the  first  week,  when  all  the  glands  are 
involved  which  are  likely  to  undergo 
change.  The  number  of  patches  in- 
volved varies  from  four  to  five  near  the 
valve  to  twenty  or  thirty  throughout 
the  whole  intestine.  The  solitary  fol- 
licles do  not  participate  in  the  infiltra-  mucou 
tion  and  swelling  to  the  same  extent  as 

fbp  Ho-Tm'nfltpfl  o-lfliidc?  ^-  ^^yf  patch    showing   the  reticulated  or 

Liit!  aguiiiifiueu  gxaiiub.  shaven-beard  appearance. 

Tn    +1t<3     QPrnnrI    oiwol-    tlia    lTTrnor5»miQ     The  mitcovs  membrane  is  hyper cemie,  and  the 
in    xne    secona    WeeiC    ine     nyperaemia        solitary  folUcles,  B,  are  only  slightly  involved. 

and  catarrh  of  the  mucous  membrane 

subside,  leaving  the  agminated  and  solitary  glands  more  elevated  ;  the 
white  lines  upon  their  surface  disappear,  and  they  assume  a  uniformly  red 
color.  An  unusually  rapid  cellular  hyperplasia  takes  place  in  the  follicles, 
by  which  they  beco"me  swollen  in  all  directions.  Usually  the  new  cell 
growth  extends  beyond  the  limit  of  the  follicles,  so  that  the  adjoining 
mucous  membrane  is  also  infiltrated  with  cells.  The  new  cells  distend  the 
glands,  and  a  vertical  section  of  a  patch  in  this  stage  shows  the  villi  in- 
creased in  length  and  width,  and  fused  together  at  their  bases  or  through- 
out their,  entire  length  by  the  embryonic  tissue.  These  newly  formed 
cells  may  wander  through  the  muscular  coat  or  penetrate  the  sub-serous 


Fig.  147. 

surface    of    a   portion  of   the  Ileum 
during  the  first  week  of  Typhoid  Fever. 


616 


ACUTE    GENERAL   DISEASES. 


tissue. 


Thus  hyperplasia  of  the  adenoid  tissue  is  the  essential  patho- 
logical change  in  the  second  week. 
By  the  middle  or  latter  part  of  the 
second  week  the  process  passes  into 
its  third  stage,  and  necrotic  changes 
are  established  in  the  newly  formed 
tissue. 

These  morbid  changes  may  ter- 
minate in  three  ways  :  first,  the  new 
elements  in  these  ductless  glands  may 
become  disintegrated  and  undergo 
absorption,  and  in  this  way  they  may 
gradually  undergo  resolution ;  second, 
either  the  tissue  between  the  follicles 
remains  infiltrated  and  elevated  while 
their  contents  are  absorbed,  or  indi- 
vidual follicles  of  the  agminated 
glands  rupture  and  discharge  their 
Mucous  surface  ofthe  Ileum  during  the  second  week  Contents  into  the  intestine,  leaving 
.   ^     ,         of  Typhoid  Fever.  dcprcssious   which  givc  the  gland  a 

A.  Peyer  s  patch  thickened  and  raised— from  hype.r-         '^  ^ 

jyiasio,.  reticulated   appearance ;     third,   the 

B.  Solitary  follicles  much  enlarged.  ,    „  ,  t      i  •    ,  ■      , 

most  irequent  and  cliaracteristic  ter- 
mination of  the  typhoid  process  is  the  separation  of  the  dead  tissue  as  a 
«longh,  or  by  ulceration  and  the 

formation  of  the  typhoid   ulcer.  ,^    .  ,^___  ,^:b 

Ulceration  which  begins  at  the 
most  elevated  portion  of  a  patch, 
already  stained  yellow  or  yellow- 
ish green  by  intestinal  fluids  or 
darker  by  sanguineous  infiltration 
advances  gradually  until  a  small 
irregular  ulcer  has  enlarged  to 
one  covering  the  whole  gland,  or 
the  entire  gland  may  slough  uni- 
formly, and  at  once  form  the  com- 
plete ulcer. 

Usually  the  sloughing  and  re- 
moval of  the  necrotic  tissue  does 
not  take  place  until  the  third 
■week  of  the  disease.  As  the 
sloughs  gradually  loosen  and  fall 
ofi:,  there  is  a  loss  of  substance 
which  extends  to  the  deeper 
layer  of  the  mucous  membrane, 
removing  the  entire  gland  and 
the  mucous  tissue  surrounding  it, 
laying  bare  the  muscular  coat  of 


ABm 


Fig.  149 

Mucous  surf  ace  of  a  portion  of  the  Ileum  in  the  third  week 

of  Typhoid  Fever. 

A.  Peyer's  patch,  ulcerated,  showing   the  overhangirig 

edges  and  the  roughened  base. 

B.  Solitanj follicles  ulcerated  at  their  apices. 

C.  A  small  oval  ulcer. 

D.  Pe7f oration  of  the  intestine. 


TYPHOID   FEVER. 


617 


the  intestine.  The  necrotic  process  may  extend  and  involve  the  muscular 
tissue,  and  end  in  perforation  of  the  peritoneal  covering.  These  ulcers 
may  be  developed  in  the  jejunum,  the  ileum,  the  stomach,  and  the  large 
intestine.  In  the  lower  part  of  the  ileum,  at  the  ileo-csecal  valve,  they  are 
usually  of  large  size— so  large  that  only  small  portions  of  healthy  mucous 
membrane  are  left  between  them  ;  in  the  jejunum,  stomach,  and  large 
intestine  they  are  usually  round  and  of  small  size.  The  form  of  the 
ulceration  corresponds  to  that  of  the  necrotic  tissue ;  if  an  entire 
Peyerian  patch  is  necrotic,  an  elliptical  ulcer  is  formed,  with  its  long  axis 
corresponding  to  that  of  the  intestine.  In  the  jejunum  and  large  intes- 
tine, the  ulcers  are  usually  small  and  round.  The  edges  of  the  ulcer  are 
sharp,  tumid,  and  overhang  the  floor  of  the  ulcer.  Sometimes  the  ulcers 
are  hemorrhagic. 

In  the  fourth  week  the  process  of  cicatrization  is  commenced.  Gradually 
the  swollen  edges  of  the  ulcers  subside,  granulation-tissue  springs  up  from 
their  base,  connective-tissue  membrane  is  formed,  and  the  edges  of  the  ul- 
cer become  united  by  a  cicatrix  which  is  covered  with  a  layer  of  e]3ithelium. 
The  gland  structure  is  never  regenerated.  The  cicatrix  which  is  formed 
by  the  healing  of  these  ulcers  is  slightly  depressed,  and  less  vascular  than 
the  surrounding  mucous  membrane.  During  the  healing  process  the  cica- 
trix becomes  more  or  less  pigmented,  and  these  pigmented  scars  may  be 
recognized  years  after  cicatrization  has  taken  place.  They  seldom  cause  any 
puckering  or  diminu- 
tion in  the  calibre  of  the 
intestine.  In  many  cases 
the  process  does  not 
pursue  this  regular 
course  ;  while  one  por- 
tion of  the  ulcer  is 
cicatrizing,  ulceration 
in  another  part  may 
be  extending ;  such 
long-continued  ulcera- 
tion prolongs  convales- 
cence, and  may  even 
cause  death  from  ex- 
haustion. 

Mesenteric  Glands. — 
Associated  with  these 
intestinal  changes,  anal- 
ogous processes  take 
place  in  the  mesenteric 
glands.  These  mesen- 
teric changes  are  also 
most  marked  in  the 
glands  situated  nearest 
the  ileo-caecal  valve ;  they  are  secondary  to  the  changes  in  the  intestinal 


Fig.  150. 
Sketch  ehowiug  Enlargement  of  the  Mesenteric  Lymphatic  Glands 
in  Typhoid  Fever. 
A,  A.  Portion  of  Small  Intestine. 
B.  Mesentery. 
O.  Glands  enlarged.    At  Da  gland  is  shown  in  section. 


618  ACUTE   GElifEEAL   DISEASES." 

glands,  and  usually  in  a  degree  corresponding  to  the  extent  of  the  intestinal 
lesions.  The  glands  are  first  congested,  then  there  is  a  production  of  lym- 
phoid and  large  cells  similar  to  those  which  are  found  in  the  enlarged 
intestinal  follicles  ;  the  glands  become  enlarged,  and  are  the  seat  of  an 
acute  cellular  hyperplasia.  When  the  enlargement  has  attained  its  full 
size,  the  hypergemia  diminishes,  and  the  cellular  elements  begin  to  disin- 
tegrate and  are  absorbed.  In  about  one-half  the  cases  the  enlargement 
reaches  its  maximum  size  by  the  middle  of  the  second  or  at  the  commence- 
ment of  the  third  week.  The  enlarged  glands  vary  in  size  from  that  of 
a  hazel-nut  to  a  small  hen's  egg.  In  the  stage  of  retrogression  some  of 
the  glands  simply  shrink  and  return  to  their  normal  condition;  in  others, 
partial  softening  takes  place  and  afterward  absorption,  leaying  a  fibrous 
cicatrix.  If  the  glands  reach  a  very  large  size,  absorption  is  incomplete, 
and  dry,  yellow,  cheesy  masses  are  left,  which  after  a  time  become  calca- 
reous and  enclosed  in  a  fibrous  capsule.  In  rare  instances  the  glands  be- 
come fluid,  their  capsules  are  destroyed,  and  the  softened  masses  escape  into 
the  peritoneal  cavity  and  cause  peritonitis.  A  calcareous  condition  of 
the  mesenteric  glands,  like  the  pigmented  cicatrices  of  the  solitary  and 
agminated  glands,  gives  evidence  of  a  previous  severe  attack  of  typhoid 
fever. 

Another  lesion  of  typhoid  fever  occurring  during  convalescence,  is  sup- 
purative inflammation  in  the  subcutaneous  cellular  tissue.  The  inflamma- 
tion is  not  of  an  active  type,  but  is  accompanied  by  some  redness  and  pain. 
Gradually  a  tumor  is  formed  at  the  seat  of  the  inflammation,  usually  where 
there  has  been  the  greatest  amount  of  pressure,  and  after  a  time  fluctuation 
becomes  distinct  as  the  swelling  increases  ;  sometimes  two  or  inore  of  these 
swellings  coalesce,  and  finally  an  immense  abscess  may  be  formed  contain- 
ing a  pint  or  more  of  pus.  Eetro-pharyngeal  ulcers  are  the  result  of  sup- 
purative inflammation  of  the  connective-tissue. 

Etiology. — According  to  the  classification  which  I  have  adopted,  typhoid 
fever  is  included  in  the  list  of  miasmatic-contagious  diseases.  Usually  it 
has  been  regarded  as  an  endemic  form  of  disease.  There  seems  to  be  no 
connection  between  its  development  and  destitution.  It  may  occur  as  an 
isolated  case,  or  whole  households  and  neighborhoods  may  be  stricken  down 
with  the  disease.  "We  must  therefore  regard  the  causes  of  its  production 
as  local  and  limited,  not  widespread.  It  is  possible  for  it  to  prevail  as  an 
epidemic,  but  it  must  first  have  been  endemic. 

In  studying  the  etiology  of  this  fever,  two  prominent  questions  present 
themselves  : — 

First :  is  it  a  contagious  form  of  disease  ? 

Second :  is  it  ever  of  spontaneous  origin  ? 

After  years  of  careful  investigation,  I  think  it  may  be  now  unhesitatingly 
stated  that  facts  do  not  sustain  the  opinion  that  typhoid  fever  is  ever, 
strictly  speaking,  a  contagious  disease.  Persons  sick  with  this  fever  are 
now  admitted  into  our  general  hospitals,  and  are  placed  by  the  side  of 
patients  with  pneumonia  or  any  form  of  chronic  disease,  without  endanger- 
ing the  lives  of  such  patients.     This  fact  shows  how  generally  the  pro- 


TYPHOID   FEVER.  619 

fession  regard  this  disease  as  non-contagious.     Typhoid  fever  is  no  longer 
restricted  by  quarantine  regulations. 

The  question  of  spontaneous  origin  has  strong  advocates  on  both  sides. 
Some  of  those  who  believe  that  it  may  have  a  spontaneous  origin  maintain 
that  the  poison  which  gives  rise  to  it  is  developed  by  the  decomposition  of 
organic  matter,  and  that  the  specific  character  of  the  fever  is  due  to  the 
particular  substances  which  are  undergoing  decomposition.  Others  main- 
tain that  decomposing  human  excrement  is  necessary  for  the  production 
of  the  peculiar  poison  which  gives  rise  to  typhoid  fever.  Again,  others 
believe  that  the  presence  of  vegetable  matter  in  certain  conditions  is  neces- 
sary for  its  production,  and  that  these  conditions  are  similar  to  those  which 
exist  when  miasmatic  fevers  are  developed,  the  difference  in  the  two  poisons 
depending  rabher  upon  the  temperature  than  upon  the  character  of  the  in- 
gredients. 

There  is  a  view,  recently  advanced,  that  sewer  gases  contain  the  poison 
which  has  the  power  of  developing  the  disease.  On  the  other  hand,  it  is 
maintained  by  those  who  do  not  believe  in  the  spontaneous  origin  of  this 
fever  that,  in  addition  to  decomposing  animal  and  vegetable  matter,  it  is 
necessary  that  the  specific  typhoid  poison  be  incorporated  in  the  decom- 
posing mass.  Observations  prove  clearly  that  vegetable  or  animal  decom- 
position alone  is  not  sufficient  for  the  development  of  this  disease,  and  facts 
do  not  sustain  the  claim  of  those  who  say  that  sewer  gases  contain  the 
typhoid  poison,  for  those  cities  in  which  the  sewerage  is  most  imperfect, 
and  those  houses  most  frequently  permeated  Avith  sewer  gases,  are  not  the 
hotbeds  of  typhoid  fever.  Moreover,  this  fever  is  more  prevalent  in  the 
country  than  in  the  city,  in  places  where  there  are  no  sewer  gases  ;  indeed, 
well-marked  cases  of  typhoid  fever  are  of  quite  rare  occurrence  in  the  city, 
and  when  they  do  occur  seem  to  be  develoj)ed  independently  of  defective 
sewerage.  In  other  words,  all  the  elements  which  favor  its  production 
may  be  present,  such  as  animal  and  vegetable  decomposition  or  sewer  gases, 
and  yet  not  a  single  case  of  typhoid  fever  be  developed,  until  the  typhoid 
poison  is  brought  Avithin  the  boundaries  favorable  to  its  development ;  then 
a  severe  epidemic  of  the  disease  may  be  developed,  but  decomposition  is 
simply  the  soil  in  which  the  specific  poison  is  developed. 

The  question  now  arises  : — what  is  the  real  nature  of  that  poison  derived 
from  a  person  sick  with  typhoid  fever,  which  has  the  power  of  indefinitely 
reproducing  itself  outside  of  the  body  in  connection  with  decomposing  or- 
ganic matter  and  thus  becoming  the  infecting  agent  when  individuals  are 
brought  within  its  influence  ?  The  history  of  epidemics  of  typhoid  fever 
leads  to  the  conclusion  that  the  poison  is  contained  in  \\\q  f cecal  discharges 
of  the  sick.  When  such  excrement  is  in  fresh  condition  the  poison  is  not 
active ;  it  must  go  through  a  stage  of  development  outside  of  the  body. 
This  may  take  place  in  the  excrement  itself,  but  it  goes  on  more  rapidly 
and  abundantly  if  the  excrement  is  collected  in  privies  or  in  earth  that  is 
already  saturated  with  organic  matter.  In  this  way  we  can  readily  explain 
how  a  typhoid  fever  patient  coming  into  a  locality  previously  free  from  the 
disease  can  establish  there  a  focus  of  infection,  from  which  many  persons 


630  ACUTE    GEXBRAL   DISEASES. 

may  become  diseased.  It  is  evident  that  this  poison  is  not  active  in  its 
fresh  state,  from  the  fact  that  the  disease  is  not  carried  directly  from  one 
individual  to  another  ; — attendants,  nurses,  and  physicians  are  no  more 
liable  to  the  disease  than  those  who  are  in  no  way  exposed  to  the  disease 
and  live  in  a  healthy  locality. 

It  is  difficult  to  determine  the  period  of  incubation,  or  length  of  time 
the  poison  must  remain  in  the  body  before  symptoms  of  the  disease  are 
manifest.  The  histories  of  isolated  cases  would  lead  to  the  conclusion  that 
the  period  varies  from  fourteen  to  twenty  days.  Undoubtedly  there  are 
two  principal  channels  of  infection,  namely,  the  air  we  breathe  and  the 
water  we  drink.  This  fever  may  be  developed  by  gases  which  emanate 
from  privies,  sewers,  etc.,  which  have  been  the  receptacle  of  excrement 
from  typhoid  patients,  and  also,  by  drinking  water  from  springs  and  wells 
which  have  become  contaminated  by  matters  from  adjoining  privies  and 
cess-pools.  It  is  an  established  fact  that  water  remains  contaminated, 
though  far  remote  from  the  point  where  it  came  in  contact  with  a  defective 
sewer  or  water-closet.  Soil  pipes  and  sewerage  may  be  defective  for  a 
long  time  and  no  case  of  typhoid  fever  occur,  when  suddenly  an  endemic 
of  typhoid  fever  breaks  out,  and  careful  investigation  shows  that  its  de- 
velopment was  preceded  by  the  introduction  of  the  excrement  of  a  single 
individual  sick  with  the  disease.  It  is  the  belief  of  some  that  milk  may 
convey  the  typhoid  poison,  and  there  is  evidence  in  favor  of  this  opinion  ; 
but  there  is  stronger  evidence  that  the  water  used  to  dilute  the  milk,  and 
not  the  milk  itself,  is  the  medium  through  which  the  poison  is  transmitted. 

This  poison  has  great  vitality.  Typhoid  fever  frequently  occurs  in  the 
same  locality  year  after  year,  when  the  surrounding  conditions  are  favor- 
able to  its  development.  Those  conditions  are  more  frequently  present  in 
the  autumn  than  in  any  other  season  of  the  year,  and  for  this  reason  it 
has  been  called  autumnal  fever.  Usually  it  makes  its  appearance  in  a 
locality,  each  year,  at  about  the  same  time  ;  case  after  case  is  developed 
until  entire  households  and  neighborhoods  become  its  victims.  Individu- 
als who  come  to  care  for  the  sick  may  contract  the  disease,  and  even  per- 
sons who  visit  houses  in  which  the  disease  is  prevailing  may  afterward  de- 
velop the  fever,  contracting  it,  not  from  the  sick,  but  from  the  infected 
atmosphere  of  the  locality. 

Age  must  be  regarded  as  a  predisposing  cause  of  typhoid  fever.  It  is 
much  more  likely  to  occur  in  young  than  in  old  persons  ;  it  occurs  most  fre- 
quently between  the  ages  of  fifteen  and  twenty-five,  and  is  rarely  met  with 
in  persons  over  fifty.  There  are  also  individual  idiosyncrasies  which  seem 
to  predispose  to  this  fever.  Some  contract  it  upon  the  slightest  exposure 
to  the  influence  of  the  poison,  while  others,  frequently  brought  in  contact 
with  it  for  a  long  time,  escape.  Again,  an  individual  may  have  repeated 
attacks  of  typhoid  fever. 

Symptoms. — I  shall  first  consider  the  prominent  symptoms  of  a  typical 
case,  and  discuss  in  detail  these  symptoms,  without  special  regard  to  the 
time  of  their  occurrence. 

This  fever  is  usually  insidious  in  its  approach,  and  comes  on  with  a  cer- 


TYPHOID   FEVER.  621 

tain  degree  of  uneasiness  throughout  the  system  ;  the  patient  feels  uncom- 
fortable, has  no  pain,  but  feels  thab  he  is  about  to  be  sick.  He  complains 
of  a  grumbling  headache,  more  or  less  aching  of  the  limbs,  "  a  tired  feeling 
all  over,"  chilly  sensations,  alternating  with  flashes  of  heat  and  loss  of 
appetite  ; — not  infrequently  nausea  and  vomiting  are  present.  The  pre- 
monitory symptoms  gradually  increasing  in  severity,  by  the  fifth  or  sixth 
day  the  patient  is  compelled  to  i;ake  to  his  bed.  At  this  early  period  there 
may  be  a  slight  diarrhoea.  In  very  mild  cases  the  disease  comes  on  so  in- 
sidiously, and  with  symptoms  so  mild,  that  the  patient  is  often  able  to 
pursue  his  ordinary  avocations,  complaining  only  of  an  undefined  indispo- 
sition. In  very  many  severe  cases  it  is  impossible  for  the  patient  to  accu- 
rately fix  upon  tlie  time  when  the  fever  commenced  ;  and  in  no  case  will 
an  early  positive  diagnosis  be  possible.  'Typhoid fever  may  be  suspected, 
but  that  is  as  far  as  one  can  safely  go. 

In  all  cases  variation  in  temperature  is  one  of  the  most  important  early 
symptoms.  Such  variations  in  temperature  in  a  typical  case  may  be  divided 
into  four  periods,  of  one  week  each,  which  correspond  to  the  four  weeks  of 
the  disease.  In  the  first  week  there  is  a  gradual  and  steady  rise  in  tem- 
perature, with  regular  morning  and  evening  variations,  each  evening  tem- 
perature being  about  2°  F.  higher  than  that  of  the  morning,  and  1^  F. 
higher  than  the  previous  night,  so  that  at  the  end  of  the  first  week  it 
is  at  its  maximum, — 104°  or  105°  F.  This  is  one  of  the  most  character- 
istic features  of  the  disease.  This  gradual  rise  of,  and  these  variations  in, 
temperature  are  not  present  in  every  case,  but  when  they  are  present 
they  will  greatly  assist  in  making  an  early  diagnosis.  It  has  been  said  that 
tj^phoid  fever  is  the  only  disease,  except  double  quotidian  intermittent 
fever,  that  gives  two  full  thermometrical  curves  within  twenty-four  hours; 
that  is,  two  remissions  and  two  exacerbations.  If  this  is  true,  it  helps  to 
explain  certain  high  temperatures  in  the  morning,  and  afPords  valuable 
assistance  in  making  a  diagnosis. 

During  the  second  week  the  variations  in  temperature  are  slight,  retain- 
ing, however,  the  same  maximum  as  was  reached  at  the  end  of  the  first 
week.  The  variations  during  the  third  week  are  remittent  in  character. 
During  the  fourth  week  they  become  intermittent,  and  the  range  of  tem- 
perature in  the  exacerbations  is  lower.  The  variations  in  pulse  correspond 
to  those  in  temperature.  During  the  first  week  the  pulse  gradually  be- 
comes more  and  more  frequent,  and  remains  at  the  height  reached  at  the 
end  of  the  first  week ;  throughout  the  second  and  third  weeks  there  are 
distinct  morning  and  evening  remissions  ;  during  the  fourth  week  it  falls 
to  its  normal  standard.  Diarrhoea  generally  comes  on  during  the  first 
week  or  is  continued  from  the  prodromal  stage.  In  some  cases  it  may  have 
ceased  by  the  second  week. 

On  the  seventh  day,  or  between  it  and  the  twelfth  day,  the  characteristic 
eruption  appears.  About  this  time  the  headache  abates  and  more  or  less 
somnolence  and  delirium  come  on.  The  delirium  at  first  is  slight,  and  is 
only  observed  during  the  night.  Day  by  day  the  patient  loses  flesh  and 
strength,  and  becomes  more  and  more  unconscious,  and  all  the  phenomena 


622  ACTJTE   GENEEAL  DISEASES. 

of  the  typhoid  state  are  developed,  viz.  :  a  dry  brown  tongue,  feeble  pulse, 
low  muttei-ing  delirium,  stupor,  tremors,  subsultus,  involuntary  evacua- 
tions, and  the  other  phenomena  of  great  prostration.  If  the  disease  is  to 
terminate  favorably,  the  amendment  is  usually  gradual.  The  first  sign  of 
improvement  is  a  decided  remission  of  the  fever. 

Such,  in  brief,  are  the  phenomena  which  attend  the  ushering-in  and  de- 
velopment of  an  ordinary  case  of  typhoid  fever  ;  they  are,  however,  sub- 
ject to  numerous  modifications.  Some  cases  are  mild  throughout  their 
entire  course ;  some  are  severe  at  first  and  mild  afterward  ;  some  are  mild 
at  first  and  severe  afterward  ;  while  others  are  severe  throughout  their  en- 
tire course. 

The  Physiognomy. — As  a  rule,  the  countenance  has  nothing  peculiar  in 
its  appearance ;  but  if  the  disease  is  of  a  severe  type,  by  the  second  week 
the  countenance  assumes  a  characteristic  appearance — there  is  a  pale,  olive, 
leaden  look,  the  eye  becomes  dull  and  the  conjunctiva  congested,  and  usu- 
ally there  is  a  small,  rose-colored  spot  in  the  centre  of  each  cheek.  The 
face  does  not  assume  the  dark  mahogany  color  seen  in  typhus,  but  in  the 
advanced  stage  of  the  fever  it  has  more  of  the  hectic  flush  of  phthisis. 

Tongue. — From  the  very  outset,  the  tongue  is  covered  with  a  light,  white 
coat,  but  there  is  nothing  special  in  its  appearance  before  the  end  of  the 
first  week  ;  then  it  may  become  red  upon  its  sides  and  tip,  and  show  a 
slight  disposition  to  dryness  in  its  centre.  As  the  disease  passes  into  its 
second  and  third  weeks,  the  tongue  becomes  more  heavily  coated,  the 
coating  becomes  brown  and  dry,  and  sordes  collect  upon  the  teeth  and 
sides  of  the  mouth  in  sufficient  quantities  to  form  crusts.  These  crusts 
may  become  thicker  and  more  abundant  as  the  disease  progresses.  At  any 
period  in  the  course  of  the  disease  the  tongue  may  suddenly  clear  off,  and 
present  a  shiny  red,  "  beef-colored  "  appearance.  The  tongue  and  lips  may 
become  dry,  cracked  and  fissured.  As  the  sordes  are  removed  from  the 
lips,  they  will  often  bleed  ;  and  in  certain  cases,  more  especially  in  the 
severer  forms  of  the  disease,  the  entire  mouth  and  tongue  may  be  covered 
with  dark-colored  incrustations.  Such  incrustations  are  seen  early  in  con- 
nection with  those  cases  where  there  are  extensive  blood  changes ;  when 
present  they  are  of  grave  significance.  One  of  the  first  indications  of  con- 
valescence is  a  moist  condition  of  the  tongue  about  its  edges ;  gradually 
its  entire  surface  becomes  moist,  and  by  the  time  convalescence  is  fully 
established  it  is  restored  to  its  natural  condition. 

Gastric  symptoms  are  always  more  or  less  prominent ;  loss  of  appetite  is 
one  of  the  earliest  symptoms,  and  nausea  and  vomiting  are  quite  common 
during  the  first  week  of  the  fever.  The  vomited  matters  usually  consist  of 
a  greenish  fluid.  When  vomiting  comes  on  late  in  the  fever,  it  is  either 
due  to  sub-acute  gastric  catarrh,  or  is  symptomatic  of  local  or  general  peri- 
tonitis. In  a  large  proportion  of  cases  thirst  is  excessive.  The  lips  are 
parched,  and  in  severe  cases  crack  and  bleed.  In  some  cases  hemorrhage 
from  the  gums  occurs. 

Diarrhoea. — Although  not  invariably  present,  diarrhoea  is  so  frequent  an 
attendant  of  this  fever  that  it  is  considered  one  of  its  characteristic  symp- 


TYPHOID   FEVEK.  623 

toms.  It  varies  with  the  severity  of  the  attack,  the  date  of  its  commence- 
ment, and  its  duration.  The  characteristic  typhoid  discharges  are  of  a 
yellowish -green  color,  described  as  -'pea-soup  discliarges."  Sometimes 
they  are  of  a  dark  color,  resembling  coffee-grounds  ;  their  react;on  is  alka- 
line. In  some  cases  diarrhcea  is  present  at  the  very  outset  of  the  disease, 
and  continues  throughout  the  entire  course.  In  others,  it  does  not  appear 
until  the  third  week.  The  second  week  is  the  ordinary  time  for  its  ap- 
pearance. When  the  diarrhoea  appears  late  in  the  course  of  the  disease, 
the  discharges  are  more  copious  than  when  it  appears  early.  A  mild 
diarrhoea  throughout  the  entire  course  of  the  fever  is  a  favorable  rather  than 
an  unfavorable  symj)tom.     In  mild  cases  diarrhoea  is  sometimes  absent. 

Intestinal  Hemorrhage. — This  occurs  in  about  one  in  twenty  cases,  and 
varies  in  quantity  from  a  mere  trace  of  blood  in  the  stools  to  a  profuse  dis- 
charge of  from  sixteen  to  eighteen  ounces.  The  slight  hemorrhages  which 
occur  early  in  the  disease  simply  indicate  a  hemorrhagic  tendency,  the  same 
as  the  epistaxis,  which  is  very  frequently  among  the  early  symj^toms.  In 
both  instances  the  bleeding  comes  from  the  capillaries  of  the  mucous  mem- 
brane. The  more  profuse  hemorrhages  are  due  to  the  opening  of  an  artery 
in  some  intestinal  ulcer.  Hemorrhages  due  to  this  cause  may  be  sudden 
and  profuse,  and  may  destroy  the  life  of  the  patient.  The  usual  time  for 
the  occurrence  of  these  profuse  intestinal  hemorrhages  is  the  latter  part  of 
the  second  and  during  the  third  week.  These  hemorrhages  are  usually 
accompanied  by  a  sudden  fall  in  temperature,  perhaps  two  or  three  degrees  ; 
if  then  in  a  patient  severely  ill  of  typhoid  fever  a  sudden  fall  in  temjDcra- 
ture  occurs  daring  the  second  or  third  week,  accomjDanied  by  extreme 
prostration,  it  is  very  conclusive  evidence  that  intestinal  hemorrhage  has 
occurred,  although  externally  the  hemorrhage  may  not  have  made  its 
appearance.  The  blood  is  usually  fluid,  rarely  clotted  ;  generally  it  is  of  a 
bright  red  color^  owing  to  the  alkaline  condition  of  the  intestinal  contents. 
Copious  intestinal  hemorrhages  are  more  frequent  in  severe  cases  that  have 
been  attended  by  profuse  diarrhoea.  Patients  may  die  of  intestinal  hem- 
orrhage before  any  blood  has  been  voided  externally.  If  the  joatient  sur- 
vive a  profuse  intestinal  hemorrhage,  there  is  great  danger  of  his  dying 
from  peritonitis.  He  may  die  unexpectedly  by  syncope  a  number  of  hours 
after  a  profuse  intestinal  hemorrhage. 

Abdominal  fain  and  tenderness  are  not  usually  present  at  the  very  outset 
of  typhoid  fever,  but  generally,  and  almost  without  exception  in  the 
severer  cases,  by  the  sixth  day  of  the  disease  some  pain  and  tenderness  will 
be  present  in  the  right  iliac  fossa.  The  pain  and  tenderness  usually  in- 
crease as  the  disease  progresses,  and  in  the  advanced  stages  it  is  sometimes 
so  marked  that  slight  pressure  over  this  region  is  unbearable.  While  ex- 
amining this  region  in  order  to  determine  the  presence  or  absence  of  pain 
and  tenderness,  the  pressure  should  be  made  with  the  palm  of  the  hand  ; 
the  expression  of  the  countenance  will  indicate  the  presence  of  ten- 
derness, long  before  an  audible  complaint  is  made  by  the  patient.  It  is 
important  to  bear  in  mind  the  possible  occurrence  of  a  more  severe  ab- 
dominal pain  arising  from  intestinal  perforation.     The  following  are  the 


624  ACUTE  GENERAL  DISEASES. 

characteristic  symptoms  of  this  lesion  :  if  in  the  course  of  a  slight  op 
severe  form  of  this  fever,  or  even  when  the  disease  has  been  latent  and  the 
diagnosis  of  typhoid  fever  has  not  been  clear,  the  patient  should  be  suddenly 
seized  with  diarrhoea,  pain  in  the  abdomen,  aggravated  by  pressure,  per- 
haps at  first  localized  in  the  right  iliac  fossa,  but  soon  extending  over  the 
entire  abdominal  cavity,  attended  by  rapid  tympanitic  distention  of  the 
abdomen,  and  symptoms  of  great  prostration,  a  rapid,  feeble  pulse,  a  sunken, 
anxious  expression  of  countenance,  nausea  and  vomiting,  quickly  followed 
by  coldness  and  blueness  of  the  extremities,  and  the  other  signs  of  sudden 
collapse,  it  is  almost  certain  that  perforation  of  the  intestine  has  occurred. 
I  have  known  this  accident  to  occur  when  convalescence  was  apparently 
progressing  satisfactorily. 

Tympanitis  is  another  very  common  symptom  of  typhoid  fever. 
Usually  it  is  not  present  during  the  first  week,  but  by  the  end  of  the  first 
or  the  commencement  of  the  second  week  a  fulness  of  the  abdomen  will 
be  noticed.  As  the  fever  advances,  the  distention  often  becomes  extreme; 
this  is  due  to  a  collection  of  gas  in  the  large  intestine,  developed 
through  some  change  in  the  mucous  membrane,  the  exact  nature  of 
which  we  do  not  fully  understand.  When  once  it  is  developed  it  remains 
until  convalescence  is  fully  established,  and  is  always  an  important  diag- 
nostic sign  of  this  fever. 

In  connection  with  the  development  of  the  tympanitis,  when  firm  press- 
ure is  made  over  the  right  iliac  fossa,  a  gurgling  sound  is  produced  ;  but 
gurgling  in  the  right  iliac  fossa  cannot  by  any  means  be  regarded  as  a 
positive  symptom  of  typhoid  fever,  as  it  may  occur  in  any  disease  where 
there  is  distention  of  the  abdomen  due  to  accumulation  of  gas  in  the  intes- 
tines. In  typhoid  fever,  so  long  as  the  abdomen  remains  tympanitic,  no 
matter  what  the  temperature  and  pulse  of  the  patient  may  be,  he  is  in 
more  or  less  danger,  for  it  shows  that  there  are  intestinal  changes  still  in 
progress,  and  the  reparative  processes  are  not  complete  ;  this  is  more  espe- 
cially the  case  when  the  tympanitis  has  continued  from  the  active  period 
of  the  disease  into  the  period  of  convalescence. 

JJrine. — Extended  and  very  careful  analyses  of  the  urine  of  typhoid 
fever  patients  have  been  frequently  made,  without  giving  any  very  practi- 
cal results.  Usually  during  the  first  two  weeks  of  the  fever  the  urine 
is  diminished  in  quantity,  and  its  color  is  dark  and  its  specific  gravity  high; 
after  the  second  week  it  is  increased,  and  when  convalescence  is  estab- 
lished, it  becomes  pale,  and  its  specific  gravity  is  lowered.  The  amount  of 
urine  excreted  daily  throughout  the  active  period  of  the  fever  is  increased. 
The  increase  is  in  proportion  to  the  intensity  of  the  fever,  subject  in  some 
degree  to  the  quantity  and  quality  of  the  food  taken.  It  will  be  greater 
when  large  quantities  of  strong  beef-tea  are  taken  than  when  the  diet 
consists  of  milk.  So  long  as  the  kidneys  are  able  to  eliminate  the  excess 
of  urea,  no  harm  results  ;  but  if  the  quantity  exceeds  their  power  of  elimi- 
nation, or  if  their  function  is  interfered  with,  uraemic  symptoms  will  be  de- 
veloped, such  as  delirium,  stupor  and  coma.  Albumen  in  the  urine  is 
only  of  occasional   occurrence  in   the   course   of   typhoid  fever.     When 


TYPHOID    FEVEE.  G25 

present  the  quantity  is  usually  small,  and  is  only  temporary.  It  rarely 
appears  before  the  third  week.  Its  appearance  is  often  marked  by  the  oc- 
currence of  cerebral  symptoms.  Renal  epithelium  and  casts  may  or  may 
not  be  present  with  the  albumen. 

Nervous  Phenomena. — The  symptoms  referable  to  the  nervous  system 
are  not  so  prominent  in  typhoid  as  in  typhus  fever ;  yet  there  are  many 
cases  in  which  these  symptoms  form  an  important  part  of  the  history.  One 
of  the  most  constant  is  headache.  In  the  majority  of  cases  it  is  one  of  the 
ushering-in  symptoms  of  the  disease.  It  is  present  in  mild  as  well  as  in 
severe  cases  ;  sometimes  it  is  confined  to  the  forehead  and  temples  ;  more 
often  it  extends  over  the  whole  head ;  it  is  not  violent,  but  a  dull,  heavy  pain. 
It  usually  increases  in  severity  until  the  middle  period  of  the  disease,  cer- 
tainly until  the  close  of  the  first  week  ;  and  generally  associated  with  it 
there  is  intolerance  of  light  and  conjunctival  injection,  pain  in  the  back 
and  limbs,  and  a  general  aching  of  the  whole  body. 

Somnolence  is  present  to  a  greater  or  less  degree  in  all  cases.  In  mild 
cases  it  does  not  appear  until  late,  and  usually  is  not  long  continued.  In 
the  severer  cases  it  appears  early  and  continues  until  convalescence  begins ; 
in  fatal  cases  it  passes  into  a  state  of  coma.  It  is  often  interrupted  by  de- 
lirium. In  children  this  symptom  is  especially  prominent,  and  is  very  val- 
uable as  a  means  of  diagnosis. 

Delirium  is  more  frequently  present  than  absent  in  typhoid  fever.  The 
character  of  the  delirium  varies ;  the  usual  form  is  known  as  the  "low- 
muttering  "  delirium,  and  is  rather  characteristic  of  this  type  of  fever,  al- 
though in  very  many  cases  the  delirium  is  violent  in  character,  and  may 
become  maniacal  to  such  an  extent  as  to  I'equire  physical  restraint.  Not 
infrequently  typhoid  fever  patients  attempt  to  jump  out  of  a  window,  or 
injure  themselves  or  their  attendants  in  their  endeavors  to  escape  from  fan- 
cied dangers.  It  is  very  common  for  the  minds  of  this  class  of  patients  to 
be  occupied  with  those  things  which  engaged  their  attention  just  prior  to 
their  illness.  The  delirium  rarely  comes  on  until  the  second  week  of  the 
fever,  and  it  commences  and  is  most  active  at  night.  After  it  has  once  ap- 
peared, it  usually  continues  until  convalescence  is  established,  and  generally 
disappears  during  a  sound  sleep  which  attends  the  early  stage  of  convales- 
cence. The  maniacal  form  of  delirium  in  typhoid  fever  is  usually  most 
marked  at  night.  During  the  low-muttering  delirium,  if  the  patient  is 
asked  questions  he  will  generally  answer  correctly. 

Muscular  Prostration  and  Paralysis. — In  all  severe  cases  of  typhoid  fe- 
ver, muscular  prostration  is  noticeable  in  the  early  stages,  and  increases 
with  the  progress  of  the  fever.  It  is  generally  most  marked  during  the 
third  week.  Where  there  is  marked  muscular  paralysis,  the  urine  and  fas- 
ces are  passed  involuntarily,  there  is  inability  to  protrude  the  tongue,  and 
more  or  less  difficulty  in  deglutition,  or  inability  to  articulate  distinctly. 
Retention  of  the  urine  may  also  occur  from  vesical  paralysis. 

Muscular  Tremors. — Tremors  of  the  hands,  tongue,  or  lips  are  most 
often  met  with  in  young  subjects  and  those  who  are  addicted  to  the  use  of 
spirits.     Severe  tremors  unaccompanied  by  much  mental  disturbance  often. 
40 


626  ACUTE    GENERAL   DISEASES. 

attend  extensive  intestinal  changes.  Spasmodic  movements,  such  as  sub- 
sultus,  hiccough,  etc.,  and  rigid  contraction  of  the  muscles  of  the  neck  or 
extremities  are  sometimes  present  in  severe  cases.  General  convulsions  are 
of  rare  occurrence,  except  in  very  young  children,  and  when  they  occur 
have  no  special  significance. 

Special  Senses. — The  symptoms  referable  to  the  special  senses  require  lit- 
tle more  than  enumeration.  As  regards  the  sense  of  sight,  there  is  nothing 
worthy  of  note,  except  that  the  eye  assumes  a  dull  expression  and  that  the 
pnpil  is  dilated  ;  some  patients  complain  of  haziness  of  vision,  which  is  in- 
creased when  they  assume  a  sitting  posture.  The  setise  of  hearing  is  always 
Inore  or  less  impaired.  This  is  most  marked  about  the  middle  period  of 
the  fever  ;  then  it  is  impossible  for  the  patient  to  hear  ordinary  conversa- 
tion. Ringing  and  buzzing  sounds  in  the  ears  are  often  complained  of  in 
the  early  stage  of  the  fever.  When  the  loss  of  hearing  is  confined  to  one 
ear,  it  is  generally  caused  by  ulceration  of  the  mucous  lining  of  the  Eusta- 
chian tube,  or  by  suppuration  of  the  middle  ear.  The  sense  of  taste  usually 
is  altered  or  perverted  ;  articles  of  food  are  tasteless,  or  have  an  unnatural 
flavor.  When  the  tongue  and  mouth  are  covered  with  a  heavy  coating  of 
sordes,  the  patient  is  unable  to  distinguish  between  bitter  and  sweet,  and 
swallows  the  most  disgusting  doses  without  complaint. 

Hypermsthesia  is  another  disturbance  of  a  special  sense.  The  surface  of 
the  body  of  a  typhoid  fever  patient  may  become  so  sensitive  that  he  will  cry 
out  with  pain  from  the  slightest  touch.  This  hypergesthesia  may  be  present 
during  the  first  week,  or  may  not  be  present  until  convalescence  is  estab- 
lished. It  is  most  marked  over  the  abdomen  and  lower  extremities,  and 
usually  occurs  in  females  of  an  hysterical  tendency.  It  is  of  importance  to 
discriminate  between  cutaneous  tenderness  in  the  abdominal  region,  and 
the  tenderness  of  peritoneal  inflammation. 

Epistaxis. — When  this  occurs  during  the  first  week,  in  most  cases  it  is 
of  little  importance  except  as  a  diagnostic  sign  of  this  type  of  fever  ;  when 
it  occurs  during  the  third  week  it  becomes  important  as  an  element  of 
prognosis,  as  it  may  be  sufficiently  profuse  to  destroy  the  life  of  the  patient. 
■Occurring  late  in  the  disease,  unless  it  can  be  promptly  arrested,  it  always 
jeopardizes  the  life  of  the  patient. 

Emaciation  is  perhaps  more  marked  and  rapid  in  this  than  in  any  other 
form  of  fever.  It  commences  early  and  is  progressive.  By  the  time  a 
patient  has  reached  the  fourth  week  of  a  typhoid  fever  of  even  moderate 
severity  he  is  usually  in  a  condition  of  extreme  emaciation.  In  this  par- 
ticular he  markedly  differs  from  a  patient  ill  with  typhus  fevp»\  for  in  the 
latter  case  emaciation  to  any  great  extent  does  not  occur. 

Temperature. — In  making  thermometrical  observations  in  this  as  well  as 
in  ^li  other  forms  of  fever,  the  thermometer  may  be  placed  in  the  axilla, 
the  mouth,  or  the  rectum.  I  shall  refer  to  axillary  temperature  whenever 
I  speak  of  temperature  without  qualification.  Usually  in  a  typical  case 
the  temperature  begins  to  rise  about  noon  on  the  first  day  of  the  develop- 
ment of  the  fever,  and  continues  so  to  do  until  between  six  and  eight 
o'clock  in  the  evening,  when  it  reaches   its  maximum  for  that  day ;  then 


TYPHOID    FEVEE. 


627 


there  is  no  change  until  midnight,  when  it  begins  to  decline,  and  by  six 
or  eight  o'clock  in  the  morning  it  has  reached  its  minimum,  which  is  a  de- 
gree higher  than  on  the  morning  of  the  preceding  day.  After  six  or  eight 
o'clock  in  the  morning  the  temperature  does  not  vary  much  until  noon  ; 
then  it  again  begins  to  rise,  and  by  six  o'clock  in  the  evening  it  has  reached 
its  maximum  for  that  day,  which  is  one  degree  higher  than  on  the  even- 
ing of  the  preceding  day.  Again,  at  midnight  it  begins  to  fall,  and  by 
morning  it  has  fallen  a  degree,  which  leaves  the  minimum,  and  the  aver- 
age for  the  day  a  degree  higher  than  on  the  preceding  day.  Thus  it  rises 
a  degree  each  day,  with  regular  morning  and  evening  variations,  until  the 
eighth  day  of  the  fever,  when,  in  most  cases,  it  has  reached  its  maximum 
for  the  whole  course  of  the  disease. 


Fig.  151. 

Temperature  Record  in  a  Typical  Case  of  Mild  Typhoid 

Fever.    Eecovery. 


During  the  second  loeeTc  the  temperature  remains  at  about  the  same  maxi- 
mum degree  which  it  has  reached  at  the  end  of  the  first  week.  There  are 
morning  and  evening  variations  of  a  degree  or  more,  but  the  maximum  of 
the  evening  exacerbation  remains  the  same. 

During  the  third  weeh  the  remission  becomes  more  and  more  marked, 
while  during  the  exacerbation  the  temperature  retains  nearly  the  same 
standard  as  during  the  second  week.  By  the  end  of  the  third  week  the 
morning  temperature  during  the  remission  will  be  two  or  three  degrees  be- 
low the  maximum  of  the  second  week. 

By  the  time  the  fourth  weeh  is  reached,  or  at  least  by  the  middle  of  that 
week,  the  temperature  becomes  intermittent,  and  with  each  exacerbation  it 
falls  lower  and  lower,  until  by  the  end  of  the  week  the  normal  standard  of 
temperature  has  been  reached,  or  it  may  fall  a  little  below  the  normal 
standard.  These  are  the  typical  thermometrical  variations  of  typhoid 
fever,  yet  they  are  not  always  present,  and  there  are  many  things  which 
will  materially  modify  them.  The  fever  does  not  always  follow  this  typi- 
cal course.  Marked  deviations  from  the  record  may  be  produced  by  com- 
plications which  would  never  have  been  discovered  but  for  the  irregular 
thermometrical  variations.  By  treatment,  the  temperature  can,  for  a  time,  be 


628 


ACUTE    GENERAL   DISEASES. 


Tery  much  lowered  ;  but  if  the  treatment  be  discontinued,  it  will  rise  again. 
In  some  cases  it  is  not  possible  to  detect  the  cause  of  the  irregularity. 

Pulse. — The  pulse  is  also  subject  to  variations,  which  correspond  very 
nearly  with  the  variations  in  temperature,  and  occur  not  only  on  different 
days,  but  at  different  hours  on  the  same  day.  During  the  first  week  the 
pulse  becomes  more  and  more  frequent ;  in  the  second  and  third  weeks  it 


Sa,^.    L  12.   a  4.  5.  6.  7.   8.  9.  m  /J. 

12.  /3.  /^.  J5. 16.  /7.  \IS.  19.  20.  21.  22 

/O^ ^ ^ ^ ^: 

l--f^-f: 

n  e  m  e  7n  e  rri  e  7n\e  m  e  Jfi  e  m.\e  fit  e  m  e^WL  €'. 

''^f  1 1  |i  H  Ml 

J 1 

„ ^ ^g. 

9S°i^ ^ 

— V it 

()■/ \z : 



-^                               1 

\ 

©  An  intestinal  hemorrhage  occurred  here. 
Fig.  152. 
Temperature  Record  in  a  Non-typical  Case  of  Typhoid  Eever. 

remains  at  its  height,  and  during  the  fourth  week  sinks  to  its  normal  aver- 
age. Throughout  the  whole  course  of  the  disease  it  is  less  frequent  in  the 
morning  than  in  the  evening.  If,  at  the  commencement  of  the  fever,  the 
pulse  is  98,  by  the  end  of  the  first  week  it  will  have  reached  100,  or  110 
per  minute,  and  there  it  remains  during  the  second  week ;  after  that  time 
it  may  become  as  frequent  as  120,  or  140..  During  the  first  and  second 
weeks  the  rate  of  the  pulse  and  the  temperature  range  correspond,  but 
after  this  time  the  parallelism  ceases  as  the  failure  of  heart-power  begins 
to  manifest  itself.  This  failure  of  heart-power  is  indicated  by  an  increase 
in  the  frequency  and  feebleness  of  the  pulse,  which  at  this  time  may  reach 
140  per  minute  and  yet  the  temperature  show  no  alarming  variation. 
Under  these  circumstances,  the  pulse  may  become  irregular  and  intermit- 
ting. Should  these  irregularities  and  intermissions  occur  during  the  third 
week,  in  most  cases  they  are  followed  by  death.  With  an  irregular  and 
intermitting  pulse,  the  first  sound  of  the  heart  will  usually  be  inaudible 
over  the  precordial  space,  and  this  indicates  that  prompt  and  judicious 
means  must  be  employed  to  restore  the  heart's  normal  action  and  to  avert 
a  fatal  issue. 

The  severity  of  the  disease  during  the  first  and  second  weeks  of  its  devel- 
opment is,  to  a  great  extent,  indicated  by  the  frequency  of  the  pulse  and 
the  height  of  the  temperature.  Although  delirium  and  extensive  tym- 
panitis are  important  symptoms  they  do  not  determine  the  result ;  but  if  a 
patient  during  the  first,  or  at  the  commencement  of  the  second  week  of  the 


TYPHOID    FEVER.  629 

disease,  has  a  pulse  of  120  per  minute,  and  a  temperature  of  one  hundred 
and  six,  it  is  very  doubtful  whether  convalescence  can  ever  be  established. 
The  pulse  may  increase  in  frequency  from  feeble  heart-power  alone  while  the 
temperature  is  steadily  falling.  On  the  other  hand,  the  pulse  sometimes 
falls  almost  to  a  normal  standard,  while  the  temj^erature  remains  high. 

Eruption. — Some  have  claimed  that  this  should  be  considered  as  a  lesion 
of  the  disease,  but  I  prefer  to  class  it  among  the  symptoms.  It  makes  its 
appearance  between  the  sixth  and  twelfth  days,  dating  from  the  commence- 
ment of  the  fever,  and  it  is  not  attended  by  any  unusual  sensation.  It  re- 
mains visible  from  eight  to  fourteen  days,  leaving  no  stain  or  mark  on  the 
surface  after  its  disappearance.  It  consists  of  isolated,  lenticular  spots 
scattered  more  or  less  abundantly  over  the  surface  of  any  part  of  the  body, 
but  usually  most  abundant  upon  the  chest  and  abdomen.  There  may  be 
only  a  few  spots  visible  at  a  time,  or  they  may  be  so  profuse  as  to  cover  the 
body  like  a  rash.  Two  or  three  well-defined  spots  of  the  eruption  are  suf- 
ficient to  establish  the  existence  of  the  fever.  Each  spot  is  circular  in 
shape,  and  varies  in  diameter  from  a  point  to  a  line  and  a  half,  rarely 
reaching  two  lines.  It  is  slightly  elevated  above  the  surface  of  the  sur- 
rounding cuticle,  is  of  a  bright  rose  color,  disappears  upon  slight  pressure, 
and  returns  as  soon  as  the  pressure  is  removed.  Each  spot  remains  visible 
for  three  days,  and  then  disappears.  Sometimes,  as  one  crop  of  the  erup- 
tion disappears  another  is  developed,  and  this  may  go  on  for  eight,  twelve 
or  fourteen  days.  There  are  many  cases  in  which  only  one  crop  appears. 
As  soon  as  one  spot  makes  its  appearance,  it  is  well  to  mark  it  with  tinc- 
ture of  iodine  or  nitrate  of  silver,  so  that  observations  will  be  always  made 
upon  the  one  point.  If  it  is  a  spot  of  typhoid  eruption,  and  one  crop  of 
eruption  is  to  follow  another,  it  will  disappear  within  three  days  from  the 
time  at  which  it  was  first  seen,  and  other  spots  will  take  its  place.  It  is 
this  feature  which  distinguishes  the  typhoid  eruption  from  that  of  all  other 
fevers. 

The  question  may  be  asked  : — is  this  eruption  essential  to  the  diagnosis  of 
typhoid  fever  ?  Many  observers  mention  that  the  eruption  is  not  constant, 
and  consequently  not  necessary  for  its  diagnosis  ;  while  others,  equally 
competent,  maintain  that,  unless  the  eruption  be  present  at  some  period 
during  the  progress  of  the  disease,  the  diagnosis  of  typhoid  fever  cannot  be 
made  with  certainty.  Jenner  states  that  he  found  the  eruption  present  in 
one  hundred  and  forty-eight  out  of  one  hundred  and  fifty-two  cases.  I 
would  not  say  that  it  is  possible  for  typhoid  fever  to  occu,r  without  the 
eruption  ;  neither  would  I  affirm  that  scarlet  fever  ever  exists  without  the 
characteristic  rash  of  the  disease  ;  but  as  regards  these  respective  fevers,  if 
no  eruption  was  present,  I  would  make  the  diagnosis  with  equal  hesitancy 
in  the  one  case  as  in  the  other.  The  eruption  is  usually  most  marked  in 
cases  of  typhoid  fever  which  occur  between  the  ages  of  ten  and  thirty.  Be- 
fore ten  and  after  thirty  years  it  is  usually  not  as  well  marked,  and  may  be 
readily  overlooked  unless  careful  search  is  made. 

The  typhoid  poison,  in  its  operation  on  the  human  body,  does  not  always 
effect  the  series  of  changes  and  symptoms  just  described.     On  the  contrary. 


630  ACUTE    GENERAL   DISEASES. 

there  are  cases  which  run  so  mild  a  course  that  they  can  scarcely  be  digni. 
fied  by  the  name  of  fever,  and,  besides,  there  are  imperfectly  developed 
cases  which  show  a  great  diversity  in  their  course,  but  they  all  can  be  in- 
cluded under  two  heads. 

First. — Mild  typhoid  fever,  in  which  the  symptoms  are  all  mild. 

Second. — Abortive  typhoid  fever,  in  which  the  duration  of  the  disease  is 
markedly  shortened. 

In  the  7nild  tyjie,  the  fever  runs  its  regular  course,  but  is  of  low  grade. 
The  temperature  rises  regularly  until  its  maximum  is  reached,  which  rarely 
exceeds  103°  F.,  then  it  remains  stationary  for  a  time,  generally  about  a 
week  ;  the  decline  follows  in  the  same  manner  as  in  a  typical  case.  This 
is  the  regular  course  of  these  cases  if  left  to  themselves,  and,  as  a  rule, 
they  should  be  left  to  themselves.  Some  of  these  cases  are  so  mild  that  the 
patients  are  not  confined  to  the  bed,  or  even  to  their  rooms,  and  perhaps 
throughout  the  entire  course  of  the  disease  are  able  to  transact  a  certain 
amount  of  business.  Such  cases  have  been  called  "  walking  cases  "  of  ty- 
phoid fever.  The  eruption  appears  in  these  cases  early,  is  of  short  dura- 
tion and  only  a  few  spots  appear  ;  usually  there  is  only  one  crop.  Diar- 
rhoea is  also  present  in  most  cases  of  this  class,  but  it  is  of  a  mild  type  and 
the  discharges  from  the  bowels  apparently  give  relief  to  the  patient.  In 
some  cases  the  diarrhoea  alternates  with  constipation,  or  constipation  may 
be  present  throughout  the  entire  course  of  the  disease,  and  the  cases  go  on 
exhibiting  a  varying  amount  of  fever  for  from  twenty  to  thirty  days,  until 
gradual  convalescence  is  established.  This  class  of  cases,  if  properly  man- 
aged, rarely  prove  fatal ;  but  if  improperly  managed,  there  is  great  danger. 
If  a  patient  walks  about  while  he  is  suffering  from  one  of  these  so-called 
mild  attacks  of  typhoid  fever,  he  does  it  at  great  risk  to  life  ;  there  should 
be  no  "  walking  cases  "  of  typhoid  fever.  A  patient  sick  with  typhoid 
fever,  however  mild  the  type,  should  take  to  his  bed  and  remain  there 
until  convalescence  is  fully  established,  as  it  is  impossible  to  say  just  how 
extensive  the  changes  may  be  that  have  occurred  in  the  intestinal  tract, 
and  in  the  mildest  type  of  the  disease  they  may  be  of  such  a  nature  that 
very  little  physical  exertion  will  cause  intestinal  perforation  which  will  be 
followed  by  a  fatal  peritonitis. 

The  abortive  form  of  typhoid  fever  is  ushered  in  with  all  the  symptoms 
of  a  typical  case — headache,  lassitude,  pain  in  the  limbs,  nausea,  etc., — 
and  the  temperature  during  the  first  week  follows  the  regular  variations  of 
the  fever.  At  the  onset  the  disease  has  every  appearance  of  a  severe  form 
of  typhoid  fever  ;  the  temperature  may  rise  as  high  as  105°  F.  or  106°  F. 
by  the  end  of  the  first  week  ;  delirium  is  often  active,  and  diarrhcea  is 
present.  By  the  end  of  the  second  week,  certainly  by  its  close,  if  recovery 
occurs,  the  fever  is  cut  short,  and  abruptly  disappears  ;  the  temperature 
falls  to  the  normal  standard,  and  the  patient  passes  on  to  a  state  of  rapid 
and  complete  convalescence.  The  eruption,  diarrhoea,  and  all  the  urgent 
symptoms  of  the  disease  may  be  present,  and  yet  before  the  end  of  the 
second  week  the  patient  may  be  fully  convalescent.  That  it  is  the  typhoid 
poison  which  thus  acts  upon  the  system,  and  gives  rise  to  the  characteristic 


TYPHOID    FEVER.  631 

symptoms  of  typhoid  fever  in  these  abortive  cases,  is  evidenced  by  the  fact 
that  at  the  post-mortem  examinations  the  characteristic  typhoid  intestinal 
lesions  are  found,  and  these,  taken  in  connection  with  the  presence  during 
life  of  the  typhoid  eruption,  establish  the  diagnosis  beyond  question. 
There  can  be  no  doubt  but  that  an  individual  may  be  affected,  overwhelmed 
as  it  were,  by  typhoid  poison,  and  yet  not  develop  well-marked  typhoid  fever. 
So,  if  only  a  moderate  amount  of  typhoid  poison  is  introduced  into  the  sys- 
tem, a  mild  or  an  abortive  type  of  fever  will  be  developed.  The  natural 
power  of  the  individual  to  resist  the  action  of  such  poisons  must  always  be  re- 
garded, and  should  be  taken  into  consideration  in  the  treatment  of  a  case. 

Differential  Diagnosis. — In  a  typical  case,  after  the  fever  is  fully  developed, 
the  diagnosis  is  not  diflBcult.  The  presence  of  febrile  excitement,  marked 
by  evening  exacerbations  and  morning  remissions,  headache,  diarrhcsa,  ab- 
dominal tenderness,  and  other  abdominal  symptoms,  and  the  presence  of 
the  characteristic  rose-colored  spots  are  sufficient  for  a  diagnosis.  In  tha 
mild  type  of  the  disease,  or  when  the  symptoms  are  developed  irregularly, 
or  during  the  first  week  of  a  typical  case,  the  diagnosis  is  often  difficult, 
and  sometimes  impossible. 

The  principal  diseases  which  are  liable  to  be  confounded  with  typhoid 
fever  are  typhus  and  relapsing  fevers,  continued  malarial  (so-called  typho- 
malarial) /ever,  acute  tuberculosis,  py(Bmia,  septiccsmia,  pneumonia,  gastro- 
enteritis, trichinosis,  and  diffuse  parenchymatous  hepatitis.  The  differen- 
tial diagnosis  between  typhoid  fever  and  g astro-enteritis  and  diffuse  hepa- 
titis have  already  been  given.  The  points  of  differential  diagnosis  between 
typhoid  and  typhus,  relapsing  and  continued  malarial  (so-called  typho- 
malarial)  fevers,  will  be  considered  in  connection  with  the  history  of  these 
fevers. 

Acute  Tuherculosis. — This  disease  is  attended  by  many  of  the  symptoms 
which  are  present  in,  and  supj)osed  to  be  characteristic  of,  typhoid  fever. 
The  fever  of  acute  tuberculosis  is  of  a  remittent  type,  attended  by  evening 
exacerbations  and  morning  remissions,  delirium,  a  dry,  brown  tongue,  a 
tendency  to  stupor,  great  prostration,  rapid  emaciation,  and  sometimes  by 
a  diarrhoea,  with  abdominal  tenderness  and  tympanitis.  All  of  these  are 
among  the  prominent  symptoms  of  typhoid  fever.  More  than  once  have 
patients  in  Bellevue  Hospital,  with  the  diagnosis  of  typhoid  fever,  pre- 
sented at  the  post-mortem  examination  the  characteristic  lesions  of  acute 
tuberculosis.  If,  therefore,  patients  with  acute  tuberculosis  may  go  through 
a  large  general  hospital,  under  the  observation  of  diagnosticians, — who  cer- 
tainly are  not  men  of  inferior  ability, — and  be  supposed  to  have  typhoid 
fever,  there  evidently  is  great  danger  of  a  mistake  in  diagnosis.  The  higher 
range  of  temperature  in  acute  tuberculosis  than  in  typhoid  fever  is  one  of 
the  distinguishing  characteristics  of  the  disease.  Usually,  early  in  the 
progress  of  the  disease,  it  reaches  106°  or  107°  F.,  while  in  typhoid  fever 
the  temperature  rarely  reaches  106°  F.,  or  if  it  does,  in  most  cases  it  is  not 
before  the  end  of  the  second  week  and  after  the  typical  rise.  There  is  no 
eruption,  neither  is  there  enlargement  of  the  spleen  in  acute  tuberculosis, 
while  both  are  very  constant  attendants  of  typhoid  fever  ;  yet  their  absence 


632  ACUTE   GENEEAL  DISEASES. 

is  not  positive  proof  that  typhoid  fever  does  not  exist.  Quinine  will  reduce 
the  temperature  of  typhoid  fevor  from  three  to  four  degrees,  while  it  has 
but  little  influence  over  that  of  tuberculosis.  Pulmonary  consolidation  is 
at  the  apex  in  tuberculosis,  at  the  base  in  typhoid  fever.  According  to 
Bouchut,  the  ophthalmoscope  reveals  the  presence  of  tubercular  granula- 
tions in  the  choroid  in  all  cases  of  acute  tuberculosis.  In  all  doubtful 
cases  the  family  history  of  the  patient,  his  immediate  surroundings,  whether 
typhoid  fever  is  prevailing  at  the  time,  and  whether  the  patient  has  been 
exposed  to  typhoid  poison,  become  important  points  in  diagnosis ;  after 
the  first  week  of  the  disease,  the  presence  of  the  rose-colored  spots  is  neces- 
sary for  a  diagnosis  of  typhoid  fever. 

Pymmia  and  Septiccemia. — In  most  cases  these  diseases  will  be  readily 
recognized,  as  the  surface  of  the  body  has  a  jaundiced  hue,  there  are  no 
lenticular  spots,  and  the  febrile  symptoms  are  irregular  in  their  develop- 
ment. There  are  exacerbations  and  remissions,  but  their  appearance  and 
disappearance  are  not  marked  by  any  regularity,  and  usually  there  is  more 
than  one  exacerbation  and  remission  in  the  twenty-four  hours.  Not  only 
are  the  variations  in  temperature  irregular,  but  the  temperature  reaches  a 
high  degree  much  sooner,  and  ranges  higher  throughout  its  entire  course 
in  pyaemia  and  septicaemia  than  in  typhoid  fever.  In  pyasmia  and  sep- 
ticaemia there  are  early  in  the  disease  recurring  chills  followed  by  profuse 
sweatings,  great  prostration,  rapid  emaciation,  delirium,  subsultus,  tym- 
panitis and  diarrhoea,  while  in  typhoid  fever  these  do  not  come  on  until 
late  in  the  disease.  Moreover,  the  history  which  precedes  and  attends  the 
development  of  pyaemia  and  septicaemia  differs  widely  from  that  of  typhoid 
fever.  In  pyaemia,  thrombi,  infarctions  and  multiple  abscesses  establish 
the  diagnosis. 

There  is  a  condition  of  septic  poisoning  occasionally  met  with  resulting 
from  the  introduction  into  the  system  of  septic  poison  through  the  drink- 
ing water,  which  so  closely  resembles  that  which  is  the  result  of  typhoid 
poisoning  that  it  is  almost  impossible  to  make  a  differential  diagnosis.  In 
these  cases  the  absence  of  the  rose-colored  spots  is  almost  the  only  distin- 
guishing feature. 

Pneumonia. — Pneumonia,  with  typhoid  symptoms,  is  sometimes  mis- 
taken for  typhoid  fever.  The  pneumonia  which  complicates  typhoid  fever 
does  not  come  on  until  late  in  the  fever,  and  is  preceded  by  the  regular 
history  of  typhoid  fever.  On  the  other  hand,  when  the  typhoid  symptoms 
are  present  from  the  beginning,  or  come  on  at  the  end  of  the  second 
stage  of  the  pneumonia,  the  physical  signs  of  the  pneumonia  will  attend 
or  precede  the  typhoid  symptoms.  There  will  be  cough  and  the  character- 
istic pneumonic  expectoration  ;  there  will  be  no  eruption,  and  no  typical 
variation  in  temperature.  If  a  patient  who  is  over  sixty  years  of  age  with 
this  type  of  pneumonia  is  not  seen  until  the  second  or  third  week  of  its 
progress,  although  evidences  of  lung  consolidation  may  be  present,  it  will 
frequently  be  very  difficult  to  decide  whether  the  pneumonia  is  or  is  not 
complicating  a  typhoid  fever.  The  diagnosis  must  be  based  upon  the  his- 
tory of  the  case. 


TYPHOID   FEVEK.  633 

Gastro-Enteritis. — In  the  adult  this  disease  is  quite  readily  distinguished 
from  typhoid  fever,  as  the  diarrhoea  and  vomiting  precede  the  febrile  move- 
ment ;  the  fever  is  irregular  in  its  development  and  progress,  and  the  tem- 
perature rarely  rises  higher  than  103°  F.  In  a  child  between  two  and  six 
years  of  age  it  is  very  difficult  to  distinguish  gastro-enteritis  from  typhoid 
fever.  The  typhoid  eruption  is  not  so  prominent  or  constant  a  symptom 
in  the  child  as  in  the  adult,  and  with  both  diseases  we  have  diarrhoea, 
tympanitis,  and  typhoid  symptoms.  When  all  the  symptoms  precede  the 
fever,  and  there  is  a  history  of  the  case,  and  a  thermometricai  record  from 
the  beginning  of  the  fever,  in  most  cases  the  diagnosis  can  readily  be  made  ; 
but  if  the  case  is  not  seen  until  it  has  reached  the  second  week  of  its  prog- 
ress, and  there  is  no  accurate  or  reliable  history  of  its  development,  a  posi- 
tive diagnosis  is  impossible. 

Trichinous  Disease. — This  condition  is  not  infrequently  attended  by 
diarrhoea,  vomiting,  and  the  development  of  other  typhoid  symptoms ;  but 
with  poisoning  by  trichinae  there  are  almost  constantly  present  intense 
muscular  pains  and  oedema  of  the  eyelids,  which  will  be  sufficient  to  arrest 
attention.  There  will  be  wanting  the  typical  temperature  trace  and  the 
rose  rash,  and  a  microscopic  examination  of  small  portions  of  the  muscular 
tissue  will  afford  a  positive  diagnosis. 

Prognosis. — Death  may  occur  at  any  stage  of  this  fever.  A  typhoid 
patient  is  not  out  of  danger  until  all  tympanitis,  diarrhoea,  and  other  ab- 
dominal symptoms  which  indicate  that  intestinal  changes  are  still  progress- 
ing, have  disappeared.  Independent  of  complications,  the  duration,  type, 
and  intensity  of  the  febrile  excitement  have  more  to  do  than  all  the  other 
elements  in  determining  the  prognosis  in  any  case  of  typhoid  fever.  The 
height  of  the  temperature  on  the  eighth  day  determines  the  range  of  tem- 
perature that  may  be  expected  on  each  succeeding  day.  If  upon  that  day 
it  is  not  higher  than  104°  or  105°  F.,  and  has  been  regular  in  its  devel- 
opment (independent  of  complications),  the  prognosis  is  good;  in  uncom- 
plicated cases  it  very  rarely  rises  higher  than  the  degree  it  has  reached  at 
that  time.  A  prolonged  high  temperature  (above  105°  F.)  after  the  first 
week  renders  the  prognosis  unfavorable.  In  mild  cases,  during  the  second 
week,  a  marked  morning  remission  occurs,  which  begins  early  and  continues 
until  midday;  the  evening  exacerbation  is  late,  and  by  the  end  of  the  sec- 
ond week  there  is  a  marked  and  permanent  fall  in  the  temperature.  In 
severe  cases,  the  opposite  conditions  are  observed.  A  sudden  rise  in  tem- 
perature, or  a  rapid  and  extreme  fall  at  any  period  of  the  fever  is  a  very 
bad  omen  ;  the  latter  often  precedes  the  occurrence  of  a  severe  intestinal 
hemorrhage.  Marked  variation  from  the  typical  temperature  of  the  disease 
indicates  the  existence  of  complications.  Slight  decline  accompanied  by 
great  fluctuation  of  temperature,  during  the  third  week,  is  an  unfavorable 
symptom.  The  natural  power  of  an  individual  to  resist  disease,  especially 
the  effects  of  prolonged  high  temperature,  is  a  very  important  element  in 
prognosis.  The  organ  which  is  the  surest  indicator  of  such  power  (espe- 
cially in  typhoid  fever)  is  the  heart. 

If  the  pulse  is  full  and  regular,  perhaps  beating  at  the  rate  of  130  or  115 


634  ACUTE    GEl^ERAL    DISEASES. 

per  minute,  if  the  cardiac  inipulse  is  good,  and  a  distinct  first  sound  can 
be  heard,  even  though  at  the  end  of  the  second  week  the  temperature  stands 
as  high  as  106°  F.,  the  prognosis  is  favorable.  If,  however,  the  pulse  has 
risen  to  120  or  130  per  minute,  if  the  apex-beat  is  feeble  or  imperceptible, 
and  the  first  sound  of  the  heart  is  indistinct  or  altogether  obscured,  with  a 
tendency  to  cyanosis  and  pulmonary  oedema,  the  indications  are  that  the 
patient's  powers  of  resistance  are  failing,  and  under  such  circumstances  the 
prognosis  must  be  unfavorable.  It  is  not  so  much  i-apidity  as  irregularity, 
a  sudden  falling  and  a  sudden  rising  of  the  pulse,  that  indicates  impending 
danger.  The  rapid  rising  of  the  pulse  upon  the  slightest  excitement  is  the 
most  unfavorable  indication,  as  it  shows  extensive  heart-failure  and  a  rapid 
giving  way  of  vital  power.  A  sudden  fall  of  the  pulse  from  any  cause  must 
always  be  regarded  as  an  unfavorable  indication.  The  abundance  or  color 
of  the  eruption  does  not  influence  the  prognosis.  Excessive  tympanitis  and 
severe  abdominal  pains  are  unfavorable  symptoms.  Severe  and  protracted 
muscular  tremors,  with  subsultus,  indicate  danger.  Sudden  collapse 
during  the  second  and  third  weeks  of  the  fever  is  always  attended  with 
danger,  as  it  is  very  likely  to  be  due  to  copious  intestinal  hemorrhages 
or  intestinal  perforation.  It  sometimes  occurs  independently  of  either  of 
these  causes,  but  nevertheless  is  very  apt  to  be  soon  followed  by  a  fatal 
result. 

The  prognosis  is  always  bad  in  those  who  are  very  fat,  and  in  those 
who  are  the  subjects  of  gout,  disease  of  the  kidney,  or  any  other  severe  form 
of  chronic  disease.  In  all  such  persons,  during  the  second  and  third  weeks 
of  the  disease,  it  is  necessary  to  be  constantly  on  the  watch  for  the  occur- 
rence of  sudden  collapse.  My  own  experience  leads  me  to  the  belief  that 
when  intestinal  hemorrhage  is  scanty  it  has  little  influence  on  the  final  re- 
sult. When  it  occurs  before  the  twelfth  day  of  the  fever,  it  is  often  of  ad- 
vantage by  relieving  the  intestinal  congestion.  But  when  profuse,  or  even 
slight,  after  the  twelfth  day,  it  is  an  unfavorable  symptom  and  renders  the 
prognosis  unfavorable.  The  occurrence  of  the  hemorrhage  renders  it  prob- 
able that  ulceration  has  extended  to  the  vessels  beneath  the  transverse  mus- 
cular fibres  of  the  intestine,  and  such  ulceration  is  very  apt  to  go  on  to  per- 
foration and  a  fatal  peritonitis. 

The  influence  of  age  is  very  great  in  determining  the  prognosis  in  any 
case  of  typhoid  fever.  It  is  much  better  in  children  than  in  adults  ;  and  in 
persons  over  forty  years  of  age  the  prognosis  is  decidedly  unfavorable,  even 
though  the  symptoms  may  not  indicate  a  severe  type  of  the  disease.  In  the 
case  of  those  individuals  who  habitually  use  alcoholic  stimulants,  whose 
power  of  resistance  to  high  temperature  is  diminished,  the  rate  of  mortality 
is  very  great.  The  puerperal  state  renders  the  prognosis  especially  unfa- 
vorable. The  danger  to  the  patient  is  equally  great,  whether  the  fever 
comes  on  prior  to  delivery  or  during  puerperal  convalescence.  The  paren- 
chymatous changes  which  take  place  in  the  different  organs  of  the  body 
during  the  progress  of  this  fever,  necessarily  influence  the  prognosis.  The 
muscular  degenerations  of  the  cardiac  walls,  and  consequent  loss  of  heart- 
power,  which  favor  pulmonary  and  other  hypostatic  congestions,  and  the 


TYPHOID    FEVEK.  635 

diminished  quantity  of  blood  sent  to  the  various  tissues  of  the  body,  inter- 
fere more  or  less  with  their  nutrition.  Necrotic  and  gangrenous  processes, 
sometimes  met  with  in  the  cellular  tissue  of  the  surface  and  along  the  line 
of  the  intestines,  as  also  the  venous  thrombi  which  so  frequently  develop  in 
a  protracted  case  of  this  fever,  are,  to  a  certain  extent,  the  result  of  this 
cardiac  weakness,  and  render  the  prognosis  unfavorable.  Excessive  cardiac 
weakness  also  favors  the  development  of  blood-clots  in  the  heart-cavities ; 
these  may  break  up  and  cause  embolism  somewhere  in  the  course  of  the 
general  circulation,  and  thus  lead  to  changes  which  may  destroy  life.  In- 
testinal perforations,  one  of  the  results  of  the  intestinal  changes  incident  to 
the  fever,  render  the  prognosis  most  unfavorable. 

Complications. — Slight  bronchial  catarrh  can  hardly  be  regarded  as  a 
complication,  it  is  so  much  a  part  of  the  clinical  history  of  the  disease, 
but  another  much  more  serious  bronchial  complication  is  capillary  bron- 
chitis. This  usually  comes  on  during  the  second  or  third  week  of  the 
disease,  and,  if  extensive,  greatly  endangers  the  life  of  the  patient.  It  is 
indicated  by  subcrepitant  rdles  suddenly  developed  over  the  whole  of  both 
lungs,  accompanied  by  great  dyspnoea  and  an  abundant  expectoration  of 
stringy  mucus.  Its  advent  renders  the  prognosis  most  unfavorable.  Ex- 
tensive osdema  of  the  lungs,  occurring  with,  or  independent  of,  capil- 
lary bronchitis  and  pulmonary  congestion,  sometimes  comes  on  suddenly 
during  the  third  week  of  typhoid  fever,  and  indicates  great  failing  in 
heart-power.  The  slighest  indication  of  its  occurrence  would  always  be 
regarded  with  suspicion.  It  is  not  infrequently  accompanied  by  more  or 
less  extensive  hemorrhagic  infarctions  of  the  lungs.  These  depend  on 
embolism  of  some  of  the  branches  of  the  pulmonary  artery  due  to  frag- 
ments of  clots  which  have  formed  in  the  right  side  of  the  heart,  the  re- 
sult of  the  cardiac  weakness,  and  often  lead  to  gangrene  of  the  lung.  It 
is  sometimes  impossible  to  diagnosticate  their  existence  during  life. 

Pneumonia,  when  it  complicates  typhoid  fever,  is  generally  latent.  It 
comes  on  very  insidiously,  and  will  be  recognized  only  by  the  most  care- 
ful physical  examination.  It  is  more  frequently  developed  during  the 
third  and  fourth  weeks  of  the  fever,  and  usually  is  lobular  rather  than  lobar 
in  character.  At  first  only  single  lobules  are  involved,  but  after  a  time 
an  entire  lobe  becomes  consolidated.  When  irregular  variations  m 
temperature  occur  during  convalescence,  or  during  the  third  or  fourth 
week  of  the  fever,  there  is  reason  to  suspect  the  development  of  pneumonia. 
In  the  majority  of  cases  the  characteristic  pneumonic  cough  and  expecto- 
ration are  absent.  Whenever  an  extensive  pneumonia  complicates  typhoid 
fever,  the  prognosis  is  especially  unfavorable. 

Pleurisy  is  not  so  frequently  a  complication  of  typhoid  fever  as  is 
pneumonia  or  bronchitis.  When  it  does  occur,  the  almost  invariable  prod- 
uct of  the  inflammatory  process  is  pus.  Usually  it  comes  on  insidiously, 
late  in  the  disease,  and  is  quite  likely  to  pass  unrecognized  unless  frequent 
physical  examinations  are  made.  In  many  instances  it  is  really  a  sequela 
of  the  fever,  not  developing  until  three  or  four  weeks  after  the  fever  has 
run  its  course.     Its  occurrence  must  always  be  regarded  as  unfavorable. 


636  ACUTE   GENEKAL   DISEASES.  ', 

for  a  year,  or  even  longer  time,  must  elapse  before  recoyery  can  take  place, 
and  even  then  complete  recovery  is  doubtful. 

Occasionally  laryngitis  is  a  serious  complication  of  this  fever.  It  gene- 
rally occurs  in  those  cases  where  the  fever  has  been  very  protracted,  and 
there  is  great  prostration.  Its  presence  is  marked  by  sudden  and  very 
intense  inflammation  of  the  mucous  membrane  of  the  glottis,  which  is 
liable  to  become  oedematous,  when  death  may  suddenly  occur.  It  may 
lead  to  ulceration  of  the  mucous  membrane.  PycBmia  may  be  met  with 
as  a  complication  during  convalescence  from  typhoid  fever,  but  it  is  not  of 
as  frequent  occurrence  as  septicaemia.  Whenever  septic  poisoning  is  de- 
veloped, with  extensive  sloughs  in  the  intestines,  the  prognosis  is  exceed- 
ingly unfavorable.  Acute  gastric  catarrh  is  another  complication  of  this 
fever.  During  the  fourth  week,  or  in  early  convalescence,  imprudence  in 
diet,  either  in  quantity  or  quality,  may  produce  irritation  and  inflamma- 
tion of  the  weakened  gastric  mucous  membrane  and  endanger  or  destroy 
the  life  of  an  already  enfeebled  patient. 

The  greatest  care  must  be  exercised  in  regard  to  the  diet  of  patients  con- 
valescing from  typhoid  fever.  They  should  be  restricted  to  milk  and 
nutritious  broths,  in  moderate  quantity,  until  all  danger  from  complica- 
tions shall  have  passed.  Disturbances  of  nerve-function  have  been  con- 
sidered under' the  head  of  symptoms,  but  not  infrequently  certain  brain 
and  nerve  lesions  are  developed  which  cannot  be  classed  under  that  head. 
Cerebral  oedema  may  complicate  a  typhoid  fever  during  its  third  week,  and 
give  rise  to  symptoms  of  a  grave  character.  A  decided  enfeebling  of  the 
mental  powers  and  a  tendency  to  stupor  announce  its  occurrence.  Hemor- 
rhagic extravasations  on  the  surface  and  into  the  substance  of  the  brain, 
the  result  of  degeneration  of  the  walls  of  the  cerebral  vessels,  occasionally 
occur  during  the  height  of  the  fever.  If  the  effusion  is  moderate,  no 
marked  symptoms  are  developed  ;  but  if  a  considerable  extravasation  takes 
place,  it  gives  rise  to  symptoms  of  cerebral  compression.  Meningeal  in- 
flammation is  a  rare  complication.  The  occurrence  of  any  of  these  com- 
plications in  any  case  renders  the  prognosis  unfavorable. 

During  the  second  and  third  weeks  of  the  fever  certain  cerebral  disturb- 
ances may  occur  which  seem  to  indicate  the  existence  of  some  one  of 
these  complications,  when  no  cerebral  lesion  exists.  Usually,  they  are 
present  in  patients  who  have  had  a  continuously  high  temperature,  and  in 
favorable  cases  they  disappear  after  a  few  days.  Various  other  disturb- 
ances of  the  nervous  system,  such  as  hemiplegia,  paraplegia,  etc.,  which 
may  simulate  those  due  to  lesions  of  the  nerve-centres,  or  forms  of  local 
paralysis  and  anesthesia  which  seem  to  be  confined  to  individual  nerves 
are  met  with,  but  as  these  functional  disturbances  do  not  depend  upon  any 
anatomical  changes,  the  prognosis  in  such  cases  is  good.  Those  changes  in 
the  kidney,  due  to  parenchymatous  degeneration,  which  usually  attend  this 
fever  have  already  been  noticed  ;  but  occasionally  nephritis  is  developed 
as  a  sequela.  The  urine  becomes  scanty,  is  loaded  with  albumen,  and  con- 
tains blood  and  casts  ;  the  face  and  extremities  become  oedematous,  and 
death  may  occur  from   uraemia.     The   occurrence   of  this   complication 


TYPHOID    FKVER.  637 

necessarily  renders  the  prognosis  bad.  In  a  few  instances  under  my  ob- 
servation, severe  catarrh  of  the  bladder  has  developed  during  convalescence, 
greatly  complicating  the  case  ;  in  one  instance  the  cystitis  was  accompa- 
nied by  pyelitis.  Cellulitis,  especially  of  the  surface,  often  complicates 
convalescence,  and  in  some  cases  causes  death.  Occasionally  it  is  met  with 
in  the  pharynx  and  along  the  line  of  the  lymphatics.  Accompanying  this 
cellular  inflammation,  or  occurring  independently  of  it,  gangrenous  inflam- 
mations of  the  integument  not  infrequently  occur,  giving  rise  to  hed-sores. 
These  gangrenous  processes  are  most  frequently  developed  at  those  points 
which  have  been  subjected  to  the  greatest  pressure,  on  account  of  the  po- 
sition of  the  patient  in  bed,  such  as  the  sacrum,  nates,  heels,  and  shoulder- 
blades.  In  the  simplest  form  of  hed-sores  there  is  only  a  superficial  loss 
of  substance  ;  in  more  severe  cases  the  subcutaneous  cellular  tissue  is  in- 
volved ;  and  in  the  worst  cases  the  muscles  and  fibrous  tissues.  I  have 
met  with  cases  where  Xhe  slough  had  involved  the  connective-tissue  and 
muscles,  and  laid  bare  the  bone.  A  considerable  number  of  typhoid  pa- 
tients who  have  lived  through  the  fever  die  either  from  the  exhausting  ef- 
fects of  these  bed-sores  or  from  the  resulting  septic  poisoning.  The  possi- 
ble occurrence  of  these  complications  must  enter  into  the  prognosis  in  every 
severe  case,  and  the  earlier  they  make  their  appearance  the  greater  the 
danger. 

The  average  duration  of  typhoid  fever  is  from  three  to  four  weeks.  It 
may  terminate  in  death  or  recovery  at  an  earlier  date.  A  typical  case  ex- 
tends over  a  period  of  four  weeks.  The  period  of  invasion  lasts  from  one 
to  five  days.  The  period  of  glandular  enlargement  continues  until  about 
the  fourteenth  day.  The  period  of  ulceration  extends  from  the  twelfth  or 
fourteenth  day  to  between  the  twenty-first  and  twenty-eighth.  When  the 
fever  is  protracted  beyond  the  middle  of  the  fourth  week,  in  most  in- 
stances this  is  due  to  some  complication,  or  to  an  extension  of  the  intestinal 
ulceration.    The  period  of  greatest  danger  is  at  the  close  of  the  third  week. 

Death  rarely  occurs  before  the  fourteenth  day.  The  prominent  direct 
causes  of  death  are  :  toxmmia  ;  asthemia ;  suppression  of  the  excretory 
function  of  the  kidneys  ;  hypercemia  and  oedema  of  the  lungs  ;  intestinal 
hemorrhage  ;  exhaustive  diarrhoea  ;  intestinal  perforation  ;  and  peritonitis 
with  or  without  intestinal  perforation.  In  nearly  all  cases  the  failure  of 
heart-power  is  directly  or  indirectly  the  cause  of  death.  In  no  case  can 
convalescence  be  said  to  be  fairly  established  until  the  temperature  remains 
normal  for  two  successive  evenings.  The  termination,  like  the  commence- 
ment, is  gradual,  and  is  not  marked  by  any  critical  evacuation  or  day  of 
crisis. 

Relapses. — After  typhoid  fever  has  run  its  course,  and  the  patient  is  en- 
tirely free  from  fever,  quite  frequently  there  is  a  new  development  of  the 
fever  ;  these  new  developments  are  called  relapses.  Their  course  corre- 
sponds with  that  of  the  primary  attack,  only  they  are  of  shorter  duration. 
The  temperature  rises  more  rapidly,  the  eruption  reappears,  the  spleen  en- 
larges, the  intestinal  and  abdominal  symptoms  return,  and  all  the  promi- 
nent symptoms  of  the  primary  fever  are  rapidly  developed.     As  a  rule,  the 


638  ACUTE   GEKERAL   DISEASES. 

relapse  is  milder  than  the  primary  attack.  If  it  terminates  fatally,  the  post- 
mortem examination  shows,  in  addition  to  the  cicatrizing  intestinal  ulcers 
of  the  primary  attack,  the  recent  intestinal  changes  of  the  relapse.  The 
lesions  of  the  relapse,  although  of  the  same  character  as  those  of  the  primary 
attack,  are  less  extensive. 

It  is  very  diflBcult  to  give  a  satisfactory  explanation  of  these  relapses. 
Some  claim  that  they  are  the  result  of  certain  plans  of  treatment,  especially 
the  cold-water  plan.  This  assertion  lacks  proof.  Others  hold  that  all  re- 
lapses depend  upon  a  new  infection.  Perhaps  this  is  possible  if  the  patient 
remains  in  the  same  locality  and  has  the  same  surroundings  as  when  he  had 
the  primary  attack ;  but  it  does  not  explain  relapses  in  those  who  are  re- 
moved from  all  the  sources  of  the  primary  infecdon.  Another  explanation 
offered  is  that  a  part  of  the  typhoid  poison  has  remained  in  the  system, 
undeveloped  during  the  primary  attack,  and  that  some  time  after  this  has 
passed  the  poison  reproduces  itself  and  sets  up  a  second  fever.  A  more 
recent  theory  is  that  the  typhoid  poison  thrown  off  in  the  faeces  of  the 
patient  is  reabsorbed  and  causes  the  relapse.  Unquestionably,  it  is  possible 
for  healthy  glands  to  become  inoculated  by  sloughs  thrown  off  from  those 
first  affected.  In  many  cases  it  is  impossible  to  account  for  the  occurrence 
of  the  relapse,  and  all  of  these  explanations  as  to  the  cause  in  any  case  are 
more  or  less  unsatisfactory.  In  those  cases  which  have  come  under  my 
own  observation,  I  have  noticed  that  the  splenic  enlargement  which  has 
existed  during  the  course  of  the  fever  does  not  subside  with  its  decline  ; 
and  that  the  tenderness  along  the  line  of  the  intestines,  especially  in  the 
right  iliac  region,  continues  during  the  period  between  the  original  attack 
and  the  relapse.  In  some  instances,  apparently,  the  relapse  has  been 
brought  on  by  indiscretion  in  diet,  or  by  injudicious  exercise  on  the  part  of 
the  convalescent  patient.  Occasionally  relapses  have  occurred  when  great 
care  had  been  taken  against  any  indiscretion  or  over-exertion.  There  is 
little  doubt  but  that  relapses  are  of  much  more  frequent  occurrence  in  those 
cases  that  are  treated  with  cathartics  during  the  first  week  of  the  fever, 
than  in  those  where  cathartics  are  not  employed. 

Treatment. — Accepting  the  theory  that  the  specific  poison  of  typhoid 
fever  is  contained  in  the  excrements  of  typhoid  patients,  the  j^rs^  indication 
in  prophylaxis  is  to  destroy  this  poison  as  soon  as  it  is  discharged  from  the 
body.  For  this  purpose  the  intestinal  discharges  should  be  received  into 
a  porcelain  bed-pan,  the  bottom  of  which  is  covered  with  a  thin  layer  of 
powdered  sulphate  of  iron  ;  immediately  after  the  discharge,  crude  muriatic 
acid,  equal  in  quantity  to  one-third  of  the  faecal  mass,  should  be  poured 
over  it.  The  discharges  of  a  typhoid  patient  (no  matter  how  thoroughly 
they  may  have  been  disinfected)  should  never  be  emptied  into  a  privy  or 
water-closet.  Trenches  should  be  dug  for  their  reception,  and  new  trenches 
should  be  opened  every  few  days ;  the  greatest  care  must  be  taken  that 
these  trenches  are  not  so  situated  that  the  drainage  from  them  can  con- 
taminate wells  or  springs  which  furnish  drinking  water. 

All  underclothing  or  bed-clothing  that  may  have  become  soiled  by  the 
discharges  from  the  bowels  should  be  immediately  immersed  in  chlorine 


TYPHOID    FEVEK.  639 

water,  and  thoroughly  boiled  within  twenty-four  hours.  These  procedures 
will  certainly  destroy  the  infective  power  of  the  typhoid  poison  contained 
in  the  intestinal  discharges,  and  in  the  majority  of  instances  will  prevent 
the  spread  of  the  fever.  Kepeated  observations  show  that  when  one  mem- 
ber of  a  family  has  typhoid  fever,  not  infrequently  it  is  developed  in  every 
other  member.  This  spread  of  the  disease  can  be  prevented,  unless  there 
is  some  local  cause  for  its  development  which  cannot  be  reached.  When 
its  origin  is  not  apparent,  the  wells,  springs,  and  all  the  sources  from 
whence  water  is  derived  for  drinking  and  cooking  purposes  should  be  care- 
fully and  thoroughly  inspected.  Care  must  be  taken  that  the  waste-pipes 
from  wells  and  springs  do  not  pass  directly  into  cess-pools  or  sewers,  and 
thus  become  a  means  for  the  conveyance  of  impure  gases  into  the  springs 
and  wells.  The  greatest  care  must  be  exercised  in  regard  to  house  drains 
and  sewer  pipes,  that  they  shall  be  free  from  leakage  and  obstruction,  and 
that  all  water-closets,  sinks,  and  other  openings  into  them  be  provided  with 
suitable  traps.  When  unpleasant  odors  are  constantly  present  in  dwellings, 
especially  in  sleeping  apartments,  disinfectants  should  be  emjaloyed,  and 
the  house  be  thoroughly  ventilated.  When  it  is  necessary  to  open  drains 
and  cess-pools  in  a  dwelling  for  purposes  of  repairing  or  cleansing,  the  same 
precautions  should  be  exercised  ;  they  are  especially  of  importance  during 
the  summer  and  autumn. 

The  question  naturally  arises  : — is  it  not  possible  to  counteract  or  neutral- 
ize the  effects  of  the  fever-poison  after  it  has  gained  admission  into  the  sys- 
tem, and  thus  prevent  the  development  of  typhoid  fever  ?  To  accomplish 
this,  blood-letting,  emetics  and  diaphoretics  have  all  been  employed ;  but 
there  is  not  the  slightest  proof  that  typhoid  or  any  fever-poison  was  ever 
removed  from  the  system  by  these  or  any  other  agents.  A  patient  with 
some  of  the  premonitory  symptoms  of  fever  may  perspire,  be  relieved,  and 
at  once  recover,  but  such  a  patient  had  not  received  the  typhoid  poison  into 
the  system,  and  was  not,  as  is  sometimes  said,  "  threatened  with  typhoid 
fever."  Notwithstanding  the  bold  affirmation  of  the  author  of  the  cold 
afPusionplan  of  treatment,  that  if  it  were  resorted  to  before  the  third  day 
of  the  disease,  it  would  invariably  arrest  its  development,  it  has  failed  to 
stand  the  test  of  practical  experience.  More  recently,  sulphate  of  quinine, 
administered  in  large  doses,  has  been  thought  to  have  the  power  of  arrest- 
ing the  development  of  tjnphoid  fever  in  the  same  way  that  it  arrests  mal- 
arial fever,  by  its  anti -periodic  power  ;  but  there  is  no  evidence  that  it  has 
any  such  power,  and  as  a  prophylactic  remedy  it  has  been  abandoned. 

After  the  poison  has  once  gained  entrance  into  the  system,  no  means 
has  as  yet  been  discovered  by  which  it  can  be  counteracted  or  neutralized 
so  as  to  prevent  the  development  of  the  disease.  The  duty  of  the  physician 
is  to  guide  the  disease,  so  far  as  he  may  be  able,  to  a  favorable  issue,  and 
prevent  injury  to  organs  essential  to  life,  keeping  in  mind  that  a  certain 
definite  period  must  elapse  before  this  result  can  be  accomplished. 

The  arrangement  of  the  sick-room  of  fever  patients,  though  often  over- 
looked, is  a  matter  of  no  inconsiderable  importance,  not  only  as  regards  the 
comfort  of  the  patient,  but  also  the  successful  issue  of  the  case.     It  is  of 


640  ACUTE    GENERAL   DISEASES. 

the  greatest  importance  that  a  properly  qualified  nurse  be  selected  ;  one 
who  has  had  experience  in  the  care  of  fever-patients  is  to  be  preferred.  The 
patient  should  be  placed  in  a  large  and  well- ventilated  apartment.  All  fur- 
niture should  be  removed  from  the  sick-room  except  those  articles  which 
are  necessary  for  the  comfort  of  the  patient  and  the  convenience  of  the  at- 
tendants. The  carpets  should  be  removed  from  the  floor  and  the  patient 
placed  in  a  bed  of  moderate  size  in  the  centre  of  the  room.  Free  ventila 
tion  during  both  day  and  night,  is  of  the  utmost  importance.  The  tem- 
perature of  the  apartment  should  be  kept  below  60°  F.  The  bed  and  body 
linen  of  the  patient  should  be  changed  daily,  and  at  once  removed  from  the 
sick-room  and  placed  in  a  weak  solution  of  chlorinated  soda ;  especially 
is  this  important  if  the  patient  is  having  frequent  discharges  from  the 
bowels.  The  apartment  should  be  kept  perfectly  quiet,  the  light  subdued, 
and  only  the  attendants  should  be  allowed  in  the  room.  Any  medicinal  in- 
terference in  a  mild  type  is  unnecessary.  The  treatment  resolves  itself  into 
the  arrangement  of  the  sick-room  and  proper  diet ;  milk  is  the  most  suit- 
able food,  Siud  fruits  are  not  to  he  alloioed  in  any  case.  Even  in  the  mild- 
est case  this  care  in  diet  is  important,  and  the  patient  should  be  kept  in 
bed  until  convalescence  is  fully  established.  This  should  be  insisted  upon 
in  the  mild  as  well  as  in  the  severe  cases. 

The  temperature  in  a  mild  type  of  this  fever  rarely  rises  above  103°  F. ; 
therefore  there  is  no  necessity  for  resorting  to  antipyretic  measures  ;  fre- 
quent sponging  of  the  surface  with  cold  or  tepid  water,  as  is  most  agree- 
able to  the  patient,  will  be  found  of  service.  By  far  the  larger  number  of 
cases  of  this  fever,  however,  are  of  a  more  severe  type,  and  though  the 
treatment  must  be  regulated  by  the  circumstances  which  attend  each  indi- 
vidual case,  more  decided  measures  will  usually  be  necessary.  Typhoid 
fever  is  a  disease  that  has  certain  stages  to  pass  through,  and  there  is 
great  doubt  whether  the  physician  can  shorten  its  duration  by  a  single  day, 
but  experience  warrants  the  belief  that  many  lives  may  be  saved  by  reme- 
dial measures,  used  at  the  proper  time,  and  combined  with  judicious  hy- 
gienic management. 

Unquestionably  one  of  the  most  important  things  to  be  accomplished  ia 
the  reduction  of  temperature,  or  rather  the  keeping  of  the  temperature  be- 
low a  certain  standard.  The  agents  which  have  been  employed  more  re- 
cently for  this  purpose,  namely,  sulphate  of  quinine  and  cold  applications 
to  the  surface,  act  powerfully  in  reducing  the  temperature  and  lessen- 
ing the  severity  of  the  disease.  It  is  claimed  by  many  distinguished  ob- 
servers of  the  present  day  that  the  parenchymatous  degenerations  of  the 
different  organs  and  tissues  of  the  body  which  are  found  in  those  who  die 
of  typhoid  fever  are  due  to  the  prolonged  high  temperature  which  is  pres- 
ent during  the  course  of  this  disease  ;  but  as  yet  there  are  no  facts  to  prove 
this  assertion,  for  the  same  parenchymatous  changes  are  found  in  the  bodies 
of  those  who  have  died  of  diseases  the  course  of  which  was  not  marked  by 
high  temperature,  and  did  not  extend  over  a  period  of  more  than  forty- 
eight  hours.  So  far  as  we  are  able  to  determine  by  analogy  upon  what 
these  parenchymatous  changes  depend,  we  are  led  to  believe  that  the  spe- 


TYPHOID    FEVER.  641 

cific  poison  of  the  disease  lias  more  to  do  with  their  development  than  the 
high  rate  of  temperature.  One  thing  must  be  apparent  to  every  clin- 
ical observer  :  that  the  injurious  effects  of  a  prolonged  high  temperature 
are  early  and  most  markedly  shown  by  disturbances  of  the  cerebro-spinal 
system,  it  is  still  an  unsettled  question  whether  these  disturbances  are  due 
to  the  primary  changes  in  the  constituents  of  the  blood,  which  always  ac- 
company a  high  range  of  temperature,  or  to  the  direct  effects  of  the  high 
temperature  or  of  the  peculiar  poison  on  the  nerve  centres.  Whichever  view 
we  adopt,  the  employment  of  those  means  which  have  the  power  of  safely 
reducing  temperature  is  indicated,  and  when  judiciously  used  they  have 
much  to  do  with  the  safety  of  the  j^atient. 

All  those  means  which  have  been  employed  for  the  reduction  of  tempera- 
ture are  included  under  the  general  term  of  antipyretics,  and  the  treatment 
of  disease  by  the  use  of  these  agents  has  received  the  name  of  antipyretic 
treatment.  Unquestionably  the  most  efficient  and  reliable  of  the  antipyretic 
agents  are  the  external  application  of  cold  by  means  of  baths,  packs  and  af- 
fusions, and  the  internal  administration  of  the  sulphate  of  quinine.  The 
quinine  is  not  administered  to  produce  any  specific  action  upon  the  typhoid 
fever  poison,  but  is  employed  for  its  antij)yretic  power.  There  are  other 
antipyretic  agents  besides  these  two,  but  they  are  of  so  little  importance 
that  it  is  necessary  to  give  them  only  a  passing  notice  after  we  shall  have 
considered  these  two  important  ones. 

At  the  present  time  the  opinion  prevails,  to  a  great  extent,  that  the  ap- 
plication of  cold  to  the  surface  is  the  great  antipyretic  in  the  treatment  of 
fever.  This  is  no  new  teaching.  Long  ago  Dr.  Currie  recommended  the 
application  of  cold  to  the  surface  of  tiie  body  for  the  purpose  of  rapidly  re- 
ducing temperature,  and  proved  that  it  had  such  an  effect ;  yet  it  was  never 
very  generally  practised,  and  soon  fell  into  disuse,  as  there  were  no  reliable 
indications  to  guide  one  in  its  application.  As  we  now  have  the  thermome- 
ter as  such  a  guide,  it  has  been  resorted  to  more  recently  with  considerable 
Buccess.  It  is  employed  in  the  following  manner.  As  soon  as  the  axillary 
temperature  in  the  evening  rises  above  103°  F.,  the  patient  is  placed  in  a 
water-bath  having  a  temperature  of  70°  E.  or  80°  P.,  which  is  gradually 
lowered,  by  the  addition  of  cold  water  or  ice,  until  the  temperature  of  the 
patient  begins  to  fall.  It  may  be  necessary  to  lower  the  temperature  of  the 
bath  to  60°  P.  before  the  temperature  of  the  patient  is  affected.  When  the 
temperature  begins  to  fall,  thermonietrical  observations  should  be  made 
every  two  or  three  minutes,  by  placing  the  thermometer  in  the  rectum.  If 
it  falls  rapidly — that  is,  two  or  three  degrcQS  in  five  or  six  minutes — as  soon 
as  the  temperature  has  reached  103°  F.  the  patient  is  to  be  removed  from 
the  bath ;  if  it  falls  slowly,  as  soon  as  it  reaches  101°  F.  he  should  be  re- 
moved and  immediately  placed  in  bed.  It  is  never  safe  to  keep  the  patient 
in  the  bath  until  the  temperature  shall  have  reached  the  normal  standard  ; 
for  he  may  pass  into  a  state  of  collapse,  since  the  temperature  continues  to 
fall  for  some  time  after  his  removal  from  the  bath.  While  in  the  bath,  cold 
should  be  applied  to  the  head  by  means  of  a  sponge  wet  in  cold  water,  or 
by  an  ice-bag.  The  cold  pack  is  much  less  effective  than  the  bath  ;  but  if 
41 


(J43  ACUTE    GENERAL   DISEASES. 

the  patient  is  too  feeble  to  be  removed,  it  may  be  employed  with  benefit. 
The  patient  is  wrapped  in  a  sheet  wrung  out  of  tepid  water,  and  over  this 
one  wrung  out  of  cold  water  is  applied.  The  latter  may  be  removed  as  it 
becomes  warmed,  and  its  application  and  removal  continued  until  the  de- 
sired fall  in  temperature  shall  be  obtained.  In  severe  cases,  during  the 
first  and  second  weeks,  after  the  temperature  has  been  reduced  by  the  ap- 
plication of  cold  to  the  surface,  it  will  soon  begin  to  rise,  and  continue  to  do 
so  until  it  reaches  its  former  height.  Usually  one  to  three  hours  will  elapse 
before  it  begins  to  rise,  and  from  two  to  six  before  it  reaches  its  former 
height.  It  will  then  be  necessary  to  repeat  the  baths  or  packs,  and  to  con- 
tinue their  use,  both  day  and  night,  from  three  to  six  times  during  the 
twenty-four  hours,  in  order  to  keep  the  temperature  below  103°  F.,  and  ac- 
complish anything  by  this  plan  of  treatment. 

My  experience  in  the  use  of  cold  applications  leads  me  to  believe  that 
unless  it  is  possible  to  maintain  a  low  range  of  temperature  after  four  or 
five  baths  very  little  is  gained  by  their  continuance.  I  am  also  convinced 
that,  after  the  second  week  of  typhoid  fever,  cold  baths  should  not  be  em- 
ployed to  reduce  temperature.  The  condition  of  a  typhoid  patient  during 
the  first  and  second  weeks  of  the  fever  is  very  different  from  that  during  the 
third  and  fourth  weeks.  During  this  latter  period  there  is  great  danger  of 
collapse  after  a  cold  bath,  and  in  several  instances  I  am  confident  that  pul- 
monary complications  have  been  the  result.  In  a  few  instances  the  tem- 
perature can  be  very  rapidly  lowered  by  the  application  of  ice-bags  to  the 
abdomen.  In  some  cases  when  the  patient  is  placed  in  the  cold  bath,  the 
temperature  will  immediately  begin  to  fall ;  in  other  cases  there  will  be  a 
gradual  reduction  of  temperature  as  the  water  is  made  cooler.  In  certain 
severe  cases,  a  patient  may  be  kept  in  a  bath  of  the  temperature  of  60°  F. 
for  the  space  of  half  an  hour  without  the  temperature  falling  a  degree. 
These  cases  are  exceedingly  grave  in  character,  and  the  bath  should  be  used 
with  great  care. 

There  is  no  remedial  agent  wMcJi  requires  greater  care  and  judgment  in 
its  use  than  the  cold  bath,  yet,  doubtless,  when  Judiciously  employed,  the 
lives  of  many  typhoid  patients  may  be  saved,  and  it  is  equally  certain  that 
when  injudiciously  employed  many  lives  may  be  destroyed.  The  general 
condition  of  a  patient  and  the  stage  of  the  fever  must  be  considered ;  also 
the  effects  of  the  first  few  baths  must  be  carefully  noted.  Should  a  pa- 
tient's temperature  range  at  104°  F.  or  105°  F.,  it  is  no  positive  indication 
for  the  resort  to  a  cold  bath,  or  that  a  cold  bath  is  the  best  agent  to  be  em- 
ployed for  its  reduction.  If  the  patient  after  the  second  or  third  bath  is 
more  quiet,  has  less  delirium  (if  delirium  previously  existed),  if  his  breath- 
ing becomes  easy  and  natural,  if  the  heart's  action  is  more  regular  and 
forcible,  and  he  falls  asleep  and  perspires,  there  can  be  no  question  in  re- 
gard to  the  beneficial  effects  of  the  bath.  If,  on  the  other  hand,  the  bath 
is  followed  by  feebler  heart's  action,  by  dusky  cheeks,  by  rapid  respiration, 
and  by  coldness  of  the  extremities,  from  which  condition  the  patient 
rallies  slowly  and  imperfectly,  it  is  certain  that,  however  high  the  tem- 
perature may  range,  harm  will  be  done  by  continuing  the  baths.     When 


TYPHOID   PEVEE.  643 

the  extremities  are  cold,  or  there  is  j)rofuse  hemorrhage  from  the  bowels, 
or  when  from  any  cause  there  is  great  feebleness  of  the  heart's  action,  and 
especially  in  the  case  of  aged  persons,  cold  baths  are  contraindicated. 

Cold  compressions  or  ice-bags  applied  to  the  abdomen,  in  addition  to 
their  beneficial  effect  on  tlie  intestinal  changes  which  constitute  such  an 
important  element  in  the  history  of  this  fever,  often  have  great  power  in 
reducing  the  general  heat  of  the  body.  I  have  also  in  some  instances 
found  the  body  temperature  rapidly  lowered  by  injections  of  ice-water  into 
the  rectum.  Care  must  be  exercised  that  the  cold  injections  are  not  ad- 
ministered too  rapidly  or  in  too  large  quantities.  Although  this  mode  of 
aostracting  heat  and  lowering  the  body  temperature  is  never  so  effective  as 
by  baths  and  paclcs,  still  it  has  this  advantage,  that  no  such  compensating 
increase  in  the  production  of  heat  follows  the  use  of  the  cold  injections  as 
follows  the  cooling  of  the  external  surface  by  the  baths.  In  many  cases  the 
extreme  obstinacy  of  the  fever,  which  resists  the  most  systematic  use  of 
cold,  as  well  as  the  fact  that  some  patients  cannot  bear  a  sufficiently  fre- 
quent repetition  of  the  baths  as  to  effect  the  desired  result,  or  that  there 
may  be  contraindications  to  their  use,  necessitates  the  employment  of  other 
means  for  the  reduction  of  the  body  temperature. 

The  antipyretic  power  of  sulphate  of  quinine  is  established  beyond  ques- 
tion. When  quinine  is  employed  as  an  antipyretic,  however,  it  must  be 
given  in  large  doses  ;  the  administration  of  two  grains  every  two  hours,  or 
a  larger  quantity  administered  in  divided  doses  within  a  period  of  twenty- 
four  hours,  will  not  act  as  an  antipyretic  ;  but  thirty  or  forty  grains  must 
be  administered  within  a  period  of  two  hours.  If  the  stomach  is  irritable, 
and  a  large  dose  produces  vomiting,  ten  grains  may  be  given  every  half 
hour  until  the  desired  quantity  has  been  administered.  Usually  from  four 
to  six  hours  after  the  antipyretic  dose  has  been  taken,  the  temperature 
will  begin  to  fall  and  in  about  twelve  hours  it  will  reach  its  minimum ; 
then  it  will  remain  stationary  from  twelve  to  twenty-four  hours.  After  the 
temperature  has  once  been  reduced  by  the  quinine,  its  administration  may 
be  discontinued  until  the  temperature  shall  again  rise  to  105°  F.  As  a 
rule,  the  temperature  rarely  ranges  as  high  as  before  the  quinine  was  ad- 
ministered. This  mode  of  administering  quinine  in  antipyretic  doses  to 
fever  patients  rarely  produces  any  symptom  of  cinchonism,  other  than  a 
transient  deafness  after  the  first  dose.  In  a  large  number  of  cases  the 
temperature  can  be  kept  below  103°  F.  by  the  sulphate  of  quinine  ;  but  in 
very  severe  cases  it  will  be  advisable,  sometimes  it  will  be  absolutely  neces- 
sary, to  employ  not  only  the  quinine,  but  at  the  same  time  the  cold  baths. 

My  rule  is,  after  I  have  reduced  the  temperature  to  101°  F.  or  102°  F., 
by  a  cold  bath,  to  administer  an  antipyretic  dose  of  quinine,  and  thus  delay 
the  recurring  rise  of  temperature.  While  the  cold  bath  more  rapidly  re- 
duces temperature,  the  effect  of  the  quinine  is  more  lasting  ;  consequently 
by  making  use  of  both  of  these  reliable  antipyretics  during  the  first  two 
weeks  it  is  possible  to  control  the  temperature  during  that  time.  After  this 
period  it  is  not  safe  to  resort  to  cold  baths  ;  but  when  the  temperature 
rises  above  103°  F.,  occasionally  the  cold  pack  may  be  used  in  connection 


644  ACUTE   GE]SrEEAL   DISEASES. 

with  antipyretic  doses  of  quinine.  If  during  the  third  and  fourth  weeks, 
these  means  fail  to  reduce  the  temperature,  from  ten  to  twenty  grains  of 
powdered  digitalis  may  be  administered  within  twenty-four  hours,  unless 
the  pulse  is  very  frequent  and  irregular — when  its  use  is  contraindicated. 

As  an  antipyretic,  digitalis  should  be  employed  only  when  quinine  is 
given.  It  seems  to  increase  the  antipyretic  power  of  the  quinine,  but  has 
little  or  no  power  when  administered  alone.  The  use  of  all  antipyretic 
remedies  must  be  persisted  in  until  the  desired  end — the  reduction  of  tem- 
perature— is  accomplished  ;  but  the  peculiarities  of  each  patient  must  be 
studied,  and  these  agents  must  be  so  administered  as  to  suit  each  individual 
case.  The  satisfactory  results  obtained  by  the  systematic  use  of  these 
remedies  justifies  their  employment  ;  but  the  exact  rules  which  are  to  gov- 
ern one  in  their  use,  as  to  manner  and  time,  can  only  be  determined  by  ex- 
perience. 

If  the  temperature  of  a  patient  can  be  kept  below  103°  F.,  during  the 
first  two  weeks  of  the  fever,  the  first  and  perhaps  the  most  important 
thing  in  the  treatment  of  this  disease  will  be  accomplished. 

Toward  the  end  of  the  second,  or  during  the  third  week,  signs  of  failure 
of  heart-power  begin  to  manifest  themselves  ;  although  the  temperature 
may  not  rise  higher  than  101°  F.,  the  pulse  frequently  becomes  extremely 
feeble  and  irregular  and  reaches  140  per  minute,  while  the  first  sound  of 
the  heart  becomes  inaudible  at  times  ;  the  surface  is  cool  and  moist ;  the 
patient  complains  of  a  sense  of  exhaustion,  and  perhaps  is  unable  to  turn  in 
bed ;  muscular  tremors,  dry,  brown  tongue,  and  all  the  symptoms  which, 
indicate  failure  of  vital  power  are  present. 

Under  these  circumstances  the  use  of  stimulants  seems  to  be  urgently 
demanded. 

A  few  simple  rules  govern  their  administration. 

First.  They  should  never  be  administered  indiscriminately — that  is, 
simply  because  the  patient  has  typhoid  fever. 

Second.  When  there  is  reasonable  doubt  as  to  the  propriety  of  giving  or 
withholding  stimulants,  it  is  safer  to  withhold  them,  at  least  until  the  signs 
which  indicate  their  use  become  more  marked. 

Third.  In  every  case,  but  especially  when  stimulants  are  not  clearly  in- 
dicated, the  effect  of  the  first  few  doses  should  be  carefully  noted.  There 
are  few  whose  experience  in  the  treatment  of  typhoid  fever  is  such  as  to- 
enable  them  to  determine  positively,  from  the  appearance  of  the  patient, 
when  the  administration  of  stimulants  should  be  commenced. 

If  under  their  use  the  tongue  becomes  dry,  the  patient  more  restless,  the 
delirium  more  active,  the  temperature  higher,  and  the  pulse  more  fre- 
quent, it  is  very  certain  that  stimulants  are  contraindicated.  If,  on  the 
other  hand,  the  pulse  becomes  fuller  and  more  regular,  if  the  first  sound 
of  the  heart  is  more  distinctly  heard,  or  if,  having  been  absent,  it  returns, 
if  the  restlessness  and  delirium  are  less  marked,  the  tongue  more  moist, 
and  the  patient  more  intelligent,  it  is  equally  certain  that  the  time  for  ad- 
ministering stimulants  has  arrived.  When  their  use  is  once  begun,  it  is  of 
the  greatest  importance  to  administer  them  at  stated  intervals,  especially 


TYPHOID    FEVER.  645 

during  the  night.  In  a  severe  case  of  typhoid  fever,  free  stimulation,  just 
at  a  critical  period  (which  may  not  lust  more  than  twenty-four  hours), 
will  often  be  followed  by  a  refreshing  sleep,  and  the  patient  may  rapidly 
pass  from  an  apparently  hopeless  condition  to  one  of  convalescence. 

The  third  important  thing  to  be  accomplished  in  the  management  of 
typhoid  fever  patients  is  the  maintenance  of  nutrition.  The  principal 
effects  of  the  typhoid  poison  are  manifested  in  the  changes  which  take 
place  in  the  lymphatics  of  the  gastro-intestinal  tract.  Experience  has 
taught  us  that  the  enfeeblement  of  the  digestive  and  assimilative  powers, 
due  to  these  glandular  changes,  which  is  manifested  from  the  very  com- 
mencement of  the  fever,  renders  the  digestion  of  solid  food  impossible,  and 
for  a  long  time  it  has  been  the  rule  of  the  profession  to  allow  typhoid  fever 
patients  only  liquid  food.  There  has  been,  and  still  is,  great  diversity  of 
opinion  in  regard  to  the  special  articles  of  diet  best  suited  to  this  class  of 
patients.  There  is  no  disease  in  which  a  waste  of  all  the  tissues  of  the  body 
goes  on  so  rapidly  as  in  typhoid  fever. 

Milk  is  an  article  of  diet  which  furnishes  the  elements  of  nutrition  neces- 
sary to  repair  this  rapid  waste,  and  there  are  not  the  objections  to  its  use 
which  are  against  animal  broths  and  gruels.  Although  there  have  been, 
and  still  are,  in  some  quarters,  strong  objections  against  its  use  as  an  article 
of  diet  in  fevers,  recently  it  has  been  regarded  with  more  favor,  and  those 
who  have  had  most  extended  opportunities  for  testing  its  nutritive  qualities 
have  come  to  regard  it  as  the  only  article  of  diet  required  by  typhoid 
patients.  In  it  we  not  only  find  all  the  elements  required  for  repairing  the 
rapidly  wasting  tissues,  but  they  are  in  a  condition  to  be  most  readily 
assimilated  by  the  enfeebled  digestive  apparatus.  In  order  that  it  shall  not 
become  distasteful  to  the  patient  some  variations  must  be  made  in  its 
preparation.  It  may  be  simply  curdled,  boiled,  frozen,  slightly  fermented, 
or  mixed  with  lime-water,  seltzer,  or  some  other  mineral  water,  and  various 
palatable  preparations  can  be  made  from  milk  which  has  been  partially 
digested  with  pepsin  or  pancreatin.  If  agreeable,  buttermilk  may  be  sub- 
stituted for  a  time.  The  quantity  of  milk  is  not  limited  ;  the  patient  may 
take  all  his  stomach  will  digest — usually  j^atients  will  take  from  four  to 
six  quarts  in  the  twenty-four  hours.  After  the  patient  has  passed  into  the 
fourth  week  of  the  disease  it  may  be  necessary  to  administer  cream  and  the 
yolks  of  eggs  in  connection  with  the  milk. 

I  now  come  to  the  treatment  of  the  accidents  of  the  disease. 

Diarrlima. — The  poison  which  produces  this  fever  unquestionably  has  a 
specific  action  upon  the  intestinal  glands  and  lymphatics.  It  is  here  that 
we  find  the  characteristic  lesions  of  the  disease,  and  it  is  scarcely  ques- 
tioned that  the  typhoid  poison,  to  a  great  extent,  gains  entrance  to  the 
system  through  these  glands  and  lymphatics,  and  here  produces  the  primary 
irritation.  Following  the  irritation  and  inflammation  of  the  follicles,  other 
portions  of  the  mucous  membrane  become  involved,  and  a  catarrhal  inflam- 
mation of  the  mucous  membrane  of  the  intestinal  tract  follows.  The  nec- 
essary consequence  of  this  is  a  diarrliffial  discharge,  which  is  simply  an  in- 
dication that  these  intestinal  changes  are  going  on  ;  it  is  not  due  to  the 


646  ACUTE    GENERAL   DISEASES. 

elimination  of  the  typhoid  fever  poison,  but  to  the  inflammation  which  the 
fever  poison  has  excited  in  the  intestinal  glands.  When  the  diarrhoea  is 
present  in  the  earlier  period  of  the  disease,  it  is  better  to  let  it  alone,  as 
during  the  first  and  second  weeks  the  danger  is  very  slight.  It  has  been 
proposed  to  treat  this  diarrhoea,  which  makes  its  appearance  early  in  the 
disease,  with  alkalies,  bismuth,  pepsin,  etc.  It  is  claimed  that  if  these 
remedies  be  administered,  diarrhoea  can  be  prevented,  or,  if  it  already 
exists,  that  it  can  be  controlled.  Theoretically,  I  see  no  reason  for  employing 
alkaline  remedies,  for  the  diarrhoeal  discharges  are  always  alkaline,  and 
from  clinical  observation,  I  am  convinced  that  bismuth,  pepsin,  etc.,  have 
little  or  no  effect  either  in  controlling  the  diarrhoea  or  in  preventing  the 
intestinal  changes  which  produce  it. 

When  diarrhoea  commences  late  in  the  disease  (during  the  latter  part  of 
the  third,  or  during  the  fourth  week  of  the  fever),  it  is  of  a  very  different 
character  from  that  which  occurs  during  the  first  and  second  weeks.  Ul- 
ceration of  the  intestinal  glands,  and  perhaps  sloughing  has  been  estab- 
lished, and,  in  addition  to  the  extensive  local  changes,  there  is  a  septic  ele- 
ment which  enters  into  the  causation  of  the  diarrhoea  at  this  stage.  Be- 
sides, the  increased  peristaltic  action  of  the  intestines,  which  attends  the 
diarrhoea,  favors  an  extension  of  the  inflammatory  processes  to  the  peri- 
toneum, especially  that  portion  which  covers  Peyer's  patches.  In  view  of 
these  facts,  the  diarrhoea  should  be  arrested  or  held  in  check.  For  the 
accomplishment  of  this,  there  is  but  one  remedy  which  can  be  relied  upon 
— that  is  opium.  My  experience  is  against  the  use  of  astringents,  if 
opium  will  not  arrest  it,  one  may  expect  little  aid  from  astringents  com- 
bined with  opium  as  they  are  usually  administered.  The  use  of  opium  is 
objected  to  by  some,  who  claim  that  it  diminishes  the  power  of  the  heart's 
action  ;  but  in  this  disease,  when  administered  in  small  doses,  it  seems  to 
me  to  increase  rather  than  diminish  the  heart-power.  It  is  acknowledged 
that  opium,  more  than  any  other  drug,  arrests  the  peristaltic  action  of  the 
intestines  ;  and  that  is  what  we  wish  to  accomplish  when  diarrhoea  is  pres- 
ent during  the  third  and  fourth  week  of  typhoid  fever. 

When  during  convalescence  diarrhoea  is  persistent,  the  patient  should  be 
kept  in  bed  and  some  of  the  vegetable  astringents,  as  catechu  or  hasmatoxy- 
lon,  may  be  employed. 

Tympanitis. — When  this  has  proved  a  distressing  symptom,  I  have 
usually  found  relief  to  be  obtained  by  the  application  of  turpentine  stupes 
to  the  abdomen.  Some  claim  that  if  turpentine  be  administered  internally 
from  the  beginning  to  the  end  of  typhoid  fever,  tympanitis  and  the  intes- 
tinal changes  which  lead  to  it  and  to  the  diarrhoea  are  much  less  severe.  I 
am  confident  that  the  turpentine  treatment,  as  it  is  called,  does  not  have 
the  controlling  influence  over  this  fever  which  has  been  claimed  for  it ;  but 
I  am  certain  that  it  is  our  most  reliable  agent  for  the  relief  of  the  tym- 
panitis. 

Intestinal  Hemorrhage. — When  this  occurs  early  in  the  fever,  it  usually 
requires  no  treatment ;  but  when  it  occurs  during  the  third  or  fourth  week, 
or  after  convalescence  is  apparently  fully  established,  it  must  be  arrested  as 


TYPHOID    FEVER.  647 

promptly  as  possible.  The  occurrence  of  severe  intestinal  hemorrhages 
may  sometimes  be  prevented  by  keeping  the  patient  in  bed.  A  typhoid 
fever  patient  should  not  be  allowed  to  get  out  of  bed  from  the  beginning  of 
the  attack  until  convalescence  is  fully  established.  Especially  is  this  of 
importance  if  the  case  is  a  severe  one,  and  attended  by  symptoms  that  indi- 
cate extensive  intestinal  lesions.  When  hemorrhage  from  the  intestines 
occurs  during  the  third  or  fourth  week  of  the  fever,  it  is  most  surely  con- 
trolled by  the  administration  of  opium  in  small  doses  at  short  intervals. 
Absolute  rest  of  the  body  must  be  insisted  on,  the  patient  must  not  be 
turned  on  the  side  or  moved  in  bed,,  and  an  ice-bag  should  be  applied 
over  the  abdomen.  I  doubt  if  any  good  results  can  be  accomplished  by 
the  use  of  astringents,  either  by  enemata  or  by  the  mouth,  as  it  is  not 
known  that  they  even  reach  the  seat  of  the  hemorrhage,  although  gallic 
acid  and  the  persulphate  of  iron  are  usually  recommended  in  cases  of  in- 
testinal hemorrhage  occurring  in  typhoid  fever.  If  the  hemorrhage  is  pro- 
fuse, it  may  be  necessary  to  keep  the  patient  under  the  influence  of  opium 
for  a  week  or  ten  days ;  in  such  cases  the  internal  use  of  turpentine  in  con- 
nection with  the  opium  will  be  found  of  service. 

Peritonitis. — When  perforation  of  the  intestine  occurs,  the  case  may  be 
regarded  as  hopeless  ;  death  takes  place  usually  within  twenty-four  hours, 
as  the  result  of  general  peritonitis  ;  no  plan  of  treatment  avails  anything. 
If  the  peritonitis  occur  without  perforation,  from  extension  of  the  inflam- 
matory process  from  the  intestinal  ulcers,  bringing  the  patient  rapidly  into 
a  state  of  semi-narcotism  and  holding  him  there  for  five  or  six  days  may 
prevent  the  occurrence  of  the  perforation,  and  thus  save  life.  Such  a  case  is 
to  be  treated  in  every  respect  as  one  of  localized  peritonitis.  After  recovery 
from  an  intestinal  hemorrhage  or  a  localized  peritonitis  in  typhoid  fever 
great  care  should  be  exercised  in  the  administration  of  cathartics  or  ene- 
mata. The  bowels  will  move  spontaneously  after  a  time,  even  though  the 
use  of  opium  be  continued,  and  no  harm  will  follow  should  two  or  three 
weeks  pass  before  they  do  so.  When  the  stomach  is  irritable,  the  hypodermic 
injection  of  morphine  is  preferable  to  opium  administered  by  the  mouth. 

Broncldtis. — For  the  catarrh  of  the  larger  bronchial  tubes  no  special 
treatment  is  required ;  but,  if  the  bronchitis  becomes  capillary,  great  relief 
will  be  obtained  from  the  application  of  dry  cups  to  the  chest  and  the  in- 
ternal administration  of  carbonate  of  ammonia.  Vapor  inhalations  will 
also  be  found  of  service  in  severe  cases. 

Pneumonia. — The  pneumonia  which  complicates  typhoid  fever  in  nearly 
every  case  is  lobular  in  character.  The  signs  which  indicate  its  occurrence 
are  sudden  rise  of  temperature,  increased  frequency  of  respiration,  and  the 
physical  signs  of  localized  pulmonary  consolidation  ;  cough  and  expectora- 
tion are  rarely  present.  Its  occurrence  is  always  an  indication  that  stimu- 
lants should  be  administered.  If  they  are  being  administered,  they  should 
be  increased  in  quantity.  To  prevent  or  relieve  the  hypostatic  congestion 
of  other  portions  of  the  lung,  which  frequently  accompanies  pneumonic  de- 
velopment, the  heart-power  must  be  increased,  and  the  position  of  the 
patient  changed. 


648  ACUTE    GENEEAL   DISEASES. 

Laryngitis. — T'or  the  relief  of  the  laryngitis  which  occasionally  compli- 
cates typhoid  fever,  a  small  blister  may  be  applied  on  either  side  below  the 
angle  of  the  jaw,  and  the  whole  neck  enyeloped  in  a  poultice.  If  these 
measures  fail,  and  suffocation  aj)pears  imminent,  tracheotomy  should  be 
resorted  to  without  delay. 

Sui-acute  gastric  catarrh,  occurring  as  a  complication  during  conva- 
lescence from  the  fever,  can  only  be  managed  successfully  by  giving  the 
stomach  rest  as  far  as  possible,  restricting  the  diet  to  a  single  tablespoonful 
of  milk  at  a  time,  and  applying  hot  fomentations  over  the  epigastrium. 

Bed-sores. — The  severer  forms  of  bed-sores  are  the  most  intractable  com- 
plications one  has  to  combat.  Fortunately  the  severer  forms  are  much  less 
frequently  met  with  under  the  more  recent  plan  of  treatment.  Scrupu- 
lous cleanliness  is  the  principal  means  for  preventing  their  development. 
So  long  as  there  are  no  erosions,  the  parts  should  be  frequently  bathed  in 
spirits  of  camphor,  and  the  points  of  attack  should  be  relieved  from  all 
pressure.  If  the  sores  penetrate  the  integument,  they  should  be  frequently 
washed  with  a  weak  solution  of  carbolic  acid,  or  brushed  over  with  equal 
parts  of  balsam  of  Peru  and  balsam  copaiva,  and  afterward  covered  with  dry 
lint,  or  lint  covered  with  vaseline.  The  most  unfavorable  cases  are  those  in 
which  the  point  of  pressure  caused  by  the  weight  of  the  body  becomes  gan- 
grenous. In  such  cases,  a  continuous  warm  bath  is  recommended  by  some. 
As  soon  as  sloughing  takes  jDlace,  and  the  parts  separate,  they  should  be 
dressed  with  lint  saturated  with  balsam  of  Peru  and  carbolic  acid. 

Constipation. — As  already  stated,  diarrhoea  is  usually  present  in  the  early 
period  of  this  fever  ;  but  sometimes  there  is  constipation.  The  question 
arises  : — is  the  administration  of  cathartics  ever  admissible  in  typhoid  fever  ? 
Quite  diverse  views  are  still  held  in  regard  to  this  question.  Eecently, 
certain  observers  of  extended  experience  have  claimed  that  there  is  suffi- 
cient reason  for  the  belief  that  a  portion  of  the  typhoid  jDoison  lodged  in  the 
alimentary  tract,  may  be  expelled  by  the  timely  administration  of  cathar- 
tics, and  thus  the  severity  of  the  fever  be  mitigated  and  its  duration  short- 
ened. Eecent  German  writers  claim  that  calomel  acts  beneficially  only  as 
a  cathartic.  Those  who  favor  the  administration  of  cathartics  recommend 
their  use  mainly  during  the  first  week  of  the  disease.  On  the  other  hand, 
equally  competent  observers  maintain  that  the  intestinal  changes  are  aug- 
mented and  rendered  more  extensive  by  the  action  of  cathartics,  that  the 
normal  course  of  the  fever  is  interfered  with,  and  that  in  a  large  proportion 
of  cases  where  intestinal  and  peritoneal  complications  occur,  hypercatharsis 
has  been  induced  at  an  early  period  of  the  fever  by  the  administration  of 
cathartics  for  the  purpose  of  shortening  its  duration.  My  own  experience 
leads  me  to  exercise  the  greatest  caution  in  the  administration  of  cathartics 
in  any  stage  of  this  fever. 

I  am  confident  that  the  routine  practice  of  administering  purgative 
medicines  in  the  early  stage  of  tyjDhoid  fever  can  only  be  followed  by 
a  threefold  injury  '.—first,  the  patient  is  weakened.  Secondly,  the  local 
intestinal  lesions  are  increased.  Thirdly,  perforation  and  peritonitis  are  more 
liable  to  occur. 


TYPHOID    FEVEE.  649 

Kervous  Phenomena. — Should  headache  be  severe,  not  readily  relieved 
by  fomenting  the  forehead  and  temples  with  warm  water,  or  should  it  give 
place  to  active  delirium  and  other  severe  nervous  disturbances,  the  ques- 
tion presents  itself  : — shall  anodynes  be  administered  ?  If  they  are  to  be 
used  the  most  reliable  is  opium,  and  usually  the  condition  of  the  pupil 
of  the  eye  will  serve  to  indicate  whether  opium  shall  or  shall  not  be  ad- 
ministered. A  contracted  or  ''pin-hole"  pupil  maybe  considered  to  contra- 
indicate  its  use,  though  there  are  exceptional  cases  in  which  opium  acts 
favorably,  notwithstanding  this  condition  of  the  iiuj)il.  Opium  should  be 
given  with  great  caution  whenever  signs  of  cyanosis  are  present.  In  all 
cases  of  typhoid  fever,  it  is  safer  to  administer  opium  in  small  and  repeated 
doses  than  to  venture  upon  the  administration  of  one  large  dose.  There 
are  other  anodynes  which  will  sometimes  be  of  service,  such  as  hyoscyamus, 
chloral  and  the  bromides.  Chloral  is  said  to  have  a  special  value  in 
quieting  active  delirium,  which  is  sometimes  so  troublesome,  but  my 
own  experience  in  its  use  has  not  been  favorable. 

When  anodynes  have  failed  to  give  relief  to  typhoid  fever  patients,  who 
have  been  delirious  and  somnolent  for  days,  they  will  sometimes  become 
quiet  and  fall  asleejD  immediately  after  the  free  administration  of  stimu- 
lants. Those  cases  in  which  the  nervous  symptoms  are  due  to  an  anaemic 
condition  of  the  brain,  associated  with  a  weak  heart  and  a  flagging  circu- 
lation, are  most  likely  to  be  benefited  by  the  use  of  stimulants.  In  those 
cases  in  which  subsultus  becomes  very  marked,  and  there  is  general 
tremor,  jactitation  and  restlessness,  I  have  seen  most  hapjoy  effects  pro- 
duced by  the  use  of  hypodermic  injections  of  sulphuric  ether.  I  would 
use,  as  an  average  quantity,  four  drachms,  given  in  injections  of  one  drachm 
each,  in  different  places.  The  same  watchful  care  should  be  taken  of  a 
typhoid  fever  patient  during  convalescence  as  during  the  active  period  of 
the  fever.  The  number  of  typhoid  patients  who  die  during  convalescence 
is  relatively  large. 

Death  is  often  due  to  the  fact  that  the  physician  has  laid  down  no 
strict  rules  to  be  observed  as  to  diet  and  exercise,  and  frequently  from  the 
non-observance  of  such  rules  when  they  have  been  given.  The  diet  of 
fever  patients  during  convalescence  should  be  carefully  watched.  Only 
small  quantities  of  food  should  be  taken  at  a  time,  so  that  the  gastric 
juice  secreted  by  the  enfeebled  stomach  may  be  sufficient  for  its  complete 
digestion.  All  indigestible  articles  of  food,  and  those  which  furnish  a 
large  amount  of  waste,  should  be  strictly  forbidden.  An  apparently  in- 
significant disturbance  of  tne  stomach,  a  slight  vomiting,  or  a  moder- 
ate diarrhoea  occurring  during  the  period  of  convalescence,  should  be 
regarded  as  dangerous,  for  any  one  of  these  may  induce  a  sub-acute 
gastritis,  or  lead  to  intestinal  perforation  and  a  fatal  peritonitis.  It  is 
obvious  that  while  the  intestinal  ulcers  are  healing  much  mischief  may  be 
done  by  improper  diet.  Notwithstanding  the  cravings  of  the  patient's 
appetite,  the  diet  must  be  restricted  to  such  articles  as  milk,  cream,  gruels, 
jellies,  and  animal  broths.  Solid  food  must  be  strictly  forbidden,  espe- 
cially meats,  vegetables,  and  fruits.     If  diarrhoea  is  present  during  conva- 


650  ACUTE   GENERAL   DISEASES. 

,a!sceiice  it  is  far  safer  to  restrict  the  patient  to  milk  and  cream.  All  ex- 
ercise, except  simple  walking  around  the  sick-room,  should  be  prohibited. 
It  is  of  the  greatest  importance  that  this  class  of  patients  should  keep  in 
the  recumbent  or  semi-recumbent  posture  until  the  cicatrization  of  the  in- 
testinal ulcers  is  completed,  which  in  some  instances  does  not  take  place 
until  two  or  three  weeks  after  convalescence  is  well  established.  If  con- 
valescence is  ."^low,  small  doses  of  quinine,  iron,  and  cod-liver  oil  are  of 
service.  They  should  be  given  after  the  patient  has  taken  food.  In  many 
cases  it  is  important  to  take  the  evening  temperature  for  at  least  two  weeks 
after  the  commencement  of  convalescence,  for  by  its  range  it  will  be  pos- 
sible to  more  accurately  determine  the  exact  condition  of  the  patient. 
When  convalescence  is  delayed,  so  that  at  the  end  of  four  or  five  weeks  the 
patient  has  not  regained  strength,  change  of  air  is  indicated. 

YELLOW    FEVEE. 

Yellow  fever  is  a  mias^natic  contagious  disease,  usually  epidemic  ;  it  pre- 
vails most  in  tropical  regions,  and  is  characterized  by  a  yellowish  discolora- 
tion of  the  skin.  From  some  of  its  more  prominent  symptoms  it  has  been 
called  typhus  iderodes,  hlack-vomit  or  Jicemo-gasiric  fever,  fehris  Jiava,  and 
also  mal  de  Siam. 

Morbid  Anatomy. — The  pathological  changes  of  yellow  fever  have  much 
that  is  common  both  to  contagious  and  miasmatic  diseases.  Its  most  con- 
stant and  characteristic  lesion  is  to  be  found  in  the  changes  which  take  place 
in  the  liver. 

The  liver  is  usually  slightly  enlarged  ;  it  may,  however,  be  normal,  or  even 
slightly  diminished  in  size.  The  most  striking  change  is  in  its  color,  which 
has  been  described  as  butter-,  cheese-,  mustard-,  or  chamois-yellow.  Some- 
times it  is  of  a  chocolate  or  bright  orange  color.  The  change  in  color 
may  be  uniform  throughout  the  entire  organ,  or  it  may  occur  in  ir- 
regular patches  of  different  hues.  Slight  extravasations  of  blood  are 
sometimes  found  on  its  surface.  In  some  few  instances  this  change  will  be 
confined  to  a  single  lobe  or  a  circumscribed  portion  of  the  organ.  The 
liver-tissue  breaks  down  readily  on  firm  pressure,  and  on  section  is  drier 
than  normal,  containing  less  blood.  Small  points  of  extravasation  some- 
times stud  its  substance. 

Under  the  microscope  the  liver  cells,  while  unaltered  in  shape,  are  seen 
to  be  filled  with  oil-globules,  so  large  that  at  times  one  globule  occupies  an 
entire  cell.  Sometimes  the  change  is  a  granular  one,  the  nuclei  of  the 
hepatic  cells  being  obscured;  or  they  have  entirely  disappeared.'  This 
change  is  an  acute  fatty  degeneration,  and  not  an  infiltration,  as  many  sup- 
pose. The  organ  in  its  gross  as  well  as  in  its  minute  anatomical  changes 
resembles  the  fatty  degeneration  of  the  drinker's  liver.  Cornil  and  Ean- 
vier^  say  this  degeneration  is  secondary  to  a  congested  and  ecchymosed  state 
of  the  liver. 

1  Yellow  Fever  considered  in  its  Histoi'ical,  Pathological,  Etiological^  and  Therapeutical  Relations,    R. 
La  Roche.    Philadelphia,  1855.     Yellow  Fever.    Fritz  Haeniscb.     Ziemssen's  Cyc.  Prac.  Med.,  vol.  1. 
*  Patholog.  Histology. 


TELLOW   FEVEE.  651 

^~fie  heart  is  lighter  in  color  than  normal,  soft,  friable  and  flabby.  It 
creaks  down  readily  under  firm  pressure,  and  resembles  strongly  in  its  gross 
and  microscopical  characters  the  heart  of  typhoid  fever.  The  muscular 
elements  undergo  the  same  granular  degeneration,  which  cannot  be  ascribed 
to  prolonged  high  temperature,  for  in  yellow  fever  the  temperature  is  neither 
high  nor  does  it  persist  above  normal  for  a  long  time.  As  in  typhoid,  so  here 
we  are  inclined  to  regard  the  degenerative  changes  as  the  result  of  the 
specific  poison  of  the  disease.  The  cavity  of  the  ^pericardium  usually  con- 
tains one  or  two  ounces  of  blood-stained  serum.  Long  coagula  or  partly 
organized  clots  extend  from  the  heart  cavities  quite  a  distance  into  the  ves- 
sels. These  coagula  are  tlie  result  of  the  heart-failure,  and  are  formed 
during  the  few  last  hours  of  life.  Sometimes  the  blood  in  the  heart  is  fluid, 
varying  in  color  and  reaction. 

The  Mood-changes  are  similar  to  those  of  typhoid  and  typhus  fever,  yet 
are  more  extensive  than  in  either  ;  the  blood  is  of  a  darker  color  than 
normal,  and  coagulates  very  much  more  slowly  and  imperfectly  than 
normal ;  a  fact  due  either  to  a  diminution  in,  or  to  a  j)artial  loss  of  the 
coagulating  power  of  the  fibrin-factors.  The  red  blood  globules  are  de- 
stroyed, or  they  are  serrated  and  shrivelled,  and  in  many  instances  broken 
down — this  explains  the  yellow  color  of  the  surface  which  gave  the  name 
to  the  disease.  A  solution  of  part  of  the  red  corpuscles  occurs,  and  the 
hsematin  is  changed  into  bile  pigment.  This  condition  of  the  blood  also 
explains  to  a  certain  extent  the  degenerations  which  are  found  in  the  dif- 
ferent organs  of  the  body.  Very  soon  after  withdrawal  the  blood  under- 
goes ammoniacal  decomposition,  due  in  part  to  the  altered  relation  of  its 
salty  constituents.  Some  affirm  that  the  blood  contains  free  ammonia.  It 
contains  no  free  pigment. 

The  mucous  memhrane  of  the  oesoiDhagus,  stomach  and  small  intestine  is 
always  the  seat  of  a  more  or  less  acute  catarrh.  The  veins  are  varicose  and 
turgid,  often  giving  rise  to  arborescent  injection  of  the  membrane ;  and 
ecchymotic  spots  of  extravasation  irregularly  stud  its  surface.  Hemorrhagic 
erosion  of  the  stomach  is  sometimes  present,  and  throughout  the  whole  in- 
testinal tract  there  is  often  a  considerable  quantity  of  dark-colored  fluid 
blood,  the  stomach,  however,  containing  matters  similar  to  those  vomited 
during  life.  The  gastric  mucous  membrane  is  aloO  not  infrequently  found 
thickened,  softened,  .and  reddened.  The  mucous  membrane  lining  the 
larynx  also  suft'ers  a  catarrhal  inflammation  ;  and  ecchymotic  sjDots  are  found 
on  the  lining  membrane  of  the  bladder. 

The  lungs  are  almost  constantly  the  seat  of  infarctions,  and  these  are 
occasionally  quite  numerous.  When  diffuse,  pulmonary  apoplexy  occurs, 
and  when  a  large  portion  of  a  lobe  is  involved,  the  lung-tissue  will  be 
broken  down  and  large  blood-clots  will  occupy  the  space. 

The  pleurcB  are  sometimes  covered  with  ecchymotic  spots,  and  occasionally 
there  is  a  blood-stained  serous  exudation  into  the  pleural  cavity. 

The  brain  and  cord  if  at  all  altered  are  only  slightly  hypergemic.  Punc- 
tate extravasations  may  occur  in  the  meninges;  and  some  affirm  that  an 
abundant  serous  exudation  is  often  present  in  the  lumbar  and  sacral  regions. 


653  ACUTE   GENERAL  DISEASES. 

attended  by  an  inflammation  of  the  membranes  of  the  cord  at  the  same 
point,  with  more  or  less  intense  inflammation  of  the  neurilemma  of  the 
nerves  in  the  coeliac  and  hepatic  plexuses. 

The  Mdneys  are  the  seat  of  parenchymatous  inflammation,  which  rap- 
idly passes  to  the  stage  of  fatty  metamorphosis.  There  are  sometimes 
small  abscesses  in  the  parenchyma.  On  microscopical  examination  oil- 
globules  are  seen  to  till  the  tubules,  whose  epithelium  is  sometimes  desqua- 
mated, or  the  seat  of  fatty  or  granular  change.  Occasionally  the  tubules 
are  filled  with  broken-down  epithelium.  The  pelves  of  the  kidneys  and 
the  ureters  are  frequently  the  seat  of  an  acute  catarrh. 

The  spleen  may  be  slightly  enlarged ;  but  is  usually  softer,  more  friable, 
and  darker  than  normal. 

The  shin  varies  in  color  from  a  bright  golden-yellow  to  a  dark  orange. 
Petechise,  ecchymoses,  vesicles,  pustules,  and  large  patches  of  extravasation 
may  be  found  upon  the  surface  of  the  body.  The  mucous  membranes  are 
not  infrequently  oi  a  distinctly  yellowish  tinge. 

The  gall-bladder  may  or  may  not  be  increased  in  size  ;  it  commonly  con- 
tains a  moderate  quantity  of  dark-colored  bile,  and  its  mucous  surface  ex- 
hibits spots  of  punctate  extravasation  as  well  as  arborescent  vascularity. 

The  ovaries  and  uterus  verj  frequently  contain  a  considerable  quantity 
of  extravasated  blood.' 

Etiology. — There  is  no  part  of  the  disease  so  uncertain  and  confusing  as 
its  etiology.  Equally  competent  observers  hold  diametrically  opposite  views 
in  regard  to  it.  I  shall  confine  my  statements  regarding  it  to  well-authen- 
ticated facts,  avoiding  the  many  controversies  on  this  subject. 

Yellow  fever  is  rarely  met  with  beyond  the  limits  of  40°  North  and  20° 
South  latitude  ;  it  prevails  in  the  West  Indies  and  eastern  part  of  the  West- 
ern Hemisphere  far  more  frequently  than  any  other  region,  and  the  locus, 
if  we  may  say  so,  of  the  malady  is  the  Antilles.  In  these  places  it  is  en- 
demic, and  to  a  comparatively  slight  extent  it  is  so  in  certain  portions  of 
Europe  and  Africa.  Commercial  seaports  are  pre-eminently  the  starting- 
points  of  great  epidemics  ;  it  is  sometimes  circumscribed  within  very  nar- 
row limits  in  the  seaports.  Crowding  is  one  of  the  essentials  to  its  develop- 
ment. The  average  temperature  of  the  locality  where  it  prevails  must  be 
at  least  73°  E.;  there  must  be  a  certain  amount  of  moisture  ;  and  animal 
and  vegetable  matter  must  undergo  decomposition,  either  on  the  surface  or 
in  the  substance  of  the  soil.  On  ship-board  there  may  be  the  greatest  un- 
cleanliness,  yet  the  fever  will  not  appear  on  the  vessel  till  it  has  touched 
land  in  an  affected  port  or  been  brought  into  communication  with  a  ship 
already  contaminated. 

The  time  of  year  during  which  the  fever  prevails  varies  with  the  climate 
and  temperature  ;  in  the  United  States  it  usually  appears  in  July  and 
August,  to  disappear  with  the  first  frost.  The  epidemic  in  New  York  City 
in  1795  began  in  August  and  terminated  in  October.  When  the  prevailing 
winds  are  southeasterly,  the  development  and  spread  of  an  epidemic  are  fa- 

1  Traite  des  Maladies  Infedieuses :  Maladie  des  Marais,  Fievre  Jaime,  Maladies  Typhoides,  Fievre 
Typhus  des  Abnees.    Willielm  Griesinger,  Paris,  1868. 


TELLOW   FEVEE.  653 

vored  ;  northwesterly  winds  check  or  arrest  it.  As  has  been  mentioned,  a 
severe  frost  or  a  "freeze"  puts  an  end  to  the  further  progress  of  the  dis- 
ease when  it  preA'ails  under  the  most  propitious  circumstances  for  its  devel- 
opment. 

There  is  much  reason  in  the  arguments  of  those  who  contend  that  yellow 
fever  is  an  "acclimation"  disease.  First  (and  here,  however,  it  should  be 
remarked  that  the  disease  is  indigenous  in  some  regions),  certain  islands  and 
seaport  towns  along  our  Southern  coast  always  suffer  from  an  ej)idemic  when- 
ever certain  atmospheric  conditions  exist;  a  resident  of  one  of  these  places 
where  yellow  fever  is  indigenous  is  far  less  liable  to  have  the  disease  than  a 
stranger,  esjDecially  one  from  the  North.  One  attack  is  usually,  not  ab- 
solutely, a  protection  against  a  second.  The  disease  is  especially  liable  to 
appear  in  those  localities  where  a  severe,  type  of  pernicious  fever  has  pre- 
vailed, and  after  a  warm,  rainy  season  rather  than  after  a  dry,  cool  one. 
Whether  the  fever  is  epidemic  or  endemic,  and  whether  the  locality  is  one 
frequently  visited  or  one  in  which  the  disease  is  indigenous,  sporadic  cases 
are  of  very  rare  occurrence. 

The  negro  race  has  a  marked  immunity  from  this  fever.  Age  and  sex 
exercise  no  influence  upon  the  etiology.  Occupation  seems  to  have  some 
effect  in  its  production,  since  those  who  work  over,  or  near,  hot  fires  are 
stricken  much  oftener  than  those  who  work  in  unhealthy,  filthy  surround- 
ings. Exposure  to  cold  and  wet,  alcoholismus,  and  venereal  excesses  here, 
as  elsewhere,  render  individuals  more  liable  to  the  fever. 

In  regard  to  the  nature  of  yellow  fever  poison,  some  assert  that  it  is  a 
malarial  miasm,  modified  by  the  person  in  whom  it  lodges.  It  is  in  many 
respects  similar  to  the  poison  of  typhoid,  both  in  etiology  and  the  manner 
of  its  conveyance.  It  is  unquestionably  a  specific  poison,  which  differs  es- 
sentially from  the  poison  of  every  other  fever.  Typhoid,  malarial  and  yel- 
low fever  may  all  prevail  at  the  same  time  in  the  same  locality,  bat  one  will 
never  merge  into  the  other;  each  runs  its  own  individual  and  peculiar  course. 
All  chemical  and  microscopical  research  has,  as  yet,  failed  to  discover  ivhat 
the  poison  is  ;  but  we  are  led  from  its  mode  of  conveyance  and  from  the 
conditions  of  its  development  to  believe  that  it  has  the  elements  both  of  a 
miasm  and  a  contagion. 

There  are  three  leading  doctrines  in  regard  to  the  contagious  character  of 
yellow  fever  -.—first,  that  it  is  contagious,  like  small-pox  and  scarlatina ; 
second,  that  it  is  non-contagious,  and  never  directly  transmitted  from  the 
sick  to  the  healthy;  and  third,  that  when  yellow  fever  is  prevailing  in  a  lo- 
cality, it  may  be  carried  from  one  person  to  another  in  that  locality.  The 
last  is  the  doctrine  of  contingent  contagion.  One  who  has  seen  the  fever 
in  hospitals  needs  no  argument  to  prove  that  it  is  not  directly  contagious. 
Some  claim  that  yellow  fever  poison,  though  not  directly  transmissible  from 
the  sick  to  the  healthy,  becomes  infectious  when  brought  in  contact  with 
decomposing  animal  and  vegetable  matter.  It  is  well  established  that  epi- 
demics of  yellow  fever  only  occur  in  those  localities  where  decomposing  ani- 
mal and  vegetable  matter  is  present ;  and  when  men  are  crowded  together 
in  shops  and  around  the  docks  and  wharves  of  seaports,  or  in  the  filthy 


654  ACUTE    GENERAL    DISEASES. 

streets  and  dwellings  of  such  localities.  In  some  few  instances  evidences 
exist  that  yellow  fever  breaking  out  in  the  hold  of  vessels  has  been  circum- 
scribed to  well-defined  and  very  narrow  limits  by  free  ventilation.  There 
are  ample  facts  to  sustain  the  belief  that  this  fever  is  infectious  only  when 
the  atmosphere  has  become  loaded  with  the  emanations  of  animal  and  veg 
etable  decomposition  to  which  has  been  added  the  specific  yellow  fever  poi- 
son. Under  such  circumstances,  the  disease  may  be  propagated  from  the 
sick  to  the  healthy. 

Whatever  view  is  taken  of  the  contagious  or  non-contagious  character  of 
yellow  fever,  all  observers  agree  that  it  \&  portable,  that  it  can  be  conveyed 
from  one  place  to  another  by  means  of  clothing  and  merchandise  and  in 
the  holds  of  vessels.  That  whenever  the  poison  is  thus  introduced  into 
healthy  localities  which  are  suited  by  temperature  to  its  reproduction,  and 
where  there  is  animal  and  vegetable  decomposition,  it  rapidly  reproduces 
itself,  and  thus  epidemics  of  yellow  fever  occur  in  localities  that  otherwise 
would  be  free  from  the  disease. 

There  is  no-doubt  that  the  poison  of  yellow  fever  retains  its  vitality  for 
a  very  long  period  ;  and  with  favoring  conditions  may  cause  an  epidemic 
in  places  very  remote  from  the  origin  of  the  poison.  The  poison  is  also 
cajjable  of  great  concentration,  for  short  exposure  to  the  contaminated 
air  that  often  fills  the  holds  of  ships  on  which  yellow  fever  is  prevail- 
ing will  be  followed  by  the  fever  in  a  few  hours.  Ordinarily  there  is  little 
danger  in  visiting  those  sick  of  yellow  fever  if  there  is  free  ventilation,  and 
one  does  not  remain  in  the  infected  locality  for  a  long  time.  The  period 
of  incubation  varies  in  duration  from  twelve  hours  to  four  or  five  days ; 
when  the  exposure  is  followed  in  a  few  hours  by  the  fever,  the  fever  poison 
must  necessarily  be  very  concentrated.  The  activity  of  yellow  fever  poison 
is  destroyed  by  cold  ;  one  or  two  hard  frosts  will  arrest  a  yellow  fever 
epidemic.  Some  claim  that  epidemics  of  yellow  fever  are  self-limiting, 
rarely  exceeding  sixty  or  seventy  days  in  their  duration.  There  is  not, 
however,  sufficient  proof  to  establish  this  statement.  ^ 

Symptoms. — As  in  typhoid  fever,  there  are  mild  and  severe  cases  of  yel- 
low fever ;  but  they  differ  only  in  degree,  not  in  kind ;  the  clinical  his- 
tory of  both  is  the  same. 

Prodromata  may  occur  ;  but  headache,  anorexia,  lassitude  and  pains  in 
the  limbs  cannot  be  reckoned  as  characteristic  of  the  fever,  and  only 
when  these  occur  during  an  epidemic  are  they  especially  significant. 
Whether  premonitory  signs  have  or  have  not  been  present,  the  disease  com- 
mences with  a  chill,  distinct  and  severe.  In  a  few  instances  a  series  of 
rigors  takes  the  place  of  distinct  chills.  Sometimes  persons  while  ap- 
pearing in  perfect  health  are  seized  with  a  severe  chill,  and  immediately 
become  seriously  ill  and  take  to  their  beds  in  a  most  dejected  manner.  Fol- 
lowing the  chill  there  is  nausea  and  vomiting,  the  face  is  flushed,  the  con- 


1  In  this  connection  see  :  The  Cause  and  Prevention  of  Yellow  Fever,  in  the  Beport  of  the  Sanitary  Com- 
mission of  New  Orleans.  Dr.  E.  H.  Barton,  New  York,  1857.  3Ie?)ioire  sur  la  Fievre  Jaune  qui  en  1857,  a 
Decime  la  Population  de  Monteviedo.  A.  Brunei,  Paris,  1860.  Account  of  the  Yellow  Fever  which  occurred 
in  the  City  of  Neiv  York  in  the  year  1822.  Dr.  James  Hardie,  New  York,  1823.  Remarks  on  the  Epidemic 
Yeilow  Fever  on  the  South  Coasts  of  Spain.    Dr.  K.  Jackson,  London,  1821. 


YELLOW   FEVER. 


Go5 


junctivae  are  injected,  there  is  circumorbital  headache,  and  violent  pains 
in  the  bones,  back  and  limbs,  especially  in  the  calves  of  the  legs.  The  eye 
has  a  peculiar  lustre  and  a  staring  look.  The  course  of  the  fever  is  the 
same  in  the  severe  and  in  the  mild  cases. 

The  temperature  rises  rapidly  after  the  chill  to  103°  or  104°F. ;  the  limits 
vary,  but  yellow  fever  is  not  a  disease  of  high  temperature.  In  a  few  epi- 
demics the  initial  rise  in  temperature  has  been  as  great  as  110°  F.,  but  these 
are  jDhenomenal  occurrences.  At  the  end,  or  beginning,  of  the  third  day 
the  maximum  fever  will  have  been  attained  ;  in  our  country  this  is  rarely 
more  than  104°  or  105°  F.  Between  this  period  and  the  fourth  day  of  the 
disease  slight  variations,  hardly  amounting  to  distinct  remissions  are  pres- 
ent;  on  the  fourth  day  there  is  a  rapid  defervescence  ;  it  is  not  an  inter- 
mission but  a  remission,  for  the  temperature  only  falls  to  100°  or  101°F. 
The  period  of  remission  lasts 
from  a  few  hours  to  two  or 
three  days,  after  which  a  sec- 
ond rise  begins,  one  that  does 
not  take  place  quite  as  rapidly 
as  the  first,  and  is  not  usually 
|)receded  by  a  chill  or  rigors  ; 
and  a  temperature  of  104°  or 
105°  is  again  reached.  The 
temperature  now  remains  sta- 
tionary from  one  to  two  days, 
it  then  falls  to  normal  and 
remains  so.  This  last  fall  is, 
like  the  first,  marked  by  a  very 
sharp  temperature  curve.  The 
range  of  temperature  is  impor- 
tant, for  it  divides  this  dis- 
ease into  three  parts;  first, 
the  stage  of  invasion,  the 
febrile  stage  or  period  of  ex- 
acerbation ;  second,  the  stage 
of  remission,  calm  or  passive  ]3eriod ;  and,  third,  the  stage  of  the  second 
exacerbation  or  collapse. 

The  piilse  in  yellow  fever  is  peculiar.  It  rarely  exceeds  110  beats  per  min- 
ute, thus  differing  from  that  of  other  fevers  in  which  the  rule  is  an  in- 
crease of  five  beats  for  every  one  degree  rise  of  temperature.  Indeed,  in 
mild  cases  the  pulse-rate  may  only  be  five  or  six  beats  above  the  normal.  It 
has  been  observed  to  fall  much  below  the  normal,  as  low  as  40  and  some- 
times 30  in  a  minute.  The  "  feel  "  of  the  pulse  is  as  if  the  arteries  were  dis- 
tended with  gas,  and  hence  the  name,  '' gaseous  pulse,-"  is  not  inajjpro- 
priate.  It  is  compressible  and  of  an  uncertain  volume,  offering  no  resist- 
ance, so  to  speak,  to  the  touch. 

The  skin,  as  soon  as  the  temperature  begins  to  rise,  maybe  either  dry  or 
bathed  in  a  cojjious  perspiration.     Following  the  chill  there  is  sometimes  an 


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Fis.  153. 
Temperature  Record  in  a  Case  of  Yellow  Fever. 


656  ACUTE    GENERAL   DISEASES. 

abnormal  coldness  on  the  surface,  while  rectal  thermometry  shows  a  marked 
rise  in  the  temperature.  At  the  close  of  the  first,  or  beginning  of  the  sec- 
ond day,  the  body  emits  a  peculiar  corpse-like  odor.  About  the  third  day 
the  skin  begins  tc  assume  a  jaundiced  hue,  noticed  first  in  the  sclera  and 
then  spreading  over  the  whole  body.  It  is  a  dark  jaundice,  like  that  of  py- 
aemia, and  is  to  be  regarded  as  hematogenous  and  not  hepatogenous.  Those 
who  maintain  that  the  jaundice  is  due  to  retention  and  reabsorption  of  bile 
have  no  proof  to  offer,  since  evidences  of  mechanical  obstruction  to  the  out- 
flow of  the  bile  are  among  the  rarest  post-mortem  appearances.  The  true 
etiology  is  found  in  the  change  which  takes  place  in  the  blood.  The  pig- 
ment thus  formed  is  deposited  in  the  tissues,  and  is  a  true  hematogenous 
icterus.  The  perspiration  now  stains  the  linen  yellow.  This  jaundice  is 
not  always  present  in  yellow  fever,  but  when  it  becomes  a  symptom  it  does 
not  run  into  the  period  of  convalescence.  In  the  third  stage  the  jaundice 
assumes  a  mahogany  hue. 

Vomiting. — Immediately  following  the  chill,  nausea  and  vomiting  are 
present.  First  the  contents  of  the  stomach  are  voided,  then  a  yellowish 
green  matter  ;  when  the  latter  color  is  present  the  vomiting  becomes  pro- 
jectile in  character,  and  the  ejected  matter  has  an  alkaline  reaction  and  is 
fluid.  The  alkalinity  is  due  to  ammoniacal  decomposition.  The  vomiting 
is  accompanied  by  burning  pains  at  the  xiphoid  cartilage.  If  the  vomiting 
comes  without  any  other  change  in  the  matter  vomited,  it  is  an  evidence 
that  the  fever  is  going  on  to  recovery ;  in  severe  cases  the  characteristic 
**  black  vomit  "  is  present,  the  result  of  hemorrhage  into  the  stomach.  Thisi 
vomit  is  brownish  black,  semi-fluid,  with  a  glistening  reflection,  and  varies 
in  amount  from  a  mere  trace  to  many  pints.  It  may  occur  on  the  second 
or  third  day  of  the  fever,  but  usually  it  does  not  come  on  until  about  forty- 
eight  hours  before  death,  or  on  the  day  of  death  ;  it  occurs  only  in  about 
one-third  of  the  fatal  cases.  It  undoubtedly  occurs  more  frequently  in  yel- 
low fever  than  in  any  other  disease,  but  it  differs  in  none  of  its  constituents. 
from  a  similar  material  which  is  sometimes  vomited  in  other  diseases  where 
small  capillary  hemorrhages  occur  in  the  stomach. 

Microscopically  '  it  is  seen  to  be  made  up  of  blood  corpuscles,  degenerated 
lymphoid  cells,  fat  cells,  epithelial  cells  from  the  raucous  membrane  of 
the  stomach,  fine  granules  of  pigment,  aggregated  non-granular  masses, 
and  serous  fluid.  The  action  of  the  gastric  juice  is  such  that  the  color- 
ing matter  escapes  from  the  corpuscles  as  small  granular  or  rounded 
masses.  It  is  claimed  that  the  black  vomit  of  yellow  fever  is  specific,  in 
that  it  contains  a  peculiar  microscopic  vegetable  organism.  This  is  yet 
lacking  confirmation.  The  enfeeblement  of  the  walls  of  the  capillary  ves- 
sels results  from  the  pathological  blood-conditions,  and  as  qualitative  al- 
terations are  likewise  added,  hemorrhagic  extravasations  occur  in  the 
stomach,  and  on  other  mucous  surfaces.  The  hemorrhages  from  the  nose 
and  gums  that  so  frequently  occur,  and  fluid  blood  in  the  discharges  from 
the  bowels  are  caused  by  the  same  changes  as  cause  the  gastric  hemor- 
rhages.    Very  rarely  hemorrhagic  extravasations  occur  during  life  from 

1  Mcroscoplc  Researches  in  the  Black  Vmnit  of  Yellow  Fever.  Dr.  M.  Michell.  Chariest.  Med.  Jour.,  1853. 


YELLOW   FEVEE.  657 

the  respiratory  organs,  the  genitals,  the  skin,  and  the  meatus  auditorius 
extern  us. 

Urine. — Early  in  the  disease  the  urine  is  scanty,  acid,  and  slight  traces 
of  albumen  may  be  found.  Later,  when  the  jaundice  appears,  its  reaction 
is  alkaline,  and  bile  pigment  is  present ;  as  the  disease  progresses  it  be- 
comes more  abundant ;  if  not  present  before,  it  makes  its  appearance  dur- 
ing the  stage  of  remission  ;  in  all  severe  cases,  leucin,  tyrosin  and  fatty 
casts  will  likewise  be  found.  Entire  suppression  of  urine  is  of  frequent  oc- 
currence in  severe  cases.  Patients  with  black  vomit  may  recover,  but  a 
fatal  result  almost  certainly  follows  urinary  suppression.  In  cases  where 
the  yellow  fever  poison  is  concentrated  and  the  nervous  symptoms  are  prom- 
inent, suppression  of  urine  may  exist  from  the  onset,  but  it  usually  does 
not  take  jjlace  until  the  second  exacerbation.  Urgemic  toxtemia  is  then 
added  to  the  yellow  fever  poison,  and  the  condition  is  almost  necessarily 
hopeless.     The  perspiration  in  this  condition  has  a  urinous  odor. 

.  The  countenance  in  some  cases  is  almost  diagnostic  :  the  eyes  are  lustrous 
and  staring,  the  face  is  flushed,  the  conjunctivae  are  injected,  the  intense 
conjunctival  congestion  giving  the  eyes  the  appearance  of  two  balls  of  fire 
set  in  a  face  of  a  dusky,  deathly  hue  ;  this  gives  to  the  countenance  a  re- 
markable expression  of  dejection  and  dulness. 

The  tongue  is  covered  at  the  outset  of  the  fever  with  a  thick,  yellowish 
white  coating,  except  at  the  tip  and  edges,  which  remain  red.  It  is  often 
indented  by  the  teeth  ;  and  as  the  disease  advances  may  become  dry,  brown, 
cracked  and  fissured,  resembling  the  typhoid  tongue.  The  buccal  mu- 
cous membrane  is  bright  red  at  first,  subsequently  becoming  oedematous. 

The  bowels  are  usually  constipated,  but  when  diarrhoea  does  occur,  fluid 
blood  is  apt  to  be  mingled  with  the  discharges.  Sometimes  when  intense 
jaundice  is  present,  the  stools  are  clay  colored,  but  this  is  an  accidental 
circumstance. 

TJie  mind  is  usually  clear  to  the  last,  but  when  delirium  sets  in  it  will 
be  wild  and  accompanied  by  a  desire  to  get  out  of  bed.  The  patient  lies 
in  a  state  resembling  collapse,  his  features  shrunken,  indifferent  both  to 
his  own  condition  and  to  what  is  occurring  about  him. 

Pain  is  quite  severe  over  the  lumbar  and  epigastric  regions ;  they  are  ex- 
quisitely sensitive  to  pressure  ;  convulsive  twitchings  of  the  muscles,  and 
diaphragmatic  contractions  are  often  present  before  death.  In  favorable 
cases  all  the  severe  symptoms  distinctly  remit  on  the  second  day  after  the 
beginning  of  the  stage  of  the  second  exacerbation,  and  then  follows  a  pro- 
tracted convalescence,  and  it  is  with  the  greatest  difficulty  that  the  stom- 
ach will  retain  the  blandest  food.  When  death  is  to  follow,  the  vomiting 
persists,  the  urine  becomes  less  and  less  in  amount  and  richer  in  albumen, 
and  uraemic  coma,  or  wild  delirium  ends  the  scene.  Just  before  death, 
in  some  epidemics,  the  temperature  falls;  hence  the  name  algid  yellow 
fever.  But  whether  coma,  algidity,  delirium,  suppression  of  urine,  or 
black  vomit  is  the  predominant  symptom  in  an  epidemic,  the  disease  is  the 
same  specific  fever.  The  mortality  varies  as  much  in  different  epidemics 
as  the  prominent  symptoms  do. 
42 


658  ACUTE    GENERAL   DISEASES. 

Differential  Diagnosis. — Yellow  fever  may  be  confounded  with  acute  yel- 
low atropliy  of  the  liver,  relapsing,  bilious  remittent,  continued  malarial 
fever,  and  the  icteric  variety  of  pernicious  fever. 

The  diagnoses  of  acute  yellow  atrophy  of  the  liver  and  yellow  fever  have 
already  been  considered. 

Relapsing  fever  is  an  inland  disease,  as  a  rule,  while  yellow  fever  is 
essentially  a  coast  disease.  In  relapsing  fever  the  temperature  rises  to  a 
high  point,  often  107°  or  108°,  the  pulse  keeping  pace  and  running  up  to 
140  or  150  beats  per  minute  ;  in  yellow  fever  a  pulse  of  over  110  is  very 
rare,  and  the  temperature  averages  104°,  often  lower.  Jaundice  and  the 
peculiar-colored  "yellow  fever  face"  are  early  symptoms  in  this  disease; 
while  there  is  no  change  in  the  face  in  relapsing  fever  and  jaundice  is  a 
very  late  symptom.  Eelapsing  fever  has  a  true  intermission,  while  yellow 
fever  has  only  a  remission.  The  spleen  is  markedly  enlarged  and  tender 
in  relapsing  fever ;  in  yellow  fever  it  is  normal.  During  the  pyrexial 
period  spirilli  are  found  in  the  blood  in  all  cases  of  relapsing  fever,  and  are 
absent  from  yellow  fever.  Bronchitis  is  a  very  common  complication  of 
relapsing  fever,  while  pulmonary  complications  are  very  rare  in  yellow 
fever.  Finally,  relapsing  fever  is  propagated  by  contagion,  and  yellow  is 
not. 

Yellow  fever  is  a  portable  disease,  and  usually  prevails  in  cities  and 
along  the  coast ;  bilious  remittent  fever  is  not  portable,  and  is  a  disease  of 
the  country  and  inland  towns.  The  pulse-rate  is  120  or  130  in  bilious  re- 
mittent ;  in  yellow  fever  it  is  rarely  over  110  ;  the  temperature  is  105°  or 
106°  in  bilious  remittent,  and  rarely  exceeds  104°  in  yellow  fever.  The 
liver  is  enlarged  in  yellow  fever,  and  normal  in  size  in  bilious  remittent ; 
the  spleen  is  invariably  enlarged  in  remittent  and  unchanged  in  yellow 
fever.  There  is  projectile  vomiting  in  yellow  fever,  while  in  bilious  re- 
mittent it  is  retching  in  character.  In  twenty-four  hours  a  remission 
occurs  in  bilious  remittent,  while  in  yellow  fever  the  remission  does  not 
occur  until  the  fourth  day.  The  urine  is  rarely  albuminous  in  remittent 
fever,  while  even  in  mild  cases  of  yellow  fever  albumen  is  rarely  absent. 
The  mind  is  clear  in  yellow  fever,  while  a  patient  with  bilious  remittent  is 
dull  and  delirious.  The  difference  in  the  invasion  of  the  two  diseases,  the 
countenance,  the  existence  of  the  hemorrhagic  tendency,  and  the  history  of 
the  epidemic  are  sufficient  to  distinguish  yellow  fever  from  the  so-called 
yellow  type  of  remittent  fever. 

Id  continued  malarial  (so-called  typho-malarial)  fever  the  temperature 
is  higher  than  in  yellow ;  there  is  diarrhoea,  which  is  absent  from  yellow 
fever,  and  the  spleen  undergoes  marked  enlargement.  Yellow  fever,  on  the 
other  hand,  is  attended  by  albuminuria  and  a  peculiar  facial  aspect  that 
are  both  absent  from  all  cases  of  continued  malarial  fever.  There  is 
periodicity  in  the  variations  in  temperature  in  continued  malarial  fever, 
and  the  disease  is  continuous  over  two  or  three  weeks ;  while  in  yellow 
fever  there  are  slight  and  irregular  variations  in  the  fever,  and  a  distinct 
remission  on  the  fourth  day,  which  removes  all  doubt.  Pain  in  the  right 
iliac  fossa  is  much  more  marked  in  continued  malarial  than  in  yellow 


TELLOW   FEVER.  659 

fever.  The  history  of  the  epidemic,  the  portability,  and  other  etiological 
points  will  also  often  greatly  aid  in  making  the  diagnosis. 

Prognosis. — The  mortality-rate  differs  in  different  epidemics ;  the  high- 
est mortality  is  given  as  one  out  of  every  three ;  while  in  mild  epidemics 
only  one  out  of  fifteen  or  twenty  dies.  The  average  duration  is  six 
days,  but  in  cases  where  a  concentration  of  the  poison  overwhelms  the 
system  at  the  very  onset,  death  may  occur  within  twenty-four  hours,  and 
between  this  time  and  six  days  there  is  a  varying  number  of  fatal  cases. 
The  conditions  that  render  the  prognosis  unfavorable  are  early  high  tem- 
perature, a  severe  period  of  invasion,  deej)  jaundice,  scanty  urine  contain- 
ing albumen  and  casts,  black  vomit,  intense  pains  over  and  irritability  of 
the  stomach,  a  gaseous  pulse,  delirium,  and,  worst  of  all,  suppression  of 
urine. 

Among  the  favorable  signs  are  diminution  in  the  quantity  of  albumen,  a 
quiet  stomach,  slight  and  late  jaundice,  a  moderate  degree  of  fever,  and 
fewer  attacks  of  black  vomit.  A  positive  prognosis  is  best  withheld  ;  but 
"black  vomit"  and  complete  suppression  render  a  case  hopeless.  Yellow 
fever,  in  some  epidemics,  is  complicated  by  numerous  boils  and  abscesses, 
and  by  cellulitis  and  inflammation  of  the  parotid  gland,  perhaps  termi- 
nating in  suppuration.  Eegarding  convalescence,  it  may  be  said,  however 
quickly  it  may  be  established,  it  is  longer  than  in  any  other  disease  in 
proportion  to  the  length  of  the  fever.  Indeed  it  is  often  two  weeks  after 
the  final  fall  in  temperature  before  the  patient  begins  to  mend,  and  five 
or  six  months  may  have  to  elapse  before  he  is  entirely  well.  Death  may 
result  from  rapid  overwhelming  of  the  system  with  the  poison,  i.e.,  from 
the  effects  of  the  blood  change,  from  uraamia,  black  vomit,  suppression, 
exhaustion  or  asthenia.^ 

Treatment. — Prophylaxis  is,  in  a  great  measure,  summed  up  in  the  word 
quarantine.  A  strict  quarantine,  that  should  include  not  only  individuals 
but  also  all  articles  that  have  been  near  the  infected  person  or  spot,  would 
be  very  desirable.  This  does  no  harm  to  the  sick  ;  they  may  be  removed 
to  a  hospital  at  once,  after  disinfection,  for  the  disease  is  not  contagious. 
To  go  into  the  details  of  quarantine,  of  ship  and  hospital  disinfection, 
would  be  out  of  the  domain  of  this  work.  A  person  who  is  in  the  yellow 
fever  region  can  take  the  best  prophylactic  measure — removal  from  the 
neighborhood.  When  this  is  impracticable,  sulphate  of  quinine  may  be 
taken  and  all  predisposing  causes  avoided  as  far  as  possible.  Mercury  is  by 
some  regarded  as  an  efficient  means  of  j)rophylaxis.^  The  variability  of  the 
mortality-rate  has  been  referred  to.  Blood-letting,  mercurials,  stimulants, 
and  quinine, — these  are  the  four  chief  methods  that  have  been  tried.  ^ 
Blood-letting,  to  the  extent  sometimes  of  180  oz.  at  a  time,  was  formerly 
practised,  but  has  been  abandoned,  as  not  only  wrong  in  theory  but  harm- 

1  "  Relati/m  de  la  Fievre  Jaune  survenve  a  Saint-Nazaire  en  1861."    M.  F.  Melier,  Paris. 

2  Yellmv  Fever;  Us  origin,  improper  treatment,  prevention  and  cure.  Dr.  W.  A.  Shubert,  Savannah,  1860. 
A  dissertation  on  the  sources  of  malignant.,  bilious  or  yellow  fever,  and  means  of  preventing  it.  Dr.  W.  G. 
Chalmell,  Philadelphia,  1799. 

'  Das  Gelhe  Fieher  heurtheilt  und  behandelt  nach  einer  neuen  Aussicht  vom  Wesen  der  Fieher  in  Allge- 
meinen.  G.  Eichbom,  Berlin,  18.?3.  The  history  of  yellow  fever,  with  themost  successful  method  of  treatment 
Dr.  J.  Mackrill,  Baltimore,  1796. 


660  ACUTE    GENEEAL    DISEASES. 

ful  in  practice.  Mercurials  are  exhibited  to-day  only  for  catharsis  at  the 
commencement.  Stimulation  is  bad  in  excess  ;  and  quinine  is  of  no  avail 
for  any  but  prophylactic  measures,  if  even  here  it  possesses  as  much 
efficacy  as  theory  attributes  to  it.  Eecently  carbolic  acid  has  been  added 
to  this  list,  but  it  has  had  so  slight  a  trial  that  nothing  can  be  said  joro  or 
con,  except  that  it  is  likely  to  go  the  way  of  all  specifics. 

The  plan  of  treatment  which  seems,  at  the  present  state  of  our  knowl- 
edge, most  reasonable,  may  be  called  a  diaphoretic  and  expectant  plan,  the 
diaphoresis  looking  toward  the  relief  of  the  grave  kidney  trouble,  and 
hence  tiding  over  the  most  serious  point  in  the  fever.  When  a  patient  is 
stricken  with  the  fever,  apply  counter-irritation  over  the  kidneys,  and  at  the 
same  time  administer  ten  grains  of  quinine  along  with  fifteen  or  twenty 
grains  of  calomel.  The  body  should  be  covered  with  flannel  and  slightly 
heated,  moderate  diaphoresis  being  continually  kept  up  by  these  methods. 
At  the  same  time  the  air  must  always  be  fresh  ;  close  quarters  are  always 
contraindicated.  The  nausea  and  vomiting  may  be  controlled  by  eating 
cracked  ice,  drinking  milk  and  lime-water,  or  by  small  hypodermic  doses 
of  morphia.  The  restlessness,  tossing,  and  jactitation  which  are  so  ex- 
hausting in  some  cases,  and  which  probably  arise  from  the  action  of  the 
urea  in  the  circulation  on  the  nerve  centres,  are  best  controlled  by  hypo- 
dermic injections  of  morphine.  Full  doses  of  opium,  producing  as  they  do 
free  diaphoresis,  may  also  be  administered,  unless  the  kidney  lesions  are 
very  grave.  Suppression  is  treated  by  the  usual  methods,  large  doses  of 
turpentine  being  given.  In  the  last  epidemic  3j  of  turpentine  in  sugared 
water  was  given  every  four  hours  in  the  case  of  a  negro,  and  recovery 
followed. 

In  copious  ha3matemesis  styptics  can  be  given  cautiously,  and  cold  com- 
presses may  be  applied  over  the  epigastrium.  When  the  various  discharges 
have  caused  much  exhaustion  the  judicious  use  of  stimulants  is  often 
beneficial.  When  the  opportunity  offers,  it  might  be  well  to  try  hypo- 
dermic injections  of  the  sulpho-carbolate  of  quinine.  Yellow  fever  runs  its 
course  in  five  or  six  days  ;  hence  the  vital  powers  must  be  sustained  until 
the  defervescence,  and  this  is  found  to  be  extremely  difficult  on  account  of 
the  extreme  gastric  irritability.  A  bland  and  highly  nourishing  diet  is  to 
be  prescribed  as  soon  as  convalescence  occurs,  and  tonics  form  an  essential 
part  of  treatment  at  this  period.  ^ 

EPIDEMIC    CHOLEEA. 

Epidemic  cholera  is  an  acute  general  disease,  which  prevails  epidemically, 
and  in  certain  localities  is  endemic.  It  is  characterized  by  copious  watery 
discharges  from  the  alimentary  canal,  by  cramps,  and  by  suppression 
of  the  excretions.  It  has  also  received  the  names  of  cholera  Asiatica, 
cholera  asphyxia,  and  epidemic,  malignant,  algid,  or  blue  cholera. 

Morbid  Anatomy. — The  post-mortem  appearances  vary  with  the  period  at 
which  death  takes  place  ;  in  the  stage  of  collapse  or  in  that  of  reaction, 

1  Tdlow  Fever  in  Charleston,  1871,  with  Remarks  upon  its  Treatment.  Dr.  F.  P.  Porcher,  Charleston, 
1872,    (Trans.  S.  C.  Med.  Asso.) 


EPIDEMIC    CHOLERA  6G1 

there  is  usually  marked  emaciation  ;  the  extremities  are  noticeably  shriv- 
elled, and  the  surface  of  the  body  in  the  dependent  portions  is  bluish  or 
mottled  ;  sub-conjunctival  ecchymoses  are  often  observed.  The  face  has  a 
pinched  and  drawn  expression,  and  the  eyes  are  deeply  sunken.  The  body 
cools  slowly  after  death,  and  frequently  there  is  a  post-mortem  rise  in  tem- 
perature of  two  or  three  degrees  Fahr. 

Rigor  mortis  is  marked  immediately  after  death,  and  muscular  contrac- 
tions often  cause  changes  in  the  position  of  the  limbs  and  body.  The  skin 
is  often  so  shrivelled  as  to  resemble  the  condition  called  "parboiled," 
■which  is  best  marked  upon  the  extremities.  Putrefaction  commences  much 
later  than  in  other  diseases,  on  account  of  the  withdrawal  of  large  quantities 
of  fluid  from  the  body. 

The  visceral  lesions  are  as  follows.  The  small  intestine  is  distended  and 
of  a  bright  red  color ;  its  muscular  coat  is  somewhat  relaxed.  Its  mucous 
membrane  is  injected  with  a  fine  aborescent  vascularity  ;  it  is  sometimes 
oedematous  and  its  folds  are  often  prominent,  especially  around  the  lower 
part  of  the  ileum.  Peyer's  patches- and  the  solitary  follicles  are  at  first  en- 
larged, the  latter  more  than  the  former  ;  if  the  solitary  glands  rupture,  the 
membrane  presents  a  reticulated  appearance.  Ulcerations  resembling  ty- 
phoid ulceration  may  occur,  the  glands  become  flattened  and  pigmented. 
There  is  an  almost  complete  detachment  of  the  epithelium;  if  any  patch  is 
left  undenuded  there  is  a  sub-epithelial  exudation  which  loosens  its  attach- 
ment to  the  villi.  The  intestine  may  be  partially  or  comiDletely  filled  with 
a  "rice-water,"  whey-like  fluid,  alkaline  in  reaction,  which  contains  an 
abundance  of  cast-off  epithelium,  and  varies  in  consistency  from  the  ordi- 
nary cholera  stool  to  that  of  putty.  The  mucous  surface  may  be  of  a 
bright  red,  grayish  or,  rarer  than  all,  a  greenish  color.  In  some  instances 
the  intestine  contains  a  moderate  quantity  of  dark  grumous  blood.  Dur- 
ing the  fever  of  reaction  gray  diphtheritic  patches,  very  difficult  of  re- 
moval, which  later  become  dry,  brown  sloughs,  are  sometimes  found  in 
both  the  small  and  large  intestine.  Similar  patches  have  also  occasion- 
ally been  observed  upon  the  mucous  membrane  of  the  biliary  passages, 
vulva,  and  vagina.  In  severe  cases  the  basement  membrane  is  wholly 
denuded. 

The  peritoneum  of  the  small  intestine  is  of  a  rosy  color  and  dry,  or  is 
covered  with  a  thin  layer  of  plastic  matter. 

The  glands  of  the  large  intestine  are  sometimes  congested,  swollen  and 
prominent ;  while  the  mucous  surface  has  large  ecchymoses  and  patches  of 
extravasation  upon  its  substance.  Diphtheritic  ulcerations  may  be  present 
in  the  colon. 

The  oesophagus  is  sometimes  congested  and  ecchymosed,  and  its  glands 
are  swollen.  It  may  have  its  epithelium  detached,  and  at  times  it  is  cov- 
ered with  a  diphtheritic  exudation. 

The  stomach  is  at  first  distended  and  filled  with  fluids  similar  to  those 
which  are  found  in  the  small  intestine  ;  later  its  mucous  lining  is  hyper- 
semic,  swollen,  often  relaxed  and  ecchymotic.  Still  later  it  is  collapsed 
and  empty. 


662  ACUTE   GElfEKAL   DISEASES. 

The  Tcidneys  are  intensely  congested  and  enlarged,  the  capsule  is  adlier* 
ent,  the  surface  presents  a  stellate  or  "marbled  "  vascularity,  and  on  longi- 
tudinal section  both  cortical  and  medullary  portions  exhibit  punctate  or 
striped  blood  injections,  and  numerous  ecchymoses.  The  small  veins,  es- 
pecially around  the  glomeruli,  are  engorged,  and  the  cortical  portion  of 
the  kidney  is  more  or  less  discolored.  The  uriniferous  tubules  have  their 
epithelium  loosened,  and  the  cells  are  cloudy,  swollen  and  filled  with  a 
granular  albuminoid  material  ;  often  transparent  cylinders  fill  the  lumen 
of  the  uriniferous  tubes.  For  the  most  part  the  lesions  resemble  those  of 
acute  croupous  nephritis.  All  these  changes  may  occur  during  the  first  day 
of  the  choleraic  attack.  Later,  during  the  secondary  fever,  the  discolora- 
tion and  tubular  changes  are  increased  ;  the  size  of  the  kidney  being  one- 
sixth  to  one-third  greater  than  normal,  and  the  epithelial  cells  undergo  pro- 
gressive fatty  degeneration,  and  the  whole  organ  becomes  soft  and  friable. 
Chemical  examinations  have  shown  the  kidneys  to  contain  an  abnormal 
quantity  of  urea,  uric  acid,  leucin,  and  some  bile-pigment. 

Tlie  hlaclder  is  at  first  contracted  and  empty  ;  but  later  it  may  be  par- 
tially filled  with  albuminous,  milky  urine.  Its  mucous  membrane  and 
that  of  the  ureters  and  pelvis  of  the  kidneys  undergo  changes  similar  to 
the  other  mucous  surfaces  ; — viz. :  hyperemia,  ecchymoses,  and  perhaps 
diphtheritic  processes. 

The  lungs  are  engorged  at  the  entrance  of  the  pulmonary  artery  ;  but 
the  parenchyma  of  the  lung  is  collapsed  and  exsanguinated,  and  crepitates 
less  than  normal  luug-tissue.  If  death  occurs  during  or  after  the  reaction- 
ary fever,  extensive  oedema,  hypostatic  congestion  and  hemorrhagic  infarc- 
tions may  be  found.  Capillary  bronchitis,  lobular  and  lobar  pneumonia, 
and  emphysema  are  present  in  those  cases  where  death  occurs  during  con- 
valescence. Pulmonary  gangrene  is  a  rare  lesion.  The  trachea  and 
bronchi  are  engorged  and  covered  with  a  muco-pus,  while  later  a  second- 
ary diphtheritic  process  may  be  established  upon  their  mucous  surface. 

The  pericardium  is  dry,  and  its  visceral  layer  is  ecchymotic,  while  the 
parietal  is  coated  with  a  sticky,  pasty  material. 

Tlie  heart  is  hard,  dry  and  contracted,  containing  in  its  right  cavity, 
which  may  be  distended,  soft  clots,  which  sometimes  extend  into  the 
pulmonary  artery  and  into  the  veins.  The  left  cavity  is  empty,  or  has 
only  a  few  small  black,  loose  coagula  in  it. 

The  tlood  is  darker  and  thicker  than  normal,  there  is  an  increase  in 
its  albumen  and  corpuscles,  as  well  as  in  its  specific  gravity  and  in 
organic  solids ;  while  there  is  a.  decrease  in  its  saline  elements  and  in  its 
coagulating  power.     Urea  is  occasionally  present. 

The  spleen  is  small,  wrinkled,  flabby  and  shrunken,  though  when  typhoid 
symptoms  co-exist,  or  when  it  is  the  seat  of  blood  extravasations  it  is  en- 
larged and  softened. 

The  liver  is  usually  pale,  containing  patches  of  commencing  fatty  de- 
generation, and  the  large  veins  are  distended  with  blood.  There  is  ex- 
foliation of  the  epithelium  of  the  mucous  surface  of  the  gall-bladder, 
which  causes  plugging  and  distention  of  the  ducts. 


EPIDEMIC    CHOLERA.  663 

The  meningeal  vessels  of  the  brain  and  the  sinuses  are  engorged,  while 
the  cerebro-spinal  fluid  is  frequently  absent.  Medullary  hyperaemia  is 
common.  But  when  death  has  occurred  late,  the  brain  contains  less  blood 
and  is  often  superficially  osdematous. 

The  suh-cntcmeous  connective-tissue  is  hard  and  dry.  Parotid  swellings, 
furuncles,  purj^uric  and  scorbutic  spots,  ulcerations  of  the  cornea,  and 
bed-sores  are  often  present. 

Etiology. — Cholera  is  an  acute,  infectious,  non-contagious  disease,  prob- 
ably of  miasmatic  origin.  It  prevails  epidemically  and  may  be  endemic. 
It  first  appeared  in  the  East,  and  thence  spread  in  all  directions,  follow- 
ing the  routes  of  commerce  without  regard  to  climate.  Xo  country 
has  been  entirely  exempt  from  its  ravages.  It  has  prevailed,  how- 
ever, chiefly  in  hot  climates,  during  wet  seasons.  In  this  country  it 
prevails  most  in  mid-summer.  It  is  more  liable  to  occur  in  low  lands 
than  in  mountain  regions.  Badly  drained  malarial  districts  favor  its  de- 
velopment, especially  where  a  cup-shaped  rock  or  clay  substratum  is  cov- 
ered by  a  thin  layer  of  permeable  earth,  favoring  the  decomposition  of 
vegetable  matter.  Bad  food,  overcrowding,  mental  depression,  excesses  in 
venery  and  alcohol  drinking,  predispose  to  cholera.  Epidemics  of  cholera 
occur  most  when  the  atmosphere  is  moist  and  sultry,  or  when  a  sultry 
period  follows  a  warm  rain  storm.  Districts  where  these  conditions  pre- 
vail are  regarded  as  favoring  the  development  of  the  cholera  germ. 

As  soon  as  the  cholera  discharges  undergo  decomposition  the  specific  in- 
fection of  the  disease  is  developed  and  may  be  conveyed  from  one  locality 
to  another  by  the  wind,  by  rivers,  and  in  clothing.  From  experiments  made 
by  Dr.  Sanderson,  it  is  evident  that  the  specific  poison  of  cholera  is 
contained  in  the  discharges  from  the  mucous  surface  of  the  alimentary 
canal,  that  it  is  not  infectious  when  fresh,  but  that  it  acquires  virulent  in- 
fectious properties  in  from  two  to  four  days,  and  that  it  is  rendered  in- 
nocuous by  cold.  There  is  no  evidence  that  the  bodies  of  cholera  patients 
are  infectious.  The  establishment  of  these  facts  readily  accounts  for  its 
sudden  appearance  in  diSerent  places  remote  from  one  another.  An  in- 
dividual travelling  rapidly  from  one  place  to  another  becomes  the  carrier 
of  the  germ,  which  is  to  develop  the  infection  in  those  localities  in  which 
the  conditions  favor  its  reproduction. 

Symptoms. — The  length  of  the  stage  of  incubation  of  cholera  is  not  de- 
termined, but  it  undoubtedly  varies  from  a  few  hours  to  as  many  days. 
Its  symptoms  may  be  divided  into  four  stages.  These  divisions  are  arbi- 
trary ;  first,  the  stage  of  invasion,  or  premonitory  stage  ;  second,  the  stage 
of  painless  diarrhoea ;  third,  the  algid  or  collapse  stage  ;  fourth,  the  stage 
of  reaction. 

The  prodromal  symptoms  are  a  feeling  of  weight  in  the  precordium, 
rumbling  of  the  bowels,  general  malaise,  a  peculiar  pallid  anxious  counte- 
nance, and  nervous  phenomena,  such  as  vertigo,  tinnitus  aurium,  head- 
ache, and  tremor.  Sometimes  there  is  apathy,  again  a  condition  of  ex- 
hilaration. Not  infrequently,  for  a  couple  of  days,  there  are  frequent  and 
moderately  fluid  dejections,  sometimes  accompanied  by  exhaustion,  rarely 


664  ACUTE   GENERAL   DISEASES. 

by  griping.  This  is  called  the  cholera  diarrhoea.  Theise  premonitory 
symptoms  continue  from  a  few  hours  to  a  week  ;  usually,  however,  about 
two  days.  They  may  be,  and  frequently  are,  absent,  the  disease  commenc- 
ing precipitately  with  a  painless  diarrhoea.  Occasionally  the  prodromata 
assume  the  character  of  cholera  morbus,  but  cramps  are  more  prominent, 
and  there  is  little  or  no  fgecal  odor  to  the  discharge. 

The  second  stage  is  characterized  by  a  profuse  diarrhoea,  generally  com- 
mencing in  the  morning  or  in  the  middle  of  the  night,  and  the  patient 
describes  the  dejection  as  passing  from  him  in  a  stream.  These  painless 
discharges  sometimes,  after  the  second  evacuation,  lose  their  faecal  odor 
and  color,  and  assume  a  light  straw-colored  or  whey-like  appearance.  They 
vary  in  number  from  three  to  twenty  a  day,  and  are  often  accompanied 
by  attacks  of  regurgitative  vomiting  with  each  evacuation.  The  average 
amount  of  fluid  discharged  in  this  stage  by  a  cholera  patient  in  twenty- 
four  hours  is  about  sixty  ounces ;  the  patient  becomes  exhausted  and  as- 
sumes a  peculiar  apathetic  condition;  dizziness,  headache,  and  vertigo  some- 
times are  present.  Complete  anorexia  is  present  from  the  onset,  and  the 
thirst  is  tormenting  and  constant.  Bile  pigment  disappears  from  the 
stools,  and  the  rice-water  appearance  is  assumed  ;  there  may  be  a  pinkish 
tint  on  account  of  the  admixture  of  blood.  The  rice-water  discharges 
often  have  a  whey-like  appearance  consisting  of  the  watery  elements  of 
the  blood;  their  specific  gravity  varies  from  1.005  to  1.012,  and  they  con- 
tain a  small  proportion  of  albumen  and  an  excess  of  sodium  chloride.  On 
standing,  the  rice-water  fluid  deposits  a  sediment  holding  fine  granular 
cells,  amorphous  granular  matter,  shreds  of  tissue,  minate  nucleated  cells, 
epithelium  and  blood  globules.  Occasionally  the  blood  globules  are  so 
numerous  that  the  vomited  matters  are  red.  Vibriones,  bacteria,  urea, 
triple  phosphates  and  a  few  leucocytes  are  also  not  infrequent  ingredients. 
The  vomited  matter,  after  the  contents  of  the  stomach  and  bilious  matters 
have  been  ejected,  is  a  clear,  watery  fluid  containing  urea  and  carbonate  of 
ammonia  ;  it  is  ejected  in  a  stream,  without  nausea  or  effort,  and  is  char- 
acteristic of  cholera.  Everything  introduced  into  the  stomach  causes  vom- 
iting. 

The  tongue  is  dry  and  covered  with  a  thick  white  coating  ;  the  coun- 
tenance becomes  pinched  and  of  a  leaden  hue,  the  expression  is  staring 
and  dull  ;  as  the  exhaustion  verges  on  collapse,  the  pulse  becomes  imper- 
ceptible at  the  wrist.  Often  there  is  distressing  hiccough,  and  more  or 
less  dyspnoea.  In  rare  instances  the  abdomen  is  tense,  hard  and  sensitive 
to  pressure  ;  it  may  be  retracted.  Suppression  of  the  urine  is  not  of  infre- 
quent occurrence  at  this  stage. 

The  algid  stage  commences  with  a  well-marked  fall  of  temperature  ;  first 
in  the  hands,  feet,  and  face,  but  soon  over  the  entire  body.  The  axillary 
temperature  may  fall  as  low  as  72°  F.,  or  even  lower,  while  the  rectal  tem- 
perature registers  101°  or  102°  F.  The  accompanying  sweat  makes  the  sur- 
face feel  colder  than  it  really  is  ;  the  patient  himself  rarely  complains  of  be- 
ing cold.  The  skin  is  in  distinct,  hard  folds  {"  washerwoman's  skin") and 
of  a  bluish  oi  livid  color.     The  features  and  extremities  are  pinched,  the 


EPIDEMIC    CHOLERA.  665 

eyes  are  deeply  sunken,  and  have  purplish  rings  about  them.  The  patient 
is  in  a  state  of  apathy  or  stupor  ;  and  is  roused  therefrom  only  by  the 
severe  cramps,  which  cause  him  to  shriek  and  throw  himself  about  the 
bed.     These  cramps  chiefly  afl:"ect  the  muscles  of  the  calf  of  the  leg. 

In  the  last  portion  of  this  stage  (called  the  asphyxial)  the  condition  of 
the  patient  is  apparently  hopeless  ;  the  deadly  coldness  is  so  marked  in  the 
tongue  and  mouth  that  the  thermometer  may  show  a  temperature  of  only 
79°  F.  The  lividity  and  cyanosis,  the  imperceptible  heart  sounds,  the  ab- 
sence of  the  radial  pulse,  the  "cholera  face, "and  the  hoarse  sepulchral 
"^cholera  whisper,"  the  agonizing  cramps  that  now  recur  oftener  than  at 
first,  complete  the  desperate  picture  of  the  disease.  The  vomiting  and  di- 
arrhoea now  markedly  diminish  and  the  discharges  are  less  fluid  when  they 
do  occur.     The  stools  are  passed  involuntarily  or  heedlessly. 

The  urine  is  either  completely  suj)pressed,  or  a  few  highly  albuminous 
drops  are  passed.  The  respirations  are  shallow  and  hurried,  often  being 
40  per  minute,  and  alternate  very  often  with  paroxysms  of  intense  dysp- 
noea. There  is  a  loss  in  weight  during  this  period,  and  so  drained  is  the 
blood  that  there  is  an  absorption  of  pathological  fluid  accumulations  as  in 
pleurisy  and  synovitis.  The  saliva  and  all  secretions  are  suppressed.  Late 
in  this  stage  of  cholera  the  stools,  from  being  odorless,  change,  and  assume 
a  smell  something  like  decayed  fish.  The  state  of  collapse  may  last  forty- 
eight  hours,  and  yet  recovery  take  place  ;  or  death  may  occur  in  two  or 
three  hours  from  the  onset  of  this  algid  condition. 

The  mind  is  clear  throughout,  and  consciousness  is  retained  till  the  last ; 
it  is  even  recorded  that  insane  p)atients  have,  in  ''cholera  collai^se,"  re- 
gained (temporarily)  their  sanity.  » 

The  "  reactive  stage,"  when  reached,  is  often  marked  by  as  speedy  a  re- 
turli  of  favorable  signs  as  was  the  algid  stage  by  unfavorable  ones.  The 
pulse  appears  in  the  carotids  and  at  the  wrists,  and  the  heart-sounds  be- 
come distinct  and  regular.  The  temperature  rises,  the  skin  becomes  warm, 
the  face  looses  its  "  deathly"  look,  the  cramps  cease,  and  the  diarrhoea  con- 
tinues ;  the  stools  soon  acquire  a  faecal  odor  and  a  brown  color ;  although 
in  cases  where  the  algid  stage  is  prolonged,  foul-smelling,  greenish,  fluid 
discharges  continue  for  some  time.  The  urine  next  appears,  although  its 
return  may  be  delayed  from  ten  to  thirty  hours  ;  at  first  it  is  scanty,  high- 
colored  and  albuminous,  containing  casts,  and  turning  pinkish  with  nitric 
acid.  Soon  it  becomes  copious  and  normal  in  character.  The  duration  of 
this  period  varies  from  one  to  ten  days.  This  is  a  history  of  a  tj^oical  case 
of  cholera.  I  shall  now  briefly  consider  some  of  the  more  common  var-ia- 
tions. 

Cholera  typhoid  is  perhaps  the  commonest  sequela  of  the  collapse  stage. 
After  a  few  days,  in  some  cases  a  week,  of  well-marked  reactive  symptoms, 
when  the  secretions  are  fully  established  and  excretion  is  being  normally 
performed,  a  quickening  of  the  pulse  is  noticed,  usually  toward  evening, 
and  soon  a  febrile  movement  is  established,  which  recurs  with  regular 
paroxysms.  These  are  accompanied  by  adynamic  symptoms,  such  as  low, 
muttering  delirium,  a  dry  tongue,  injected  conjunctivse,  coma,  and  often 


666  ACUTE    GENERAL   DISEASES. 

bed-sores  and  purpuric  spots.  The  patient  sinks  into  a  state  of  extreme  ex- 
haustion, and  gradually  the  coma  deepens,  the  bowels  and  bladder  are  in- 
voluntarily evacuated  and  death  occurs.  If  patients  recover  from  cholera 
typhoid,  the  convalescence  is  very  protracted  and  uncertain. 

Urmmia  is  a  frequent  condition  ;  following  the  stage  of  collapse  no  urine 
is  secreted  in  the  reactive  stage ;  and  in  about  thirty-six  or  forty-eight 
hours  the  pulse  becomes  abnormally  slow,  the  face  slightly  flushed,  and  the 
eyes  darkly  injected.  The  urine  is  entirely  suppressed  or  very  scanty,  and 
will  be  found  to  contain  albumen  and  casts  in  abundance.  There  is  con- 
stant headache,  rarely  a  mild  delirium.  The  patient  becomes  drowsy  and 
listless,  vomiting  a  spinach-green  material.  Epileptiform  convulsions  are 
followed  by  coma  and  death.  The  bowels  are  constipated,  and  the  febrile 
symptoms  are  negative. 

A  "  cholera  eruption,"  so-called,  sometimes  makes  its  appearance  either 
in  the  typhoid  variety,  or  in  the  stage  of  reaction.  This  eruption  varies  in 
character  :  it  may  be  an  erythema,  or  resemble  urticaria  or  roseola.  It  ap- 
pears first  on  the  hands  and  feet,  then  spreads  to  the  trunk,  the  face  being 
very  slightly  affected.  Macular,  papular  and  vesicular  eruptions  sometim_es 
occur ;  in  all  cases  the  appearance  of  a  cholera  eruption  is  a  favorable 
symptom.  The  eruption  lasts  about  two  days,  and  is  often  accompanied  by 
a  "burning"  sensation.  Although  va.  children  the  disease  runs  the  same 
general  course,  collapse  supervenes  much  more  rapidly,  and  death  often  oc- 
curs after  a  few  choleraic  discharges. 

Cholerine  is  a  mild  form  of  cholera  occurring  during  a  cholera  epidemic, 
and  attended  by  all  the  characteristic  symptoms  of  the  disease,  except  that 
there  is  no  algid  stage.  There  is  often  a  slight  coolness  of  the  extremities 
and  cramps  in  the  calves  of  the  legs.  Eecovery  is  usually  rapid.  It  may 
be  followed  by  a  severe  and  well-marked  attack  of  cholera. 

Differential  Diagnosis. — During  an  epidemic,  cholera  is  not  likely  to  be 
mistaken  for  any  other  disease  ;  but  when  it  occurs  in  isolated  cases,  it  may 
be  confounded  with  acute  poisoning,  as  from  arsenic  or  antimony,  and  with 
the  g astro-enteric  variety  of  pernicious  fever. 

In  cases  of  poisoning  there  will  be  the  evidences  of  the  action  of  the 
poison  on  the  mouth  and  pharynx  which  are  absent  in  cholera.  The 
vomiting  in  cholera  is  regurgitative  and  painless,  whereas  in  cases  of 
poisoning  it  is  distressing,  and  is  preceded  by  an  intense  burning  pain 
in  the  oesophagus  and  stomach.  Diarrhoea,  if  it  occurs  in  poisoning, 
is  never  of  a  "  rice-iuater''  character,  but  mucous  and  blood-stained.  A 
chemical  analysis  of  the  ejected  matters  will  detect  the  presence  of  a 
poison. 

In  the  g astro-enteric  variety  of  pernicious  fever  the  first  two  or  three 
discharges  from  the  bowels  are  bloody ;  while  in  cholera  they  are  never 
bloody  at  first,  and  soon  assume  the  "rice-water"  appearance.  In  gastro- 
enteric pernicious  fever  vomiting  is  rare,  but  if  present,  is  painful  and 
retching  in  character;  while  in  cholera  it  is  regurgitative.  The  temperature 
in  pernicious  fever  is  high,  often  reaching  106°  or  107°  F.,  while  febrile 
movement  in  cholera  is  slight.     There  is  free  pigment  in  the  blood  in  per- 


EPIDEMIC   CHOLERA.  667 

nicious  gastro-enteric  fever,  which  is  never  found  in  the  blood  of  a  cholera 
patient. 

Prognosis. — The  mortality-rate  varies  in  different  epidemics  from  20  to  80 
per  cent.  ;  generally  one-half  recover.  The  more  dense  the  population  in 
any  locality  and  the  nearer  the  sea-coast  the  higher  the  mortality-rate. 
The  mortality-rate  is  always  less  toward  the  end  than  at  the  commence- 
ment of  an  epidemic  ;  it  is  greatest  in  those  under  one  or  over  fifty  years  of 
age.  Habits  of  life  and  hygienic  surroundings  influence  very  greatly  the 
prognosis.  The  duration  of  an  attack  varies  from  a  few  hours  to  two  weeks. 
Fatal  cases  usually  terminate  within  two  or  three  days,  while  the  aver- 
age duration  of  those  that  recover  is  nine  days.  Each  ej^idemic  in  this 
country  has  been  milder  than  the  preceding. 

The  symptoms  which  indicate  recovery  are  a  general  improvement  in  the 
appearance  of  the  patient ;  he  becomes  less  restless,  his  breathing  slower 
and  more  natural,  the  radial  pulse  returns,  the  lividity  of  the  surface  dis- 
appears, the  shrunken  tissues  expand,  the  temperature  rises  to  normal,  the 
urinary  secretions  are  re-established,  the  discharges  from  the  bowels  are 
again  stained  with  bile,  and  the  patient  falls  into  a  quiet  sleep.  The  un- 
favorable symptoms  are  involuntary  pinkish  discharges  from  the  bowels, 
absence  of  the  radial  pulse  and  the  second  sound  of  the  heart,  extreme  cy- 
anosis, a  complete  suppression  of  urine,  coma,  persistency  of  the  vomiting 
and  diarrhoea,  and  the  occurrence  of  complications. 

Cholera  may  be  complicated  by  capillary  bronchitis,  lobular  pneumonia, 
oedema  and  congestion  of  the  lungs,  pericarditis,  peritonitis,  and  pleurisy. 
The  sequelse  are  uraemia,  membranous  enteritis,  cerebral  oedema  and 
hypersemia,  gangrenous  or  purpuric  patches,  ulcerated  corner,  furuncles, 
bed-sores,  and  gangrene  of  the  lungs.  Death  may  result  from  the  direct 
effects  of  the  cholera  poison  without  the  occurrence  of  the  diarrhoea,  from 
the  exhaustion  produced  by  the  diarrhoea,  from  heart-failure,  and  from  any 
of  its  complications  or  sequelse. 

Treatment. — Prophylactic  and  hygienic  measures  may  limit  the  duration, 
extent,  and  the  mortality-rate  of  a  cholera  epidemic.  When  a  cholera 
epidemic  is  prevailing  quarantine  regulations  must  be  vigorously  enforced, 
and  those  attacked  by  the  disease  should  be  isolated.  All  cess-pools, 
privies,  and  bodies  of  stagnant  water  in  the  neighborhood  should  be  drained 
or  disinfected,  and  each  member  of  the  community  should  be  placed  under 
the  best  hygienic  conditions,  and  his  diet  carefully  regulated.  All  excesses 
in  food  and  drink,  and  all  sources  of  intestinal  ii'ritation  should  be  avoided. 
A  diarrhoea  occurring  during  a  cholera  epidemic  should  be  immediately 
checked. 

Cholera  stools  should  be  immediately  disinfected  and  buried  in  trenches, 
as  in  typhoid  fever.  The  linen  and  all  tin  utensils  used  in  the  sick  room 
must  also  be  thoroughly  disinfected.  Instead  of  sulphate  of  iron  and  hydro- 
chloric acid  mingled  with  the  faeces,  carbolic  acid  may  be  used  .  indeed, 
many  regard  it  as  superior  to  any  other  disinfectant  for  the  purpose.  All 
persons,  who  are  able,  should  be  inimediately  removed  from  the  infected 
district. 


668  ACUTE    GENERAL   DISEASES. 

The  first  great  object  of  medicinal  treatment  is  to  control  the  prodrO' 
mal  diarrhoea.  For  the  accomplishment  of  this,  opium  is  the  most  reliable 
drug  ;  it  may  be  combined  with  nitrate  of  silver,  sulj)huric  acid,  small 
doses  of  calomel,  or  with  vegetable  astringents.  Brown-Sequard  states  that 
morphine  hypodermically  in  sufficient  doses  at  the  onset  will  jjr event 
cliolera.  The  patient  is  to  be  at  once  placed  in  bed,  kept  absolutely  quiet, 
and  the  abdomen  swathed  in  flannel  bandages.  If  there  are  slight  signs  of  ex- 
haustion early,  stimulants  may  be  given  carefully.  Turpentine  stupes  over 
the  stomach  and  bowels  in  the  early  stage,  when  the  symptoms  are  urgent, 
are  often  serviceable.  Nausea  in  the  premonitory  stage  is  often  allayed  by 
carbonic-acid  water,  cracked  ice,  or  effervescing  draughts. 

When  the  disease  is  fully  established,  as  indicated  by  the  projectile  vomit 
and  rice-water  stools,  the  treatment  becomes  "symptomatic"  or  "ex- 
pectant." To  relieve  the  agonizing  thirst  patients  may  take  freely  of 
cracked  ice,  very  cold  seltzer  water,  or  carbonic-acid  water  combined  with 
lime  water.  If  the  pulse  becomes  imperceptible  at  the  wrist,  indicating 
heart  insufficiency,  stimulants  are  indicated,  but  they  must  be  carefully 
administered.  English  physicians  in  India  give  opium,  calomel,  and  acetate 
of  lead  (or  tannin)  during  the  stage  of  painless  diarrhoea.  If  the  cramps 
are  not  severe,  they  may  be  relieved  by  friction.  But  when  they  become 
severe,  hypodermics  of  morphia  combined  with  chloral  are  indicated.  If 
the  extremities  become  cold  they  should  be  wrapped  in  hot  cloths,  or  hot 
water  bags  may  be  placed  around  them,  or  they  may  be  rubbed  with  stim- 
ulating liniments  or  capsicum  preparations.  In  the  stage  of  collapse  iced 
brandy  or  champagne  given  repeatedly  and  in  small  doses  is  the  best  stimu- 
lant ;  musk  and  ammonia  are  also  recommended.  The  inhalation  of  amyJ 
nitrite  has  been  tried,  and  found  very  efficient  in  combination  with  alcohol, 
in  the  advanced  stage  of  collapse.  When  death  is  impending,  whiskey 
may  be  injected  hypodermically,  or  milk  maybe  administered  intravenously. 
In  the  use  of  stimulants  one  must  be  guided  by  the  pulse,  and  the  effects 
of  the  stimulation.  The  India  cholera  pills,  given  in  the  collapse,  are 
made  of  camphor,  asafoetida,  pepper,  and  the  essential  oils  or  ether. 

As  the  reactionary  fever  comes  on,  and  the  temperature  begins  to  rise, 
nourishment  must  be  given  with  the  greatest  care  ;  the  rule  being  to  post, 
pone  a  solid  diet  as  long  as  consistent  with  maintenance  of  strength  j 
milk,  beef -juice,  and  very  light  broths  are  the  only  articles  of  diet  admis- 
sible for  some  time.  When  the  stomach  is  weak  and  irritable,  and  there 
is  a  tendency  to  vomiting,  bismuth  and  cherry-laurel  water  can  be  given  ■ 
with  advantage.  Cerebral  symptoms  must  be  promptly  treated  by  ice-bags 
about  the  head,  heat  to  the  feet,  and  bromide  of  potassium  internally. 
The  surroundings  of  the  patient,  the  maintenance  of  cheerfulness  and 
calm,  and  even  temperature — these  are  important  points  to  be  observed. 

DIPHTHERIA, 

Diphtheria  is  a  specific  constitutional  disease,  characterized  by  a  granular, 
fibrinous  exudation  upon  the  surface  and  into  the  substance  of  mucous  mem- 


DIPHTHERIA.  G6D 

branes,  and  upon  abraded  surfaces.  Various  countries  of  Europe  were 
visited  by  epidemics  of  diphtheria  in  the  sixteenth  and  seventeenth  cen- 
turies. In  the  middle  of  the  last  century  it  reached  England,  and  in  the 
early  part  of  the  present  century  it  prevailed  at  different  points  in  the  Xew 
England  States. 

Dr.  Samuel  Bard,  of  New  York,  gave  the  first  accurate  description  of 
the  disease  in  this  country,  and  brought  clearly  before  the  profession  its 
specific  contagious  character;  his  clear  accounts  tally  perfectly  with  the 
experience  of  the  present  day.'  The  labors  and  investigations  of  Louis, 
Trousseau,  Rilliet,  Graefe,  and  Virchow  have  done  more  than  those  of  any 
Qther  investigators  to  perfect  our  knoAvledge  of  diphtheria. 

Morbid  Anatomy. — The  characteristic  pathological  lesion  of  diphtheria' 
consists  in  a  membranous  or  granular  infiltration  of  some  mucous  surface. 
Of  the  mucous  surfaces,  those  of  the  pharynx,  tonsils,  uvula,  and  nasal 
passages  are  its  most  usual  seats ;  beginning  on  the  tonsil  and  anterior 
wall  of  the  pharynx  the  diphtheritic  process  may  extend  upward  into  the 
posterior  nares,  forward  into  the  anterior  nares,  or  pass  down  the  larynx, 
larger  bronchi,  bronchioles,  and  even  enter  the  air-cells.  From  the  pharynx 
it  may  pass  down  into  the  oesophagus,  the  larynx  often  escaping  ;  or  it  may 
first  appear  in  the  larynx  and  extend  upward  into  the  pharynx  ; — this  latter 
is  rare.  Occasionally  the  mucous  membrane  of  the  mouth,  stomach,  va- 
gina, rectum,  and  biliary  passages  is  the  seat  of  the  diphtheritic  process. 
If  the  skin  is  abraded  it  may  become  covered  with  diphtheritic  exuda- 
tion. 

The  first  change  in  the  part  that  is  to  be  the  seat  of  this  exudation,  is  a 
passive  hypercemia  ;  the  capillary  vessels  are  gorged,  and  the  mucous  mem- 
brane is  of  a  dark,  purplish-red  color ;  somewhat  swollen  at  the  point 
where  the  membrane  is  to  develop.  The  hyperaemia  is  not  active,  the  color 
is  not  the  bright  red  of  active  inflammation,  but  dark,  livid,  and  ''angry." 
The  amount  of  serous  infiltration  of  the  sub-adjacent  tissues  determines,  in 
each  case,  the  amount  of  tumefaction.  On  the  surface  of  the  afPected  part 
there  is  an  abnormal  secretion  of  mucus,  and  the  epithelial  cells  covering 
it  become  enlarged  and  cloudy,  from  exudation  into  them.  Little  by  little 
they  lose  their  nuclei  and  become  transformed  into  a  homogeneous  mass, 
presenting  numerous  ramifications — in  other  words,  the  metamor|)hosed 
epithelium-cells  form  a  reticulated  membrane. 

The  first  and  most  superficial  diphtheritic  exudation  is  into  the  epi- 
thelium. The  cells  of  the  deeper  structures  may  be  simultaneously  or 
secondarily  involved.  The  surface  exudation  becomes  thicker  and  of  a 
grayish  color  as  the  sub-epithelial  mucous  and  sub-mucous  coats  become 
successively  involved.  In  mild  cases  the  membrane  first  resembles  a  gauzy 
film,  then  it  assumes  a  light  yellow  color,  or  occurs  as  white  patches  of 
varying  size.  In  severe  cases  a  leathery,  gray  exudation  from  one-eighth 
to  one-fourth  of  an  inch  in  thickness  will  form  in  five  or  six  hours,  which 
can  be  removed,  and  when  removed  leaves  a  raw  bleeding  surface  which  will 
immediately  be  covered  by  a  "(v^a^  exudation.     The  membranous  exudation 

1  He  publisht;d  his  pamphlet  iu  1812. 


670  ACUTE    GEISTERAL   DISEASES. 

may  become  infiltrated  with  blood,  and  'assume  a  black  color  ;  this  is  not  a 
condition  of  gangrene,  but  gives  evidence  of  great  blood  changes.  Absorp- 
tion of  the  exudation  is  only  possible  when  the  epithelial  layer  is  alone  in- 
volved ;  when  the  mucous  and  submucous  tissue  is  involved,  the  mem- 
branous exudation  can  only  be  removed  by  a  suppurative  or  gangrenous 
process. 

As  the  exudation  is  taking  place  into  the  epithelium,  micrococci,  or 
spherical  bacteria  will  be  found ;  as  the  diphtheritic  process  involves  the 
deeper  tissues,  the  bacteria  greatly  increase  in  number.  Some  regard  the 
bacteria  originating  within  the  epithelial  cells  as  the  result  of  the  path- 
ological processes;  others  that  they  cause  the  pathological  changes. '  It 
seems  reasonable  to  regard  the  diphtheritic  exudation  as  a  granular  fibrin  of 
low  vitality,  which  possesses  no  power  of  organization. 

The  arrest  of  the  diphtheritic  process  may  be  first  by  suppuration.  Un- 
derneath the  diphtheritic  exudation,  there  may  be  a  suppurative  process 
established,  which  separates  the  layer  of  exudation  from  the  tissues  which 
it  involves.  In  such  a  case  the  membranous  exudation  becomes  more 
sharply  defined  at  its  boundary,  the  tumefaction  of  the  surrounding  mucous 
membrane  subsides,  the  inflammatory  zone  draws  closer  and  closer  to  the 
margin  of  the  patch,  whose  edges  curl  up,  and  finally  the  mass  is  removed 
from  its  base,  and  is  thrown  off  spontaneously.  The  duration  of  this  exfo- 
liative process  varies  from  two  to  five  days.  In  some  cases  the  diphtheritic 
process  is  so  mild  that  while  the  exudation  occupying  the  epithelium  is 
thrown  off,  that  in  the  subjacent  structures  is  absorbed,  no  suppurative 
process  occurring.  In  this,  the  mildest  form,  there  is  absorption  accom- 
panied by  a  simple  epithelial  desquamation. 

Another  termination  of  the  local  diphtheritic  process  is  in  gangrene. 
The  nutrition  of  the  tissues  is  so  extensively  and  rapidly  interfered  with 
by  the  abundant  exudation  that  the  blood  supply  is  cut  off  and  death  of  the 
parts  is  the  result.  Some  observers  claim  that  gangrene  is  caused  by  the  ob- 
struction of  the  lymphatics  with  bacteria.  With  the  gangrenous  process 
large  numbers  of  putrefactive  bacteria  develop  in  the  membrane  and  in  the 
tissues  underneath,  which  break  down  into  a  semi-fluid,  dark  mass,  which 
has  the  peculiar  odor  of  gangrene.  Sometimes  the  sloughs  are  quite 
firmly  attached  to  the  adjacent  tissues.  The  so-called  septic  variety  is 
characterized  by  the  formation  of  an  extensive  necrotic  membrane,  the 
color  of  which  is  a  dark  gray,  or  brown  with  streaks  of  capillary  hemor- 
rhages throughout  its  entire  extent.  Larger  colonies  of  micrococci  are 
found  in  its  deeper  layers,  and  pressing  against  the  fibrinous  bands  they 
form  alveoli,  in  which  myriads  of  the  bacteria  lie.  The  exudation  in  this 
variety  occurs  most  frequently  in  the  nasak cavities,  where  in  and  beneath 
the  Schneiderian  mucous  membrane  is  an  extremely  rich  j)lexus  of  lym- 
phatic and  blood-vessels.     This  variety  may  involve  tissues  other  than  the 

1  Zahn  thinks  he  can  distinguish  three  varieties  of  diphtheritic  membrane  :  (1)  one  that  is  the  result  of 
morbid  processes  situate  in  the  pavement  epithelium  ;  (2)  one  that  arises  from  solidification  of  a  muco- 
fibrinous  exudation  ;  (3)  and  one  that  is  the  result  of  solidification  of  a  fibrino-puruloid  exudation.  This 
careful  histolo-pathologist  states  further  that  any  or  all  forms  of  the  bacteria  rnay  be  found  in  each  of  Ms 
varieties,  that  they  may  also  be  absent,  and  that  they  are  not  an  essential  factor  in  diphtheria. 


DIPHTHERIA.  G71 

mucous  and  submucous  layers  ;  cases  are  recorded  where  the  vomer  was 
eroded,  and  little  depressions  in  it  were  filled  with  nests  of  micrococci. 

A  piece  of  membrane  on  examination  will  be  found  soft  and  friable, 
breaking  down  into  an  ichorous,  semi-fluid,  dirty  brown  pulp.  If  a  por- 
tion of  "septic"  diphtheritic  membrane  is  removed,  ulcers  are  found  in 
the  tissue  beneath,  which  may  be  shallow  or  deep.  When  shallow,  they 
bleed  very  readily ;  when  deep,  they  are  covered  by  dirty  gray  sloughs. 
The  variety  of  the  epithelium,  and  the  number  of  mucous  glands  in  the 
mucous  membrane  involved  in  the  dij^htheritic  process,  modify  the  patho- 
logical course  of  the  exudation.  When  diphtheria  invades  the  bronchioles 
and  alveoli,  the  characteristic  microscopical  appearances  of  the  exudation 
are  discovered,  and  some  air  cells  are  filled  with  micrococci. 

The  heart  is  pale,  flabby,  and  friable,  presenting  changes  similar  to  those 
in  typhoid  fever.  The  right  heart  is  often  filled  with  clots  ;  and  the  peri- 
cardium may  be  the  seat  of  numerojis  ecchymotic  sjDots,  rarely  of  large 
size.  Endocarditis  is  not  an  infrequent  complication,  and  when  present  it 
is  in  many  cases  ulcerative,  particularly  if  the  disease  has  been  severe  and 
there  are  extensive  blood  changes. 

The  hlood  sometimes  is  but  slightly  altered ;  in  the  severer  forms  it  is 
thick,  of  a  dirty  brown  color,  slightly  coagulable,  and  after  death  contains 
micrococci.  The  arteries  and  veins  are  equally  filled.  A  transient  increase 
in  the  number  of  the  white  blood  corpuscles  is  very  common. 

The  spleen  is  usually  enlarged,  the  capsule  is  tense,  shining,  and  covered 
with  numerous  points  of  capillary  hemorrhage.  The  splenic  parenchyma  is 
congested,  softened,  and  friable,  darker  than  normal,  and  often  the  seat 
of  multiple  infarctions. 

The  lymphatic  glands  become  swollen  and  inflamed  on  account  of  their 
free  communication  with  the  infected  parts.  The  hyperj^lasia  occurring 
within  the  gland  causes  a  swelling  which  may  be  tense  and  hard  or  doughy. 
This  doughy  feel  results  from  oedema  of  the  peri-glandular  and  subcutaneous 
connective-tissue,  in  which  vegetable  parasites  are  frequently  found.  The 
lymph  vessels  are  often  clogged  with  micrococci.  Suppuration  in  the 
lymphatics  is  of  very  rare  occurrence. 

The  kidneys  are  congested  or  the  seat,  in  severe  cases,  of  parenchymatous 
nephritis,  differing  in  no  respect  from  that  occurring  in  scarlatina,  which 
has  received  the  name  of  scarlatinal  nephritis.  Those  who  favor  the  para- 
sitic origin  of  diphtheria  regard  the  micrococci  as  the  starting-point  of  the 
morbid  nephritic  processes ;  yet  they  state  that  if  a  child  die  rapidly  from 
suffocation,  only  a  cloudy  swelling  of  the  epithelium  exists;  but  if  the  disease 
shall  have  progressed  for  several  days,  attended  by  severe  symptoms  of  in- 
tense blood  poisoning,  then  the  micrococci  are  discovered.  Thus  the 
morbid  processes,  by  their  own  statements,  are  shown  to  be  primary  and 
not  secondary  to  bacterian  developments  or  migration. 

The  Brain  and  Cord. — In  severe  cases  there  are  numerous  small  spots  of 
capillary  hemorrhage  scattered  throughout  the  meninges  of  both  brain  and 
cord.  These  extravasations  may  sometimes  be  large  enough  to  form  clots, 
and  then  softening  of  the  brain  in  localized  spots  will  occur.     Cells  and 


672  ACUTE    GEKEEAL   DISEASES. 

nuclei  swell  the  spinal  nerves  at  the  point  where  their  roots  join  so  that 
their  thickness  may  be  twice  the  normal  ;  blood  may  be  extravasated  at 
this  point  and  then  the  swelling  will  be  distinctly  red.  Punctate  hemor- 
rhages into  nerve  centres  where  white  matter  is  predominant  are  said  to  be 
the  cause  of  diphtheritic  paralysis,  and  after  degenerative  processes  have 
occurred  in  these  hemorrhagic   spots  the  paralysis  gradually  disappears.' 

Etiology. — Diphtheria  is  a  miasmatic  contagious  disease,  often  prevailing 
epidemically.  Many  of  its  etiological  conditions  are  identical  with  those 
of  typhoid  fever :— filth,  bad  sewerage,  over-crowding,  etc., — and  yet  we 
are  not  prepared  to  state  that  either  of  these  diseases  is  of  spontaneous 
origin.  I  have  met  with  diphtheria  in  houses  where  the  water  and  sewer- 
age pipes  were  defective,  and  where  no  other  causative  factor  could  be 
found  ;  nevertheless  I  have  a  belief  that  the  miasm  of  diphtheria  must 
be  present  with  the  other  etiological  conditions  before  diphtheria  will  be 
developed.  Trousseau  claims  that  the  infectious  element  is  confined  to 
the  exudation,  but  many  clinical  facts  indicate  that  it  is  present  in  the  ex- 
halations and  in  the  excretions,  as  well  as  in  the  exudation  itself.  Di|)h- 
theritic  contagion  clings  to  the  objects  that  have  been  in  contact  with  the 
diseased  individual,  and  may  thus  be  carried  a  long  distance. 

Another  vexed  question  in  its  etiology  : — is  it  first  local,  and  then  consti- 
tutional, or  vice  versd  f  From  a  clinical  stand-point  it  seems  that  the 
disease  starts  locally  ;  that  some  particle,  for  instance,  of  the  exudation, 
too  small  to  be  detected  with  the  unaided  eye,  is  received  upon  the  mu- 
cous membrane  of  the  pharynx,  nose,  mouth,  larynx,  trachea,  vagina,  or 
upon  a  cut  or  abraded  surface  ;  and  thence  contaminates  the  whole  system. 
The  point  of  infection  cannot  be  determined  until  after  constitutional  in- 
fection has  taken  place.  It  seems  to  be  well  established  that  when  the  lo- 
cal signs  of  diphtheria  are  present,  there  is  already  a  constitutional  infec- 
tion. The  experiments  of  Oertel  ^  and  others  show  that  the  point  of  inoc- 
ulation is  the  point  from  whence  radiates  the  disease.  Experiments  are 
now  being  made  which  tend  to  show  that  in  virulent  fluids  it  is  not  the 
bacteria  but  the  chemical  element  which  is  capable  of  inducing  the  grave 
symptoms  which  sometimes  follow  inoculation. 

The  stage  of  incubation  usually  varies  from  one  to  eight  days  ;  it  may  last 
one  month;  when  the  disease  is  directly  communicated,  as  in  some  recorded 
instances  when  a  piece  of  diphtheritic  membrane  is  dislodged  and  coughed 
into  the  mouth,  nose,  or  eye  of  the  physician  or  attendant,  the  disease  has 
developed  within  twenty-four  hours.  Bat  the  question  arises:— may  not  the 
one  thus  attacked  have  been  under  the  influence  of  the  diphtheritic  poison 
for  some  time,  and  thus  be  prepared  for  the  rapid  reception  of  the  local 
poison  ?  During  epidemics  the  period  of  incubation  is  shorter,  and  there 
is  reason  to  believe  that  the  more  virulent  the  poison  the  less  time  elapses 
between  exposure  and  the  initial  symptoms.  As  a  rule,  the  latent  period 
of  diphtheria  rarely  exceeds  five  days. 

1  Einidex  iiber  Biphthene.    L.  Buhl,  Zeit.  fur  Berl.,  iii.,  4.    1867. 

2  ExpeHmentaUe  UnUrsuchungen  iiber  Diphtlierie.  M.  J.  Oertel,  Deutsch.  Arch,  fur  klin.  Med.,  viiu 
1871. 


DIPHTHERIA.  673 

Diphtheria  may  prevail  as  an  epidemic,  or  be  endemic.  It  also  occurs 
sporadically.  Sporadic  cases  occur  most  frequently  in  those  localities 
where  the  disease  has  prevailed  as  an  epidemic.  Climatic  influences  have 
little  to  do  with  its  development,  but  autumn  and  spring  are  the  seasons 
when  the  disease  is  most  fatal.  Age  is  a  powerful  predisposing  cause ; 
from  the  second  to  the  fifth  year  is  the  period  of  greatest  susceptibility  ; 
but  no  age  is  exempt.  Previous  attacks  afford  no  immunity  against  sub- 
sequent ones ;  certain  individuals  seem  to  be  perfectly  proof  against  the 
diphtheritic  infection.  Filth,  bad  sewerage  and  drainage,  over-crowding 
and  a  general  bad  hygienic  condition  favor  the  development  and  spread  of 
diphtheria.  Exposure  to  cold  and  wet,  and  sudden  chilling  of  the  body, 
may  bring  on,  or  hasten  an  attack  of  diphtheria  during  an  epidemic.  In  a 
region  where  the  soil  is  porous,  the  spread  of  the  disease  is  much  less  ex- 
tensive than  in  clay  soil. 

Symptoms. — The  symptoms  of  diphtheria  are  local  and  constitutional. 
The  constitutional  may  precede  the  local  ;  or  both  may  appear  at  the  same 
time.  In  some  cases  the  local  are  the  primary,  and  for  a  time  the  only 
signs  of  the  disease.  The  ushering-in  symptoms  vary  not  only  in  different 
epidemics,  but  in  different  cases  during  the  same  epidemic.  It  is  a  dis- 
ease which  has  no  typical  course. 

The  local  symptoms  begin  with  a  sensation  of  dryness  and  prickling  in 
the  throat,  with,  perhaps,  slight  pain  independent  of  attempts  to  swallow. 
There  is  more  or  less  stiffness  along  the  angle  of  the  jaw.  Deglutition  be- 
comes more  and  more  painful;  solids  do  not  cause  as  much  dysphagia  as 
fluids.  There  may  be  marked  and  painful  swelling  of  the  glands  at  the 
angle  of  the  Jaw — in  the  bifurcation  of  the  common  carotid  artery — but 
many  severe  and  fatal  cases  are  accompanied  by  only  slight  glandular  en- 
largement, and  occasionally  the  disease  runs  its  entire  course  without  any 
glandular  swellings.  In  some  epidemics  most  of  the  cases  will  be  attended 
by  extensive  glandular  swellings,  while  others,  of  equal  severity,  only 
exhibit  this  symptom  in  a  slight  degree.  However  the  disease  may  com- 
mence, when  fully  established  there  will  be  noticed  upon  the  anterior  pil- 
lars of  the  soft  palate,  the  velum,  and  tonsils,  sometimes  also  upon  the 
posterior  pharyngeal  wall,  whitish  patches,  surrounded  by  a  livid,  tumefied 
and  congested  mucous  membrane.  At  this  early  stage  the  exudation  can 
be  removed  without  causing  even  punctate  hemorrhage  ;  and  under  the 
microscope  the  epithelial  cells  will  exhibit  the  appearances  that  have 
already  been  described.  The  sub-epithelial  tissue  becomes  oedematous,  and 
later,  both  tonsils,  the  uvula,  and  the  anterior  part  of  the  soft  palate  will 
become  oedematous.  At  this  period  the  membrane  may  be  easily  removed, 
but  soon  after  its  removal  it  will  reappear  in  the  same  situation,  and 
have  the  same  extent.  As  a  rule  the  more  extensive  the  exudation,  the 
thicker  will  be  the  membrane  and  the  firmer  its  attachment. 

When  the  posterior  nares  are  involved  it  is  usually  the  'result  of  the  ex- 
tension of  the  diphtheritic  process  upward  :  the  tonsils,  uvula,  and  pos- 
terior pharyngeal  wall  having  been  the  primary  seat  of  the  exudation.  A 
coryza  is  soon  developed,  and  the  sanious,  ichorous  discharge  irritates,  red- 


674  ACUTE   GENERAL   DISEASES. 

dens,  and  excoriates  the  surfaces  over  which  it  flows.  At  the  same  time 
rapid  swelling  of  the  cervical,  lymphatic,  and  sub-maxillary  glands  occurs  ; 
and  there  is  undoubtedly  a  special  connection  between  enlargement  of  the 
glands  at  the  angle  of  the  jaw,  and  diphtheria  of  the  nares  and  posterior 
wall  of  the  pharynx.  The  nostrils  are  soon  clogged,  often  completely  so, 
and  repeated  attacks  of  epistaxis  may  mark  the  later  stages  of  nasal  diph- 
theria. When  the  disease  extends  upward  the  parotid  is  not  infrequently 
swollen  and  tender.  Xasal  diphtheria  is  in  a  few  instances  primary.  The 
nose,  in  cases  of  invasion  of  the  posterior  nares,  is  often  swollen  and  red,  or 
shining  and  oedematous  ;  the  parts  excoriated  by  the  flow  from  the  nostrils 
are  soon  covered  with  ulcers,  and  the  latter  are  often  covered  with  the  gray 
diphtheritic  exudation. 

When  the  Eustachian  tubes  are  involved,  there  will  be  tinnitus  aurium, 
darting  pains  on  attempts  to  swallow,  marked  loss  of  hearing,  and  perhaps 
otitis  ;  perforation  of  the  tympanum,  and  caries  of  the  adjacent  bones  may 
result.  The  external  ear  has  in  rare  cases  been  the  seat  of  secondary  and 
also  of  primary  diphtheria.  The  middle  ear  has  also  sometimes  been  im- 
plicated. The  eye  may  be  invaded  in  diphtheria  when  the  nasal  duct  is 
the  seat  of  the  exudation  ;  or  a  piece  of  membranous  exudation  being 
coughed  into  the  eye  of  the  examiner  may  excite  a  diphtheritic  conjunc- 
tivitis. If  the  diphtheritic  process  passes  downward  it  may  enter  either 
the  digestive  or  the  respiratory  tract. 

If  the  cesopliagus  is  involved  there  will  be  a  marked  dysphagia,  and  fluids 
■will  be  regurgitated  ;  accompanying  paralysis  of  the  muscles  of  deglutition 
in  many  instances  increases  the  dysphagia.  If  no  special  signs  of  pharyn- 
geal exudation  are  present  in  a  suspected  case  of  oesophageal  diphtheria, 
portions  of  the  exudation  may  appear  in  the  vomited  matters,  for  vomiting 
is  an  important  sign  of  oesophageal  diphtheria.  Portions  of  membrane  in 
the  fgecal  discharges  point  to  the  existence  of  the  oesophageal  diphtheria 
when  there  are  evidences  of  tonsillar  and  pharyngeal  exudation. 

When  the  vagina,  rectum  or  ktbia  is  involved  there  will  be  more  or  less 
swelling  of  the  inguinal  glands  in  the  immediate  neighborhood. 

The  diphtheritic  process  may  extend  from  the  pharynx  into  the  larynx 
and  trachea.  Sometimes  laryngeal  diphtheria  is  developed  when  the  pri- 
mary seat  of  the  diphtheria  is  in  the  nasal  passages,  or  in  the  mouth. 
Laryngeal  diphtheria  occurs  most  frequently  in  children  ;  the  younger  the 
child  the  greater  the  liability  to  laryngeal  comj)lication  ;  when  adults  are 
attacked,  it  is  the  weak  and  feeble  and  the  aged.  The  epiglottis  becomes 
hypergemic,  livid,  and  swollen,  its  edges  are  harder  than  the  remainder  of 
its  substance,  and  the  diphtheritic  patches  are  developed  irregularly  upon 
its  surface. 

The  first  symptom  indicative  of  laryngeal  diphtheria  is  a  change  in  the 
voice,  which  loses  its  volume,  becomes  hoarse,  rough  and  indistinct, 
then  falls  to  an  inarticulate  whisper.  The  respirations  become  noisy  and 
whistling,  and  dyspnoea  becomes  more  and  more  urgent  as  the  exudation 
advances.  The  cough  is  first  dry  and  stridulous — "  brassy," — but  soon 
changes,  losing  the  brassy  tone,  and,  indeed,  it  has  no  distinct  tone  what- 


DIPHTHERIA.  (,-i/5 

ever,  and  is  so  peculiar  as  to  be  almost  diagnostic  of  laryngeal  diphtheria. 
In  children  the  invasion  of  the  larynx  is  often  sudden.  In  a  short  time 
there  is  complete  aplionia ;  a  cough  is  developed  that  is  '^  barking"  or 
"  croupy  "  in  character,  but  (as  in  adults)  it  soon  becomes  abortive.  The 
dyspnoea  is  extreme ;  all  the  auxiliary  muscles  of  respiration  are  called 
into  play.  The  attacks  of  difficult  breathing  assume  a  paroxysmal  form, 
and  in  one  of  the  paroxysms  death  may  occur.  If  the  upper  part  of  the 
larynx  only  is  involved  there  is  difficulty  of  inspiration,  but  when  the 
whole  larynx  is  involved  expiration  is  also  affected.  There  is  falling  in  of 
the  supra-  and  infra-clavicular  sjiaces  during  inspiration,  showing  that  im- 
perfect inflation  of  the  lungs  results  from  the  mechanical  obstruction  to 
the  entrance  of  the  air  into  them.  Cyanosis  becomes  marked,  and  there 
is  either  stupor,  or  restlessness  and  Jactitation.  When  the  child  dies  it  is 
with  all  the  symptoms  of  croup  {q.  v.).  Death  is  not  from  the  action  of 
the  poison  but  from  local  obstruction  which  has  mechanically  forestalled 
its  constitutional  effects. 

A  laryngoscopic  examination  shows  epiglottis,  vocal  cords,  and  the  in- 
terior of  larynx  to  be  the  seat  of  a  diphtheritic  exudation,  the  ventricle  being 
usually  wholly  obliterated. 

Auscultation  reveals  abnormal  laryngeal  sounds,  together  with  rales  of 
various  kinds,  and  a  loss  of  vesicular  respiration.  In  some  instances  the 
diphtheritic  process  may  have  its  primary  seat  in  the  larynx,  and  then  ex- 
tend upward,  the  same  processes  occurring  upon  the  tonsils,  uvula,  and  soft 
palate,  as  when  they  are  the  primary  seat  of  the  disease.  In  such  cases 
laryngeal  symptoms  are  present  from  the  onset  of  the  disease. 

Constitutional  Symptoms. — There  are  no  regular  stages  in  the  develop- 
ment of  diphtheria,  therefore  no  typical  clinical  sketch  can  be  given  which 
shall  include  all  cases.  The  division  of  diphtheria  into  the  catarrhal, 
croupous,  gangrenous  and  septic  forms  can  only  be  made  at  the  expense  of 
facts,  for  they  may  rapidly  merge  into  each  other,  and  are  only  stages  of 
one  and  the  same  diseased  process.  Diphtheria  may  begin  with  well- 
marked,  active  symptoms,  as  a  chill,  fever,  pain  in  the  head  and  back, 
nausea,  vomiting,  and  even  convulsions.  Or  it  may  come  on  insidiously, 
the  patient  complaining  only  of  the  throat  symptoms.  It  may  run  so  mild 
a  course  that  the  patient  at  no  time  feels  sick  ;  the  throat  symptoms  are 
not  marked  ;  and  there  is  a  small  patch  of  exudation  upon  the  tonsils,  but 
it  does  not  extend. 

There  is  little  or  no  febrile  movement,  and  at  the  end  of  a  week  the 
patient  is  fully  convalescent.  In  those  cases  where  well-marked  symptoms 
usher  in  the  disease,  the  temperature  ranges  higher  than  in  any  other  form 
of  the  disease  ;  in  rare  cases  it  may  reach  105°  F.  by  the  end  of  the  second 
day.  Insidious  cases  are  marked  by  a  gradual  rise  in  temperature,  102° 
or  103°  F.  being  the  highest  point  reached  during  the  whole  course  of  the 
disease.  Mild  and  severe  cases  often  occur  in  the  same  household  during 
the  same  epidemic. 

In  whatever  manner  diphtheria  is  established,  the  constitutional  and  local 
symptoms  do  not  always  progress  with  the  same  severity.     In  some  cases 


676  ACUTE    GE^STEEAL   DISEASES. 

while  the  exudation  is  rapidly  extending  the  temperature  falls  to  normal, 
the  pulse  diminishes  in  frequency,  the  patient  seemingly  having  decidedly 
improved  in  every  respect — in  fact,  the  constitutional  symptoms  remit  if 
they  do  not  intermit.  The  pulse,  however,  will  show  the  influence  of  the 
poison  on  the  nervous  system,  either  in  irregularity  or  abnormal  frequency, 
or  both.  But  during  all  this  time  the  membranous  exudation  is  spreading. 
After  a  time  the  temperature  rises  to  103"  or  104°  ¥.,  the  pulse  to  120  or  130, 
and  all  the  severe  constitutional  symptoms  reappear.  Death  often  occurs 
early  in  such  cases.  In  another  class  of  cases  the  constitutional  symptoms 
are  severe  from  the  onset,  while  the  local  manifestations  of  the  disease  are 
but  slight  and  not  progressive.  In  some  cases  the  nervous  system  may  be 
overwhelmed  by  the  intensity  of  the  diphtheritic  poison  at  the  onset  of  the 
disease,  and  death  result  before  any  local  manifestations  of  the  disease  have 
had  time  to  make  their  appearance. 

In  the  more  common  forms  of  diphtheria  the  first  symptom  will  usually 
be  the  soreness  of  the  throat,  which  will  be  found  congested ;  and  either 
upon  a  tonsil  or  at  some  point  in  the  pharynx,  a  small  white  patch  of  ex- 
udation will  be  seen.  Slight  febrile  movement  may  accompany  the  throat 
symptom,  or  it  may  not  come  on  for  forty-eight  hours.  The  exudation 
gradually  extends  until  a  large  surface  is  covered  with  a  thick  layer  of 
membrane,  which  assumes  a  gray  or  brown  color.  The  sub-maxillary  glands 
become  more  or  less  swollen.  There  is  always  some  obstruction  in  the 
throat  and  difficulty  in  swallowing.  As  the  disease  becomes  fully  developed, 
patients  are  unable  to  sit  up.  There  is  nausea  and  often  vomiting.  The 
urine  is  usually  albuminous.  The  pulse  becomes  frequent  and  feeble  ;  the 
temperature  ranges  from  101°  to  103°  P.  The  membranous  exudation 
continues  to  extend,  involving  more  and  more  of  the  throat.  The  patient's 
general  condition  becomes  worse  each  day  until  about  the  end  of  a  week  ; 
when  the  membrane  is  thrown  off,  the  pulse  becomes  less  frequent  and  the 
patient  slowly  recovers.  Or,  as  happens  in  some  instances,  as  the  exuda- 
tion disappears  from  the  tonsils  it  extends  into  the  larynx  :  then  are  de- 
veloped all  the  symptoms  of  laryngeal  obstruction,  the  breathing  becomes 
difficult,  cerebral  symptoms  are  prominent,  and  patients  die  in  a  few  days 
after  the  laryngeal  symptoms  appear.  Occasionally  after  the  local  mani- 
festations of  diphtheria  have  disappeared,  patients  experience  a  degree  of 
prostration  and  feebleness  that  is  met  with  in  no  other  disease.  The  pulse 
becomes  feeble,  frequent  and  intermitting  :  and  the  heart-sounds  are 
muffled  and  indistinct.  Death  occurs  in  such  cases  as  if  a  poison — such 
as  prussic  acid  for  instance — had  been  taken. 

Symptoms  luMch  indicate  danger.  —Diarrhoea,  although  not  often  present 
in  diphtheria,  may  be  so  profuse  as  to  cause  exhaustion  which  will  hasten  the 
fatal  termination.  Nausea  and  vomiting  coming  on  late  are  most  unfavor- 
able symptoms.  Albuminuria  occurs  in  mild  as  well  as  in  severe  cases, 
rarely  lasting  longer  than  a  week,  except  in  those  severe  cases  where  oedema 
is  present,  and  where  epithelial,  granular,  small  hyaline  and  exudative 
casts  are  found  in  the  urine.  It  is  stated  by  some  that  the  amount  of 
albumen  in  the  urine  is  in  direct  proportion  to  the  intensity  of  the  diph- 


DIPHTHEfllA.  677 

theritic  infection.  In  a  few  rare  instances  diphtheritic  nephritis  has  been 
so  intense  that  death  has  resulted  from  it,  before  either  the  constitutional 
or  local  symptoms  of  the  disease  were  present.  Albuminuria  generally 
comes  on  toward  the  end  of  the  first  week  of  the  disease.  Coma  may  occur 
as  the  result  of  the  nej)hritis.  An  erythematous  eruption  sometimes  makes 
its  appearance  in  diphtheria  between  the  first  and  third  days.  Its  usual  seat 
is  the  upper  part  of  the  chest  and  back. 

The  pulse  is  peculiar-  and  varies  greatly  in  different  cases.  There  are 
three  distinct  varieties  : 

I.  In  a  large  number  of  cases  the  pulse  from  the  very  commencement  is 
feeble,  small,  and  rapid,  ranging  from  120  to  160,  or,  in  young  children, 
even  to  170  in  the  minute. 

II.  There  is  a  class  of  cases  where  the  pulse  rises  to  120  or  130  early  in 
the  disease,  but  falls  to  60  or  even  40  within  twenty-four  or  forty-eight 
hours  from  its  onset. 

III.  There  is  a  class  of  cases  in  which  the  pulse  is  irregular  and  inter- 
mittent throughout  the  entire  course  of  the  disease.  The  prognosis  in  the 
latter  variety  is  always  bad. 

If  the  temperature  falls  to  normal,  or  below,  and  the  exudation  shows 
no  signs  of  exfoliating,  no  matter  how  trifling  its  amount,  or  how 
slight  the  glandular  swelling,  the  case  is  grave  and  death  is  not  usually 
long  delayed.  Convulsions  occurring  late  in  diphtheria  are  always  un- 
favorable symptoms,  while  as  usheriug-in  symptoms  they  have  no  special 
significance.  Swelling  of  the  lymphatic  glands,  although  not  present  in 
all  cases,  is  so  frequently  present  that  it  must  be  regarded  as  one  of  the 
symptoms  of  the  disease.  If  it  is  extensive  so  as  to  interfere  with  degluti- 
tion and  respiration,  the  prognosis  is  unfavorable. 

After  the  exudation  disappears  and  convalescence  is  apparently  estab- 
lished, sequelae  may  develop,  which  may  continue  for  months  and  even 
years.  The  commonest  h  paralysis  of  some  of  the  voluntary  muscles  ;  the 
muscles  most  frequently  affected  are  those  of  the  soft  palate  and  pharynx. 
Usually  the  first  thing  indicating  the  occurrence  of  this  paralysis  will  be 
difficulty  in  swallowing — first  fluid  and  then  solid  food — with  an  inability 
to  articulate  clearly.  "When  paralysis  is  unilateral  the  velum  is  drawn'  to 
the  healthy  side  ;  when  both  sides  are  involved  the  velum  hangs  pendulous 
and  motionless  ;  there  is  also  a  loss  of  sensation  as  well  as  of  motion,  for 
pricking  it  causes  no  pain.  The  voice  is  altered,  and  children  cry  as  with 
a  cleft-palate,  while  adults  have  a  sort  of  nasal  twang.  These  changes  come 
from  paralysis  of  the  velum,  anterior  pillars  of  soft  palate,  and  pharyngeal 
wall.  Fluids  are  only  partially  swallowed,  the  greater  portion  being  re- 
gurgitated through  the  nose,  especially  if  the  individual  is  standing  or 
leaning  forward  while  drinking.  This  variety  of  paralysis  sometimes  comes 
on  while  the  exudation  is  yet  visible  in  the  fauces,  just  as  it  is  disappear- 
ing, or  in  a  week  or  ten  days  after  it  has  entirely  disappeared.  With  the 
dysphagia  there  is  sometimes  difficulty  in  expectorating  ;  the  patient  will 
choke,  cough  and  strangle  in  vain  endeavors  to  get  rid  of  mucus  that  has 
collected  in  the  pharynx. 


€78  ACUTE   GENERAL   DISEASES. 

As  the  pharyngeal  paralysis  is  disappearing, — or  from  two  to  ten  days 
after, — the  muscles  of  some  other  part  of  the  body  will  be  involved — the 
lower  extremities  being  much  more  frequently  affected  than  the  upper. 
Though  usually  beginning  in  the  feet,  diphtheritic  paralysis  follows  no 
regular  order  ;  a  hand  may  first  be  affected,  then  a  leg,  and  subsequently 
the  other  hand,  arm  and  leg.  Before  the  occurrence  of  the  paralysis  there 
will  be  a  sensation  of  coldness,  pricking,  crawling  (formication)  and 
numbness  in  the  part  about  to  be  affected.  The  patient  cannot  determine 
precisely  where  he  has  placed  his  foot — on  the  floor  or  some  object  higher 
than  the  floor ;  movements  are  ungainly  and  hesitatingly  made,  the  gait 
becomes  tottering,  and  finally  he  cannot  stand,  the  paralysis  becoming  com- 
plete. Sensation  is  likewise  more  or  less  impaired.  The  hand  loses  its 
usual  dexterity  ;  the  patient  being  unable  to  button  his  coat,  or  even  write 
his  name.  When  the  muscles  of  the  neck  are  involved  the,  head 
"  wobbles,"  or  is  held  upright  with  the  greatest  diflficulty.  The  neck  is 
usually  the  last  part  to  be  attacked.  The  power  of  ocular  accommodation 
is  often  seriously  interfered  with  on  account  of  the  paralysis  of  some  of  the 
ocular  muscles.  The  ciliary  and  recti  suffer  oftenest.  First,  sight  is 
diminished  or  lost  for  objects  close  at  hand  ;  and  later,  distant  objects  be- 
come invisible.  There  is  always  diminished  refraction,  and  there  may  be 
strabismus  and  double  vision. 

When  diphtheritic  paralysis  is  general  the  laryngeal  muscles  will  usually 
be  wholly  or  partially  involved.  The  voice  is  hoarse,  non-resonant,  and 
often  there  is  complete  aphonia.  There  is  no  loss  of  sensation  until  the 
superior  laryngeal  branch  of  the  pneumogastric  is  involved  ;  this  is  attended 
with  danger,  for  particles  of  food  may  pass  into  the  bronchi,  and  suffocative 
dyspnoea  may  result  in  death.  In  nearly  all  forms  of  laryngeal  paralysis 
there  is  more  or  less  dyspnoea,  greatly  increased  by  exercise.  If  the  paraly- 
sis involves  the  sphincters  there  will  be  involuntary  discharges  from  the 
bladder  and  rectum.  The  genital  organs  may  be  paralyzed,  and  all  sexual 
desire  and  power  may  be  lost  for  months.  Paralysis  of  the  muscles  of  the 
thorax,  trunk  and  diaphragm  gives  rise  to  grave  symptoms,  pulmonary 
oedema  and  death  usually  resulting.  Finally,  paralysis  of  the  heart  may 
occur. 

Diphtheritic  paralysis  is  always  entirely  recovered  from.  In  mild  cases 
its  duration  is  two  or  three  weeks,  while  in  others  it  has  continued  one 
or  two  years.  Another  sequel  of  diphtheria  is  parenchymatous  nephritis. 
When  developed  during  the  exudative  stage  it  usually  ends  in  complete  re- 
covery. Earely  does  it  directly  cause  death.  When  so  developed  it  may 
be  regarded  as  part  of  the  active  history  of  the  disease.  But  when  it 
occurs  during  convalescence  it  may  lead  to  chronic  Bright's  disease.  In- 
flammation of  a  serous  membrane  may  complicate  or  be  a  sequel  of  diph- 
theria ;  the  most  frequent  serous  inflammation  is  endocarditis. 

Pleurisy,  peritonitis  and  pericarditis  are  of  rare  occurrence.  Chronic 
pharyngitis  is  a  sequela  only  in  those  cases  wliere  there  has  been  paralysis 
of  the  pharyngeal  muscles. 

Differential  Diagnosis. — The  diagnosis  of  diphtheria  rests  on  the  presence 


DIPHTHEKIA.  679 

of  a  membranous  exudation.  When  it  prevails  as  an  epidemic,  a  form  of 
"  sore  throat,"  a  pharyngeal  catarrh  usually  prevails  at  the  same  time, 
sometimes  called  ''diphtheritic  sore  throat." 

This  sore  throat  is  ushered  in  by  a  chill,  followed  by  a  more  or  less  in- 
tense febrile  movement.  There  is  a  sense  of  fulness  in  the  throat  with 
swelling  of  the  sub-maxillary  glands,  and  more  or  less  dysphagia.  The 
mucous  membrane  over  the  tonsils  is  intensely  congested,  the  uvula  is 
oedematous,  and  a  few  points  of  whitish  exudation  stud  the  mucous 
membrane.  If  these  little  dots  are  examined  closely  they  are  found  to 
be  mucus,  exuded  from  the  enlarged  follicles.  The  process  is  purely 
catarrhal,  and  not  membranous.  This  is  called  by  some  "catarrhal  diph- 
theria," but  is  nothing  more  than  a  catarrhal  pharyngitis.  It  is  never 
contagious,  but  is  due  to  atmospheric  influence,  and  has  none  of  the  char- 
acteristic local  or  constitutional  features  of  diphtheria. 

The  points  of  differential  diagnosis  between  diphtheria  and  croupous 
laryngitis  are  the  following  :  croupous  laryngitis,  or  membranous  croup,  is 
a  local  affection,  while  diphtheria  is  a  constitutional  disease.  Croup  is 
not  contagious  or  inoculable  ;  while  dij)htheria  is  markedly  so.  In  croup 
the  exudation  is  07i  the  surface  of  the  mucous  membrane  ;  in  diphtheria  it 
is  in  its  substance  as  well  as  on  its  surface.  Laryngeal  symptoms  are 
primary  in  croup,  while  in  diphtheria  they  usually  follow  severe  con- 
stitutional symptoms,  and  in  the  majority  of  cases  also  follow  the  ap- 
pearance of  the  exudation  upon  the  nasal  or  pharyngeal  membranes. 
Croup  rarely  attacks  those  who  have  passed  the  age  of  puberty ;  diph- 
theria attacks  all  ages.  Croup  is  sporadic  ;  diphtheria  is  often  epidemic. 
The  sub-maxillary  glands  may  be,  and  often  are,  enlarged  in  diphtheria, 
but  never  in  croup.'  From  a  clinical  standpoint  they  must  be  regarded  as 
distinct  diseases. 

Diphtheria  may  be  distinguished  from  scarlatinal  sore  throat  by  the 
following  points  : — in  scarlatina  there  is  a  diffuse  redness  of  the  mouth 
and  pharynx ;  in  diphtheria  the  redness  is  local  and  of  a  darker  color.  In 
scarlatina  the  exudation  is  mucus,  and  on  the  surface  of  the  tonsils  soft 
palate  and  pharynx  ;  in  diphtheria  it  commences  at  one  point,  and  spreads, 
is  adherent  and  tough,  and  has  a  grayish  or  brown  color.  When  an  erup- 
tion occurs  in  diphtheria  it  will  have  the  characteristics  already  referred 
to,  will  last  but  a  few  days,  and  will  appear  on  the  trunh  only.  In  scarlet 
fever  the  characteristic  eruption  rapidly  spreads  over  the  whole  surface, 
lasts  three  to  four  days  and  is  followed  by  desquamation.  In  dijihtheria 
there  is  no  characteristic  eruption,  only  occasionally  transient  roseola.  The 
temperature  is  far  higher  in  scarlet  fever  than  in  diphtheria,  the  ushering- 
in  symptoms  more  severe,  and  there  is  the  peculiar  strawberry  tongue  in 
scarlatina  which  is  not  present  in  diphtheria. 

Typhoid  or  typhus  fever  may  be  suspected  when  intestinal  diphtheria 
exists.  The  only  means  of  diagnosis  is  to  watch  the  passages  for  the  mem- 
brane, and  take  the  temperature  carefully  ;  in  typhoid  there  will  be  the 

1  The  Bides  of  the  neck  are  to  be  examined  for  enlarged  glands  ;  those  at  the  anterior  border  of  the 
Kterno-mastoid  are  always  palpable,  but  it  is  important  to  note  that  the  glands  at  the  angle  of  the  jaw  are 
not  enlarged. 


680  ACUTE   GENEEAL   DISEASES. 

typical  range,  and  in  typhus  the  rise  will  be  sudden  and  higher.  Finally 
idiopathic  erysipelas  of  the  throat  is  very  difficult  to  distinguish  from  diph- 
theria. In  erysipelas  the  tongue  is  blackish  brown,  dry  and  fissured  ;  and 
there  is  more  puffy  swelling  of  the  parts  than  in  diphtheria.  The  glands 
are  not  enlarged  and  the  process  is  limited  in  its  extent  in  erysipelas. 

Prognosis. — The  prognosis  in  diphtheria  yaries  with  different  epidemics, 
and  with  the  type  of  the  disease.  The  prognosis  is  more  unfavorable  the 
younger  the  subject,  since  extension  into  the  larynx  is  more  frequent  in 
the  young  child.  The  death  rate  varies  in  different  epidemics  from  twenty 
to  fifty  per  cent.  A  peculiar  fact,  and  one  to  be  remembered,  is  that  a 
mild  case — one  where  all  things  are  progressing  favorably — is  liable  to  as- 
sume, in  a  few  hours,  a  most  malignant  type.  The  system  may  be  over- 
whelmed with  the  poison  even  when  the  exudation  shall  have  disappeared ; 
and,  again,  in  convalescence  heart-paralysis  may  suddenly  occur ;  all  of 
these  points  make  a  very  guarded  prognosis  not  only  safest  but  necessary. 
Its  duration  varies  from  three  to  twelve  or  fourteen  days,  but  death  may 
occur  within  thirty-six  hours  ;  and  again  the  disease  may  continue  three  or 
four  weeks. 

The  symptoms  which  may  be  regarded  as  unfavorable  are  extreme  gland- 
ular swellings,  huskiness  of  the  voice,  a  dark-colored  extensive  exudation, 
and,  above  all,  laryngeal  implication  ;  when  diphtheria  extends  into  the 
larynx,  about  95  per  cent,  of  the  cases  end  fatally.  Repeated  convulsions 
are  unfavorable  ;  and  a  pulse  that  is  irregular  and  intermittent,  or  one  that 
drops  to  60  after  having  been  rapid  at  the  onset,  indicates  danger.  When 
at  the  same  time  that  the  exudation  is  extensive,  it  has  a  dark  gray,  green, 
or  black  color,  and  when  it  emits  a  gangrenous  or  sickly,  sweet  odor,  the 
prognosis  is  unfavorable.  JSTausea,  vomiting,  diarrhoea  and  epistaxis,  when 
they  occur  late  in  the  disease  are  very  serious  symptoms.  Coma,  ac- 
companied by  casts  and  albumen  in  the  urine,  or  by  entire  suppres- 
sion of  urine,  is  a  most  dangerous  occurrence.  If  pharyngeal  paralysis 
occurs  before  the  exudation  has  disappeared,  the  case  is  a  very  serious 
one  ;  the  future  course  will  be  troublesome,  owing  to  intense  involve- 
ment of  the  nervous  system,  and  these  cases  are  often  fatal.  The 
temperature  is  not  a  reliable  element  in  prognosis  :  in  the  most  malig- 
nant types  of  the  disease  it  may  range  low,  between  101°  and  102' F.  A 
sudden  rise  or  a  sudden  fall,  especially  to  sub-normal  limits,  is  exceedingly 
unfavorable.  Primary  diphtheria  of  a  wound,  in  which  the  throat  shows 
no  manifestations  of  the  disease,  generally  runs  a  favorable  course.  Pri- 
mary infection  of  a  wound  with  diphtheria,  in  which  the  throat  becomes 
secondarily  involved,  is  always  unfavorable.  Secondary  wound  infection, 
•during  the  course  of  a  pharyngeal  diphtheria,  shows  an  intense  degree  of 
poisoning,  and  is  a  bad  prognostic  omen. 

All  complications  render  the  prognosis  unfavorable.  Among  the  com- 
plications are  meningitis,  endocarditis  (usually  ulcerative),  pleurisy,  peri- 
tonitis, pericarditis,  pneumonia,  bronchitis,  tracheitis,  laryngitis,  pulmon- 
ary cedema  and  congestion,  oedema  glottidis,  acute  Bright's  disease,  and  a 
septic  fever  that  ordinarily  complicates  the  malignant  form.     Septicaemia 


DIPHTHERIA.  G81 

and  pyasmia  may  occur,  and  intestinal  hemorrhage,  purpura  and  jaundice 
are  occasional  and  very  grave  complicatioas.  Deatli  may  occur  from  any 
of  these  complications,  from  paralysis  of  tho  heart,  from  inanition,  espe- 
cially in  children  where  deglutition  is  interfered  with,  or  from  asthenia. 
The  nervous  system  may  be  overwhelmed  with  the  poison  at  the  onset.  The 
exhaustion  from  vomiting,  diarrhoea  or  hemorrhage  may  sometimes  be  so 
great  as  to  cause  death.  The  patient  may  be  asphyxiated  from  intercostal 
and  diaphragmatic  paralysis  or  from  getting  a  bit  of  solid  food  in  the 
larynx  or  trachea. 

Treatment. — The  treatment  of  diphtheria  will  be  considered  under  four 
heads  :  I.  Hygienic  ;  II.  External  local  ;  III.  Internal  local ;  IV.  Inter- 
nal constitutional  treatment. 

Hygienic. — A  patient  sick  with  diphtheria  should  be  kept  in  bed  from 
the  advent  of  its  first  symptom  until  convalescence  is  fully  established, 
and  the  pulse  is  normal  in  frequency  and  regular  in  its  rhythm  and  force. 
The  membranous  disappearance  is  not  the  guide  ;  it  is  the  exhausted  and 
anemic  condition  which  demands  absolute  rest  in  bed.  Only  attendants 
that  are  agreeable  to,  and  can  manage  the  child  well  should  be  admitted 
into  the  sick  room,  which  must  be  large,  well  ventilated,  and  have  a  tem- 
perature of  70"  to  75°  F.  Perhaps  one  of  the  most  important  indications  is 
cleanliness  ;  the  patient  should  be  kept  scrupulously  clean, — eyes,  nose, 
ears  and  mouth,  as  well  as  the  face  and  limbs.  All  utensils  of  whatever 
kind,  all  clothing  and  linen,  must  be  frequently  cleansed  and  disinfected. 
The  disinfection  may  be  accomplished  as  in  typhoid  (q.  v.).  The  patient 
must  be  strictly  quarantined,  the  attendants  must  mingle  as  little  as  jDossi- 
ble  with  the  rest  of  the  household,  and  must  avoid  taking  the  breath  of, 
and  unnecessary  manipulation  of,  the  patient.  The  rule  is,  not  to  disturb 
a  diphtheritic  patient  except  so  far  as  it  is  necessary  for  cleanliness.  The 
physician  should  be  careful  not  to  make  unnecessary  examinations  of  the 
throat.  The  instruments  used  in  the  examination  should  be  thoroughly 
cleansed  after  each  examination.  Freshly  slacked  lime  mixed  with  pow- 
dered charcoal  may  be  placed  about  the  room  as  disinfectants.  Fresh 
air  and  sunlight  are  important,  and  should  be  so  admitted  into  the  sick 
room  so  as  to  avoid  draughts.  A  grate  fire  in  cold  weather  is  the  best 
method  to  attain  ventilation. 

External  Local  Treatment. — This  treatment  may  be  considered  under 
four  heads  : — 1.  llood-letting  by  means  of  leeches  at  the  angle  of  the  jaw  ; 
2.  cold  applications — ice-bags — to  the  throat ;  3.  counter -irritation — 
blisters,  etc. — over  the  neck  and  enlarged  glands  ;  and  4,  Jiot  poultices  or 
other  hot  applications  to  the  throat. 

Blood-letting,  local  or  general,  while  it  does  not  arrest  the  exudative 
process,  diminishes  the  resisting  power  of  the  patient ;  clinical  experience 
teaches  us  that  all  antiphlogistic  remedies  are  contraindicated  in  the 
treatment  of  this  disease. 

Ice  to  the  throat  is  with  some  a  favorite  plan  of  local  treatment.  It  is 
to  be  remembered  that  the  exudation  is  a  local  manifestation  of  a  consti- 
tutional disease,  and  that  its  extension  is  arrested  and  its  removal  accom- 


682  ACUTE   GENEEAL  DISEASES. 

plished  by  the  establishment  of  a  suppurative  process  ;  and  for  this  reason 
the  local  application  of  cold  is  contraindicated.  It  may  relieve  pain,  but 
it  does  not  arrest  the  diphtheritic  process. 

Counter-irritation  is  also  powerless  to  check  the  membranous  exuda- 
tion ;  besides,  whenever  a  surface  becomes  abraded,  the  diphtheritic  process 
is  liable  to  be  established  upon  it. 

If  the  diphtheritic  exudation  is  arrested  and  removed  by  a  suppurative 
process,  the  external  application  of  heat  is  indicated,  and  may  be  of  service. 
Hot  fomentations  must  be  regarded  as  the  safest  and  best  means  of  hasten- 
ing the  removal  of  the  membrane,  and  they  afford  the  greatest  relief  to  the 
patient. 

Internal  Local  Treatment  may  be  considered  under  three  heads  : — 1.  Me- 
chanical means  employed  for  removing  the  membrane.  2.  Escharotics 
employed  for  its  destruction.  3.  Astringents  to  prevent  an  extension  of 
the  exudation  by  their  action  on  the  unaffected  mucous  membrane. 

It  is  not  diflBcult  to  pull  off  a  patch  of  diphtheritic  exudation  hj  mechan- 
ical means ;  but  the  membrane  will  reappear  as  soon  as  the  removal  is 
effected  ;  and  the  second  membrane  has  a  deeper  intimacy  with  the  tis- 
sues than  the  primary.  For  this  reason  no  attempt  should  be  made  to  re- 
move a  diphtheritic  exudation  unless  it  hangs  loosely  detached,  and  then 
the  dependent  portion  may  be  carefully  snipped  off.  Any  irritation  pro- 
duced by  instruments  favors  the  extension  of  the  diphtheritic  process.  It 
is  to  be  remembered  that,  however  pleasant  it  may  be  for  parents  and 
friends  to  see  patches  of  the  membrane  removed,  after  each  removal  the 
diphtheritic  process  is  increased  both  in  depth  and  extent. 

The  powerful  escharotics  which  have  been  used  for  the  destruction  of 
the  diphtheritic  exudation  are  hydrochloric  and  nitric  acids,  nitrate  of 
silver,  bromine,  chromic  acid,  etc.  It  is  claimed  by  partisans  of  this  plan 
that,  when  seen  very  early,  and  when  the  diphtheritic  patches  are  small, 
extension  of  the  exudation  may  be  arrested  by  the  destruction  of  its  local 
manifestations.  There  seems  no  more  reason  for  the  use  of  escharotics 
than  for  the  mechanical  removal  of  the  exudation  ;  for  each  one  of  the 
escharotic  sloughs  leaves  an  ulcer,  which  is  a  favorite  spot  for  the  develop- 
ment of  a  new  membrane  in  the  deeper  tissues. 

Astringents,  by  constringing  the  mucous  membrane  about  a  diphtheritic 
patch,  thus  prevent  the  spread  of  the  exudation.  But  as  the  primary 
action  of  all  astringents  is  to  cause  irritation  of  the  mucous  surface,  and 
as  the  irritation  favors  the  development  of  the  diphtheritic  membrane, 
their  use  is  contraindicated. 

The  thing  to  be  accomplished  by  local  internal  treatment  is  to  hasten 
the  suppurative  process ;  the  locajl  means  which  will  aid  the  process  of 
suppuration  is  the  inhalation  of  the  vapor  of  hot  water.  The  external  and 
internal  local  treatment  of  diphtheria  resolves  itself  into  the  application 
of  poultices  externally  and  vapor  inhalations  internally.  The  vapor  in- 
halations should  be  commenced  as  soon  as  the  exudation  is  detected,  and 
continued  until  all  signs  of  it  have  disappeared.  As  the  steam  inhalation 
increases  mucous  secretion,  it  favors  the  removal  of  the  membrane,  and 


DIPHTHERIA.  683 

furnishes  another  reason  for  its  use.  To  jorevent  or  limit  septic  poisoning 
antiseptics  are  to  be  used,  and  those  that  are  non-irritating  are  to  be  pre- 
ferred. The  diphtheritic  surfaces  should  be  frequently  sprayed  with  chlo- 
rine water,  or  with  weak  solutions  of  carbolic  and  salicylic  acid,  boric  acid, 
benzoate  of  soda,  or  muriated  tincture  of  iron.  Lime  water,  glycerine, 
and  lactic  acid  have  been  used  with  benefit  ;  and  when  an  atomizer  is 
not  at  hand,  disinfectant  gargles  and  washes  may  be  substituted.  It  is 
especially  important  that  disinfectants  should  be  employed  in  nasal  diph- 
theria, after  thoroughly  cleansing  the  nasal  cavities. 

The  constitutional  treatment  of  diphtheria  consists  essentially  in  sup- 
porting the  vital  powers  of  the  patient.  There  are  no  specifics  for  its 
treatment,  any  more  than  for  scarlet  fever  or  smallpox.  All-depressing 
remedies  are  contraindicated.  The  alcoholic  treatment  is  a  favorite  j^lan 
with  a  large  number  of  practitioners  ;  under  this  plan  alcohol  is  given,  not 
merely  to  sustain  the  patient,  but  for  its  constitutional  effects.  With  this 
end  in  view,  it  is  given  in  large  quantities  ;  one-half  an  ounce  of  brandy 
may  be  given  to  an  adult  every  half  hour  ;  to  a  child  two  years  old  from 
one-half  to  one  drachm  every  hour.  The  amount  to  be  given  must  be  de- 
termined only  by  its  effects.  The  object  is  to  get  the  physiological  effects 
of  the  alcohol  as  quickly  as  possible.  The  beneficial  effect  of  the  stimulants 
will  be  indicated  by  the  pulse  becoming  slower  after  its  use,  by  a  diminu- 
tion in  its  tremulousness,  by  an  increased  desire  for  food,  and  by  a  manifest 
feeling  of  general  amelioration.  The  stimulating  plan  should  be  carried 
out  more  strictly  in  diphtheria  than  in  any  other  infectious  disease.  An 
intermittent  and  irregular  pulse  demands  freer  stimulation  than  a  rajDid 
and  feeble,  but  regular,  pulse.  An  increasing  apathy,  a  feeble  pulse,  ir- 
regular at  times,  a  dry  tongue,  a  dark  and  offensive-smelling  exudation, 
often  indicate  a  crisis  that  may  be  tided  over  by  crowding  stimulants. 

The  diet  should  be  milk  and  yolk  of  eggs  ;  when  there  is  great  dysphagia, 
food  may  be  administered  per  rectum.  Ether,  musk,  and  camphor  are  re- 
garded by  some  as  valuable  adjuncts  to  the  alcoholic  plan  of  treatment.  When 
the  temperature  ranges  high,  quinine  and  cold  sponging  may  be  emjDloyed. 
The  tincture  of  the  chloride  of  iron  and  chlorate  of  potassa  are  favorite  in- 
ternal remedies  in  the  treatment  of  diphtheria.  From  five  to  twenty  drops 
of  the  tincture  of  iron  are  given  in  glycerine  or  water  every  hour ;  and 
from  two  to  twenty  grains  of  the  chlorate  of  potassa  every  two  hours.  The 
use  of  these  drugs,  given  either  alternately  or  in  connection,  is  at  the  pres- 
ent time  a  ruling  practice  in  the  profession.  The  internal  use  of  the  ben- 
zoate of  soda,  and  solution  of  the  bromides,  to  neutralize  the  dij^hth critic 
poison,  although  strongly  advocated  by  some,  is  not  sustained  by  the  ex- 
perience of  the  profession  generally. 

If  nutrition  be  kept  at  a  high  standard,  and  if  the  use  of  tonics  be  per- 
sistently kept  up,  the  paralyses  that  are  the  chief  sequelae  of  diphtheria 
will  usually  soon  be  recovered  from.  Porter  is  one  of  the  best  tonics  in 
the  treatment  of  the  sequelae  of  diphtheria,  especially  the  paralyses.  When 
pharyngeal  paralysis  occurs,  the  food  is  to  be  given  through  an  oesophageal 
tube. 


684  ACUTE    GENEKAL    DISEASES. 

When  the  nose  is  the  seat  of  diphtheritic  exudation,  the  nasal  chambers 
must  be  thoroughly  cleansed.  Lime  water  or  dilute  carbolic  acid  are  the 
best  washes  to  accomplish  this,  the  washings  must  he  frequently  and  care- 
fully employed. 

When  the  larynx  is  invaded,  exudations  may  be  mechanically  removed, 
if  suffocation  is  imminent.  Inhalations  of  alkalies,  lactic  acid,  etc.,  are 
beneficial  only  in  theory.  Tracheotomy,  if  performed  at  all,  should  be 
performed  early,  as  soon  as  suffocative  symptoms  or  signs  of  asphyxia  be- 
gin to  show  themselves.  The  hypersesthesia  which  is  often  so  troublesome 
is  best  relieved  by  large  doses  of  bromide  of  potassium,  and  if  restlessness 
and  jactitation  are  marked,  moderate  opium  narcosis  may  be  beneficial. 

To  sum  up  :— a  diphtheritic  patient  should  be  quarantined  in  a  large, 
well-ventilated  apartment,  attended  by  a  well-trained  nurse;  poultices 
should  be  applied  externally  to  the  throat ;  steam  inhalation  should  be  con- 
stant from  the  onset  of  the  disease  until  the  exudation  has  disappeared ; 
iron  and  brandy  should  be  given  freely  ;  the  diet  should  be  fluid,— milk 
preferably,— and  the  patient  kept  in  bed  until  the  convalescence  is  com- 
plete. 

EPIDEMIC    CEREBRO-SPIlSrAL    MENINGITIS. 

Epidemic  cerebro-spinal  meningitis,  or  cerebro- spinal  fever,  historically 
belongs  exclusively  to  the  nineteenth  century,  although  it  unquestionably 
prevailed  prior  to  this  period.  French  writers  were  the  first  to  accu- 
rately describe  it.-  It  is  a  continued  fever  belonging  to  the  class  of  mias- 
matic-contagious diseases,  which  generally  prevails  in  quite  limited  areas. 
It  has  received  various  names  ;  as  spotted,  petechial  and  congestive  fever  ; 
malignant  purpuric  fever  ;  cerebro-spinal  and  syncopal  typhus. 

Morbid  Anatomy. — Pathologically  as  well  as  etiologically  there  are  two 
forms  of  cerebro-spinal  meningitis  ;  the  first  is  simply  an  acute  inflam- 
mation involving  the  meninges  of  the  brain,  spinal  cord  and  medulla. 

Its  local  symptoms  predominate  over  the  constitutional,  and  it  occurs 
exclusively  as  a  sporadic  disease  ;  the  second, — epidemic  cerebro-spinal 
meningitis, — is  accompanied  by  all  the  signs  of  an  infectious  disease,  and, 
at  the  autopsy,  are  found,  in  addition  to  lesions  that  are  the  counterpart  of 
those  occurring  in  simple  cerebro-spinal  meningitis,  those  grave  visceral 
and  sanguineous  changes,  which  are  present  in  other  acute  infectious  diseases. 

On  examining  the  brain  of  one  who  has  died  of  epidemic  cerebro-spinal 
meningitis,  the  convexity  and  base  will  be  found  most  extensively  involved. 
Its  dura  mater  is  tense,  shining,  and  studded  with  numerous  punctate  spots 
of  extravasation.  The  cerebral  convolutions  are  flattened  and  the  sulci 
deepened.  The  pia  mater  of  the  brain  and  spinal  cord  is  thickened.  The 
vessels  of  the  pia  mater  are  always  more  or  less  intensely  injected  and  the 
surface  of  the  membrane  roughened.  In  some  cases  extreme  hypersemia 
may  be  the  only  discoverable  lesion.  The  exudation  is  the  characteristic 
lesion  of  this  disease.  A  more  or  less  abundant  sero-fibrinous  or  sero- 
purulent  exudation  takes  place  into  the  meshes  of  the  pia  mater.  Clear 
serum  is  first  effused,  then  it  becomes  milky  and  clouded,  then  yellowish, 


EPIDEMIC    CEREBKO-SPIXAL   MENINGITIS.  685 

and  finally  a  thick,  viscid,  greenish -yellow  mass,  consisting  of  granular 
fibrin,  pus-cells  and  red  blood  globules,  which  gives  to  the  surface  a  "  leek- 
green  "  color.  In  the  severest  cases  the  fibrin  and  pus  form  a  continuous 
sheet  in  the  sub-arachnoidean  space,  always  thickened  above  the  sulci.  The 
vessels  are  inclosed  in  the  exudation,  looking  like  red  threads  in  a  gelatin- 
ous filmy  mass.  When  the  layer  is  removed,  the  subjacent  gray  substance 
is  dotted  with  red  points.  In  rare  cases  the  exudation  is  deeply  stained 
with  blood  ;  at  other  times  it  is  a  thin,  colorless  fluid.  The  sinuses  are 
full  of  dark,  soft  coagula,  or  thin  fluid  blood.  Hard  thrombi  are  occa- 
sionally found  in  them. ' 

The  brain  substance  is  frequently  softened,  especially  near  the  largest 
patches  of  exudations.  This  is  the  "mechanical  softening"  of  French 
authors. 

On  sectiofi  there  is  more  or  less  congestion  and  punctate  extravasation 
in  the  brain  substance,  and  the  ventricles  are  usually  full  of  serum  ;  more 
rarely  of  pus  ;  and  this  pus  enters  the  ventricles  by  means  of  the  velum  in- 
terpositum,  or  along  the  cerebellar  or  choroid  plexuses.^  All  the  local  changes 
have  their  primary  starting  point  in  the  pia  mater.  Finally,  if  absorption 
occur,  the  pia  mater  often  remains  thickened.  In  prolonged  cases  cheesy 
metamorphosis  occurs  in  various  spots  in  the  thickened  pia  mater. 

The  changes  in  the  spinal  canal  are  similar  to  those  within  the  cranium. 
The  dura  nmter  is  injected,  and  extravasations  of  blood  are  often  found 
upon  its  parietal  surface ;  it  is  tense  and  shining.  The  meshes  of  the 
spinal  pia  mater  are  occupied  by  the  exudation,  which  occurs  either  as 
stringy,  interlacing  bands  forming  a  network,  or  in  the  form  of  a  thick 
sheet  completely  enveloping  the  cord's  substance.  The  color  and  char- 
acter of  the  exudation  are  the  same  as  that  in  the  cranial  cavity.  The  largest 
collections  of  pus  are  about  the  second  and  last  dorsal  and  the  lumbar  ver- 
tebrae. The  posterior  portion  of  the  cord  is  the  part  most  involved;  the 
anterior  portion  suffering  only  in  those  cases  where  the  whole  cerebro- 
spinal tract  is  involved.  The  pia  mater  itself  is  hypersemic  ;  it  may  be 
thicker  than  normal,  shaggy  and  adherent  to  the  cord.  In  some  instances 
the  exudation  occurs  in  the  form  of  lozenge-shaped,  irregular  masses  whose 
ends  are  connected  to  one  another  by  bands  of  fibrino-pus.  In  the  severest 
cases  suppuration  is  so  rapid  that  a  complete  sheath  of  pus  is  formed  about 
the  whole  cord  in  a  few  hours  after  the  onset  of  the  malady.  The  gray 
substance  of  the  cord  is  of  a  pinkish  color,  and  may  be  infiltrated  with 
serum.     It  is  sometimes  reduced  to  a  mere  pultaceous  mass. 

In  addition  to  these  local  changes  there  are  blood  and  visceral  changes. 
The  fibrin-factors  of  the  blood  are  diminished,  and  hence  there  is  a  loss  in 
its  coagulating  power.  The  number  of  white  corpuscles  is  increased,  and 
the  red  ones  are  shrivelled,  serrated  and  partly  disorganized.  The  blood 
is  darker  than  normal,  fluid,  and  rapidly  decomposes  when  taken  from  the 
body. ' 

•  Merkel  states  that  he  has  found  "  a  nuclear  proliferation  in  the  vessels,  extending  from  the  cerebral 
meninges  to  the  spinal  cord." 

2  Virchow'B  Arch.     Be.  34,  Ileft  31,  866. 

>  The  ventricular  fluid  contains  chloride  of  sodium,  phosphate  of  soda  and  ammonia  and  oxalate  of  urea. 
—Meschede. 


686  ACUTE   GENERAL   DISEASES. 

The  heart  and  the  voluntary  muscles  undergo  the  same  degeneration  and 
present  the  same  appearances  as  in  typhoid  fever. 

The  lungs  are  frequently  the  seat  of  oedema,  and  hypostatic  congestion 
is  present  when  the  disease  is  prolonged.  Passive  hypersemia,  lobular, 
and,  less  frequently,  lobar  pneumonia,  are  often  found  at  the  post-mortem. 

The  liver  is  congested.  The  liver-cells  are  often  cloudy  and  granular — 
i.e.,  there  is  albuminoid  or  fatty  degeneration. 

The  spleen  is  enlarged  and  softened  ;  the  lymphatics  are  usually  hyper- 
semic,  having  a  fleshy  look. 

The  intestinal  mucous  membrane  is  hyperaBmic  and  the  follicles  are  con- 
gested. The  projecting  agminated  glands  are  sometimes  ulcerated.  There 
is  more  or  less  congestion  of  the  kidneys  ;  the  microscopical  changes  are 
those  of  the  first  stage  of  acute  Bright's.  Abscesses  (as  in  typhoid)  often 
form  in  the  subcutaneous  connective  tissue.  Bed-sores  are  not  rare  in  those 
parts  subjected  to  pressure,  and  gangrene  is  sometimes  present. 

The  integument  is  often  the  seat  of  petechial  spots,  and  large,  irregular, 
discolored  patches  are  sometimes  seen  over  the  body.  Herpetic  spots  are 
frequently  seen  on  the  surface  of  the  body,  on  the  face,  and  about  the  lips 
especially.  Rigor  mortis  is  marked  and  very  much  prolonged.  Finally 
the  serous  membranes  are  frequently  all  covered  with  petechial  spots  and 
small  extravasations. 

Etiology. — I  have  included  cerebro-spinal  meningitis  in  the  list  of  mias- 
matic contagious  diseases,  as  it  has  more  in  common  with  this  class  than 
with  any  other.  It  has  prevailed  as  an  epidemic  and  as  an  endemic  dis- 
ease, and  occasionally  sporadic  cases  have  occurred  in  localities  where  it  has 
been  epidemic.  Epidemics  have  occurred  at  all  seasons  ;  by  far  the  greater 
number,  however,  occur  in  cold  weather.  All  classes  and  ages  are  subject 
to  it,  but  it  is  most  likely  to  attack  those  between  ten  and  eighteen  years  of 
age.  Young  troops  on  the  march  are  especially  liable  to  it. '  Its  strongest 
predisposing  causes  are  over-crowding,  bad  ventilation,  insufficient  or  im- 
proper food,  dampness,  and  all  other  bad  hygienic  surroundings.  Mental 
excitement,  excessive  brain-work  or  bodily  fatigue,  exposure  to  excessive 
cold  or  heat,  are  also  predisposing  causes.  Cerebro-spinal  meningitis  is  in 
no  sense  a  contagious  disease.  It  is  more  closely  allied  etiologically  to  lobar 
pneumonia  than  to  any  other  disease,  although  some  have  regarded  it  as  a 
variety  of  typhus  fever  ;  others  of  malarial  fever. 

Symptoms. — Cerebro-spinal  fever  follows  no  regular  order,  either  in  its 
prodromata  or  in  its  subjective  symptoms.  Arbitrary  classifications  and 
many  subdivisions  have  been  made,  such  as  the  typhoid,  the  paralytic,  the 
adynamic,  the  intermittent,  the  petechial,  etc.  Such  classifications  are 
useless  and  confusing,  for  cases  differ  in  the  same  epidemic.  If  the  gene- 
ral phenomena  of  the  disease  be  known,  the  accidental  circumstances  that 
are  the  basis  of  this  complex  nomenclature  will  be  of  very  little  impor- 
tance. 

The  premonitory  symptoms  of  cerebro-spinal  meningitis  vary  in  differ- 
ent epidemics.     In  some  the  invasion  is  abrupt ;  the  patient,  apparently  in 

1  Out  of  forty-seven  French  epidemics,  Hirsch  attributes  forty-six  to  the  military  population. 


EPIDEMIC    CEREBRO-SPI-NTAL   MENIISTGITIS.  687 

perfect  health,  is  suddenly  seized  with  a  chill,  loss  of  consciousness,  becomes 
comatose  and  dies  in  a  few  hours.  In  others  a  feeling  of  lassitude,  dull 
headache,  pains  in  the  joints  and  muscles,  and  sometimes  nausea  and 
vomiting  precede  its  development.  Again,  patients  complain  of  pains  in 
the  back  of  the  head  and  neck — they  have  no  chills,  but  after  twenty-four 
hours  a  febrile  movement  is  developed  and  they  pass  raj)idly  into  the 
active  symptoms  of  the  disease.  The  prodromata  may  last  from  a  few 
hours  to  three  or  four  days.  In  sporadic  or  endemic  cases  there  is 
generally  a  period  preceding  its  invasion  during  which  patients  suffer 
from  a  feeling  of  general  indisposition. 

When  its  onset  is  sudden  its  advent  is  marked  by  a  distinct  chill,  in- 
tense headache,  pain  in  the  back  and  upper  part  of  the  spine,  nausea, 
vomiting,  a  rise  in  temperature  and  an  acceleration  of  pulse.  The  chill 
may  last  an  hour  or  more,  but  is  usually  of  short  duration.  The  skin  is 
abnormally  cool  and  dry  in  its  early  stage. 

Headache  in  most  cases  is  a  prominent,  agonizing  and  persistent  symp- 
tom, and  the  pain,  even  in  a  condition  of  coma,  causes  the  patient  to  groan. 
In  rare  instances  the  headache  intermits,  and  frequently  it  remits.  Ver- 
tigo almost  always  is  an  attendant,  and  the  patient  may  suddenly  stagger 
and  fall  during  the  period  of  the  headache. 

Pain  in  the  hach  and  upper  part  of  the  spine  is  a  characteristic  symp- 
tom of  the  disease  ;  attempts  to  flex  the  head  on  the  chest  increase  the 
pain  during  the  first  twenty-four  hours  of  the  disease,  and  pressure  np 
under  the  ligamentwm  nuchce,  against  the  cord,  often  induces  excruciating 
agony.  Soon  the  muscles  at  the  back  of  the  neck  become  stiff,  then 
rigid,  the  neck  becoming  fixed,  and  the  head  extremely  extended — opistho- 
tonos. So  intense  may  be  the  opisthotonos  that  attempts  to  swallow  are 
so  painful  that  the  sufferer  soon  ceases  to  make  the  effort.  The  signs  of 
prostration  are  present  early. 

The  temperature,  as  a  rule,  is  loiv  ;  although  107°,  109°  and  110°  ¥., 
are  recorded  by  trustworthy  observers.  It  may  rise  rapidly  to  104°  or  105° 
F.,  and  then  suddenly  fall  to  102°  or  103°  F.,  there  to  remain,  with  un- 
important and  irregular  variations  until  a  gradual  return  to  normal  marks 
the  beginning  of  convalescence.  Often,  before  death — and  an  almost  sure 
indication  of  it — a  low  temperature  will  suddenly  give  place  to  a  high  one, 
and  death  will  occur  during  the  time  of  the  highest  temperature.  In 
children  the  febrile  movement  is  less  marked  than  in  adults. 

The  pulse  at  first  is  slightly  accelerated,  beating  from  90  to  100  per 
minute  ;  but  in  twenty-four  hours  after  the  commencement  of  the  attack 
it  may  range  between  120  and  150,  It  bears  no  relation  to  the  range  of 
temperature,  often  varying  40  or  50  beats  in  a  few  hours.  It  is  feeble, 
rapid  and  compressible  in  those  cases  where  there  are  early  symptoms  of 
exhaustion.  In  many  cases  it  is  small  and  wiry  in  character  ;  sometimes  it 
is  dicrotic.  In  children  the  pulse  is  more  accelerated  and  much  more  ex- 
citable than  in  adults.  In  a  few  cases  the  pulse  is  slow  at  the  onset  of  the 
attack,  but  soon  becomes  accelerated,  irregular  and  intermittent.  Pho- 
tophobia,   contracted    pupils,   great    and    increasing  restlessness,  nausea 


bob  ACUTE    GENEBAL    DISEASES. 

and  urgent  vomiting,  and  abdominal  neuralgia,  are  among  the  early 
symiDtoms. 

The  pu-pils  are  often  unequal  in  size,  and  usually  respond  slowly  to  light. 
The  face  is  pale  and  anxious,  and  the  features  have  a  fixed,  rigid  expres- 
sion ;  in  some  the  countenance  has  a  dusky  hue  like  that  of  one  who  is 
tinder  the  influence  of  narcotic  poison ;  indeed,  in  some  instances,  the 
patient  believes,  from  the  severity  and  suddenness  of  the  attack,  that  he  is 
the  victim  of  wilf  al  poisoning.  About  the  second  or  third  day  of  the 
disease,  if  the  headache  has  been  very  severe,  delirium  comes  on  ;  it  may 
be  mild  and  muttering,  wild  and  uncontrollable,  or  "■  maudlin,"  like  that 
of  a  drunken  man.  In  women  the  delirium  may  be  attended  by,  or  merge 
into,  a  form  of  hysteria.  The  most  fanciful  hallucinations  often  visit  the 
minds  of  such  patients,  and  if  left  to  themselves  they  are  constantly  getting 
out  of  bed.  These  patients  are  frequently  roused  from  their  wanderings  by 
excruciating  pains  in  the  head  and  extremities.  Muscular  contraction  is 
rarely  absent  even  in  the  mildest  cases. 

By  the  third  or  fourth  day  a  tetanic  and  contracted  state  of  the  muscles 
of  the  extremities  begins,  and  then  the  arms  become  flexed  on  the  chest, 
the  forearm  on  the  arm,  the  thumb  on  the  palm,  the  knee  on  the  abdomen, 
and  the  leg  on  the  thigh.  When  these  excito-motor  spasms  of  a  tonic 
character  are  marked  in  the  groups  of  muscles  in  the  back  of  the  neck  and 
in  the  back,  trismus  may  occur,  and  then  the  case  is  hopeless.  Twitching 
of  groups  of  muscles  often  causes  the  patient  to  start  from  a  state  of  semi- 
stupor.  General  convulsions  are  absent  in.  adults,  but  are  frequent  in 
children.  Pains  in  the  extremities  and  in  the  abdominal  region  are  always 
more  or  less  severe.  They  are  shooting  and  lancinating  in  character. 
Pains  when  located  over  the  abdominal  region  cause  vomiting,  and  dyspnoea 
when  in  the  thoracic  region.  The  skin  may  be  hyper-  or  anaesthetic,  and  is 
early  the  seat  of  an  eruption.  In  the  majority  of  cases  the  surface  is  so 
sensitive  that  palpation  and  percussion  are  exceedingly  painful  ;  the  patient 
cries  out  and  starts  at  every  attempt,  and  will  usually  say  that  it  is  that 
particular  spot  which  is  the  "sorest."  Voluntary  movements  cause  pain. 
Cutaneous  ansesthesia  rarely  exists  throughout  the  course  of  the  disease, 
but  follows  the  hyper-sensitiveness. 

The  eruption  is  usually  limited  to  the  face,  neck,  and  lips  ;  it  is  herpetic 
in  character.  It  may  appear  on  the  trunk  and  limbs.  Vesicles  appear 
earliest  on  and  about  the  lips,  and  may  be  confined  to  them.  Sometimes 
the  eruption  is  mottled  like  that  of  typhus,  and  covers  the  body  ;  it  may 
have  a  distinctly  petechial  character.  Ecchymotic  spots  are  often  scattered 
irregularly  over  the  body,  especially  on  those  parts  that  are  subjected  to 
pressure.  Purpuric  maculae,  erythema  and  urticaria  are  sometimes  present 
(indeed,  there  are  many  varieties  of  the  eruption),  but  herpetic  and  pete- 
chial spots  are  the  most  common.  As  there  is  no  definite  time  for  the 
appearance  of  these  eruptions,  so  their  duration  varies  ;  sometimes  they  last 
only  for  a  day — at  other  times  they  are  visible  throughout  the  whole 
course  of  the  disease.  Epidemics  in  which  eruptions  are  marked  have 
given  ric    to  the  name  of  spotted  fever. 


EPIDEMIC   CEREBKO-SPIKAL   MENINGITIS.  689 

With  the  photophobia  the  eye  is  subject  to  many  disturbances.  Paralysis 
of  the  orbicularis  palpebrarum  may  result  in  keratitis  ;  there  may  be  more 
or  less  intense  conjunctivitis  ;  or  a  neuro-retinitis  or  choroiditis,  the  result 
of  an  impIi<3ation  of  the  optic  nerve,  may  occur.  Ptosis  is  present  in 
nearly  every  case.  Temporary  or  permanent  blindness,  squint,  double 
vision,  and  nystagmus  are  not  infrequent  optical  lesions.  Atroj^hy  of  the 
eyeball  and  cataract  are  occasional  sequelae. 

Taste  is  perverted  or  entirely  lost ;  yet  the  jiatient  will  often  take  with  avid- 
ity any  article  of  food  which  may  be  placed  in  his  mouth.  Thirst  is  often 
a  constant  and  tormenting  symptom.  Deafness  is  even  more  frequent  than 
loss  of,  or  disturbances  in  sight.  There  is  always  intolerance  to  noise,  and 
tinnitus  aurium  exists  from  the  very  commencement.  Otorrhoea  may  be 
extensive  enough  to  result  in  tympanic  perforation  ;  and  the  internal  ear 
may  become  the  seat  of  an  inflammatory  process  which  sometimes  ends  in 
suppuration.  The  semicircular  canals  would  seem  to  be  involved  here,  for 
in  many  recorded  cases  "an  uncertain  gait"  is  mentioned  as  accompany- 
ing the  deafness.  The  respiratory  tract,  as  a  rule,  is  involved,  the  respira- 
tions generally  being  accelerated  out  of  proportion  to  the  frequency  of  the 
pulse,  but  when  the  exudation  presses  on  the  medulla  and  respiratory 
centre,  dyspnoea  and  slowed  respiration  occur,  and  in  some  few  cases  the 
Cheyne-Stokes'  breathing  is  noticed.  Usually  the  violent  headache  and 
the  "wandering"  are  attended  by  great  restlessness,  tossing  and  jactita- 
tion that  frequently  demand  restraint.  Insomnia  is  a  common  symptom. 
There  is  often  great  tremulousness  and  subsultus  tendinum  ;  in  the  ad- 
vanced stage  of  the  disease  the  pupils  are  dilated,  the  resjiiration  markedly 
sighing,  deglutition  diflBcult,  the  sphincters  relaxed,  or  there  is  retention 
of  urine  and  faeces,  the  removal  of  which,  by  means  of  the  catheter  or 
copious  enemata,  causes  a  slight  return  of  consciousness. 

The  tongue,  at  first,  is  moist  and  covered  with  a  whitish  coating ;  soon 
it  becomes  dry  and  brown  ;  the  joarotids  may  enlarge,  and  even  suppurate ; 
the  abdomen  is  flattened.  Eigidity,  contraction  and  opisthotonus  give  way 
to  palsies.  The  skin  becomes  cyanotic  as  in  the  asphyxia  stage  of  cholera. 
In  other  cases  tetanic  spasms  are  the  most  prominent  signs,  the  rigidity 
and  contraction  of  the  muscles  of  the  back  and  neck  are  excessive,  and 
the  sufPerer  dies  with  the  grin  of  lock-jaw  upon  his  face.  In  protracted 
cases  the  patient  becomes  emaciated  and  loses  strength  in  a  degree  out  of 
proportion  to  the  duration  of  the  disease. 

The  joints  are  usually  tender,  and  often  inflamed  ;  suppurative  arthritis 
occurs  in  a  few  instances. 

The  urine  is  but  slightly  altered.  There  is  an  increase  in  the  urates 
and  phosphates,  and  albuminuria  not  infrequently  occurs,  especially  late  in 
the  disease.     Polyuria  is  often  present  in  children. 

The  bowels  are  constipated ;  exceptions  to  this  rule  are  seen  only  in 
children.  If  the  disease  is  prolonged,  the  symptoms  assume  a  typhoid 
character;  and  so  "typhoid  cerebro-spinal  fever"  is  one  of  the  many 
varieties.  The  term  intermittent  cerebro-spinal  meningitis  has  been  ap- 
plied to  those  cases  where  all  the  symptoms  remit  on  the  second  or  third 
44 


690  ACUTE    GENEEAL   DISEASES. 

day  from  the  onset  of  the  attack,  and  soon  reappear  or  exacerbate  and  the 
patient  rapidly  passes  into  stupor  and  coma.  As  an  epidemic  advances  the 
cases  grow  milder,  so  that  toward  its  end  the  patients  may  hardly  be  ill 
enough  to  be  confined  to  their  beds. 

In  the  form  called  "  meni7igitis  foudroyante "  the  patient  is  struck 
down  in  full  health,  and  death  may  occur  within  twenty-four  hours  from 
the  first  symptom.  The  initial  chill  and  headache  are  severe,  there  is 
stasis  in  the  capillary  circulation  of  the  surface,  purpuric  maculae  soon 
appear  over  the  body,  and  active  delirium  is  followed  by  profound  coma 
and  death.  The  course  is  often  so  rapid  that  there  are  no  tetanic  exhibi- 
tions. Exhaustion,  paralysis,  and  anaesthesia  are  complete  before  the  fatal 
issue  ;  albuminuria  is  rarely  absent  in  such  cases.  In  fact  all  the  prominent 
severe  symptoms  of  the  disease  are  crowded  into  a  few  hours,  and  the  pa- 
tient rapidly  passes  into  a  state  of  collapse. 

When  recovery  is  to  occur,  the  restlessness,  jactitation,  insomnia  and 
headache  remit  and  finally  disappear,  or  the  patient  emerges  from  a  condi- 
tion of  coma  into  consciousness.  The  muscular  paralysis  continues,  how- 
ever, as  well  as  the  pains  in  the  head  and  back  of  the  neck,  and  in  all 
cases  the  convalescence  is  tedious.  Stiffness  of  the  muscles  of  the  nape 
of  the  neck  is  a  persistent  symptom  during  convalescence.  Mental- 
psychical  disturbances  are  also  common  attendants  of  the  convalescence. 
Sometimes  when  the  disease  has  pursued  a  mild  course  for  a  week  or  ten 
days  and  convalescence  seems  about  to  be  established,  the  patient  gradu- 
ally gets  worse,  and  after  weeks  of  suffering,  death  will  occur  from  inani- 
tion and  general  marasmus,  the  respirations  becoming  more  and  more 
irregular,  and  deglutition  often  becoming  impossible. 

Differential  Diagnosis. — Cerebro-spinal  fever  may,  in  children,  be  con- 
founded with  pneiiinonia,  since  convulsions  and  opisthotonus  may  occur 
in  either.  It  may  be  mistaken  (at  any  age)  for  typhus,  small-pox,  tuber- 
cular meningitis,  the  cerebral  ioTm.  ot pertiicious  malarialieYer,  and  acute 
myelitis. 

When,  from  the  ushering-in  symptoms,  doubt  arises  as  to  whether  a  child 
lias  thoracic  or  cerebral  disease,  a  careful  physical  examination  of  the  chest 
will  at  once  remove  the  doubt. 

The  differential  diagnosis  between  cerebro-spinal  fever  and  typhus  and 
pernicious  malarial  fever  will  be  considered  in  the  history  of  those  fevers. 

In  small-pox  the  pain  in  the  head  is  confined  to  the  frontal  region,  while 
in  cerebro-spinal  meningitis  it  has  its  seat  in  the  occipital  region.  In  men- 
ingitis there  is  early  stiffness  and  rigidity  of  the  muscles  at  the  back  of  the 
neck.  In  small-pox  this  is  a  later  symptom  if  it  occurs  at  all.  In  small- 
pox, on  the  fourth  day  of  the  fever,  the  characteristic  eruption  appears  about 
the  roots  of  the  hair,  while  in  cerebro-spinal  meningitis  there  is  no  peculiar 
eruption,  and  no  regularity  in  the  date  of  its  appearance.  The  tempera- 
ture in  small-pox  is  much  higher  than  in  cerebro-spinal  meningitis.  On 
the  second  day  of  small-pox  there  are  redness,  swelling,  and  soreness  of  the 
throat ;  in  spinal  fever  these  are  absent.  Coma  may  occur  early  in  cerebro- 
spinal meningitis,  but  is  a  late  symptom  in  small-pox.     After  the  initial 


EPIDEMIC    CEREBRO-SPINAL   MEN^INGITIS.  691 

pains  in  the  back  and  limbs,  pain  is  not  a  prominent  symptom  of  small- 
pox ;  while  the  severe  and  excruciating  pains  in  the  head,  limbs,  and 
trunk  increase  in  severity  with  the  advance  of  cerebro-spinal  menino-itis. 

The  diagnosis  between  tuhercular  and  cerebro-spinal  meningitis  is  always 
difficult  and  often  impossible.  A  careful  study  of  the  previous  history, 
the  insidious  and  characteristic  slow  advent  of  tubercular  meningitis,  the 
slowed  i3ulse  at  the  beginning,  the  ''hydrocephalic  cry,"  the  absence  of 
eruptions,  the  very  mild  delirium,  and  the  late  appearance  of  muscular 
rigidity,  are  the  points  on  which  we  may  differentiate  the  otherwise  analo- 
gous diseases. 

The  ushering-in  symptoms  of  acute  myelitis  are  very  similar  to  those  of 
cerebro-spinal  meningitis  ;  but  when  the  myelitis  is  fully  established  there 
are  the  peculiar  "girdling"  pains — the  feeling  as  if  an  iron  band  were 
around  tlie  waist — with  paralysis  of  the  lower  limbs,  which  rapidly  extends 
upward.  The  temperature  of  the  paralyzed  limbs  is  first  elevated,  but 
subsequently  falls  below  the  normal ;  there  is  almost  complete  anaesthesia 
of  the  surface,  and  impaired  muscular  contractibility  ;  later  there  is  atrophy 
of  the  muscles  of  the  paralyzed  parts  ; — all  of  these,  symptoms  are  in  strong 
contrast  with  the  symptoms  of  cerebro-spinal  fever.  Again,  pressure  on 
the  spine  in  myelitis  causes  severe  pain  which  is  not  increased  by  motion  ; 
while  in  meningitis  motion  rather  than  pressure  causes  pain.  The  recta'' 
and  vesical  sphincters  are  involved  in  myelitis,  so  that  ammonaemia,  pye- 
litis, cystitis,  and  various  urinary  complications  are  early  attendants  on  the 
disease  ;  these  are  rarely  present  in  cerebro-spinal  fever.  Trophic  nerve  de- 
rangement is  shown,  in  myelitis,  by  the  extensive  formation  of  acute  bed- 
sores, while  this  is  a  comparatively  rare,  and  always  a  late,  occurrence  in 
cerebro-spinal  meningitis.  Eefiex  power  is  diminished  or  wholly  absent  in 
myelitis,  while  it  is  exaggerated  in  spinal  meningitis. 

Prognosis. — Cerebro-spinal  meningitis  is  always  a  grave  form  of  disease, 
and  a  guarded  prognosis  should  be  given.  The  death  rate  in  severe  epi- 
demics is  80  per  cent.,  and  about  30  in  mild  ones.  Toward  the  close  of  all 
epidemics  the  death  rate  markedly  diminishes.  Hence,  the  period  as  well 
as  the  severity  of  an  epidemic  will  influence  the  prognosis.  Its  average 
duration  is  about  fourteen  days,  but  cases  are  recorded  where  death  has  oc- 
curred in  five,  twelve,  fifteen,  twenty-four,  and  thirty  hours  after  the  first 
symptoms.  In  the  majority  of  cases  which  prove  fatal,  patients  die  during 
the  second  week ;  if  recovery  takes  place  the  disease  is  apt  to  last  two  or 
three  weeks.  In  quite  mild  cases  the  disease  lasts  about  two  weeks  ;  and 
in  the  intermittent  form,  when  the  so-called  relapses  occur,  the  disease  may 
be  protracted  seven  or  eight  weeks. 

Age  influences  the  prognosis.  Statistics  show  that  under  fifteen,  the 
mortality-rate  is  much  greater  than  between  fifteen  and  thirty-five  ;  and 
that  after  thirty-five,  each  year  diminishes  the  chances  of  recovery.  Every 
day  that  is  passed  after  the  seventh  renders  recovery  m.ore  and  more  proba- 
ble ;  the  symptoms  that  tend  to  render  the  prognosis  unfavorable  are  a 
rapid,  and  especially  an  irregular  or  intermitting  pulse,  an  abundant  erup- 
tion, excessive  hyperaesthesia  and  nervous  excitement,  absolute  insensibility 


692  ACUTE    GEKEEAL    DISEASES. 

of  the  pupils,  as  well  as  symptoms  of  great  mental  depression  and  prostra- 
tion early  in  tlie  disease.  Convulsions,  a  low  temperature  with  attendant 
collapse,  paralysis  of  the  muscles  of  deglutition,  continued  vomiting,  shal- 
low and  irregular  respirations  and  the  occurrence  of  any  of  the  complica- 
tions, all  render  the  prognosis  unfavorable. 

The  co7npUcations  of  cerehro- spinal  fever  are  bronchitis,  broncho-pneu- 
monia, croupous  pneumonia,  pulmonary  oedema,  pulmonary  atelectasis  aris- 
ing from  obstruction  in  one  or  more  bronchi,  and  pleurisy.  Endocarditis 
or  pericarditis  and  nephritis  are  frequent  complications  ;  the  lesions  of  the 
eye,  ear,  joints,  and  subcutaneous  areolar  tissue  can  be  regarded  as  belong- 
ing to,  and  complicating  the  ordinary  course  of  the  disease. 

The  sequels  of  cerebro-spiual  fever  are  numerous  :  even  in  the  most 
favorable  cases  basilar  headaches  and  attacks  of  dizziness  are  liable  to  occur 
for  years  after  recovery.  Deafness  or  blindness  may  result,  and  in  chil- 
dren deaf -mutism  is  a  not  uncommon  sequence,  especially  if  the  disease 
occur  before  the  child  has  learned  to  talk.  The  eye  lesions,  already  men- 
tioned, may  become  permanent.  The  psychical  disturbances  may  vary 
from  complete  idiocy  to  .stupidity,  impaired  memory,  and  marked  diminu- 
tion in  intelligence.  General  motor  weakness  is  rather  unusual ;  but 
paralysis  of  various  muscles  or  groups  of  muscles  is  a  frequent  sequel. 
Single  nerves  are  sometimes  paralyzed.  Death  may  result  from  the  pul- 
monary complications,  from  paralysis  of  the  muscles  of  deglutition  and  of 
the  thoracic  groups,  from  heart  failure,  and  consequent  oedema  of  the 
lungs,  from  intensity  of  poisoning  at  the  onset,  from  asthenia,  and  from 
coma. 

Treatment. — The  propliylactic  measures  to  be  observed  during  an  epi- 
demic of  cerebro-spinal  meningitis  may  be  summed  up  in  careful  attention 
to  the  surroundings  : — remove  all  anti-hygienic  influences,  and  when  possi- 
ble isolate  the  sick.  Indeed  the  general  principles  of  prophylaxis  are  the 
same  as  in  all  miasmatic-contagious  diseases. 

A  patient  with  cerebro-spinal  meningitis  should  be  immediately  put  to 
bed,  in  a  dark,  cool,  well- ventilated  room,  removed  from  noise  and  con- 
fusion. During  the  entire  course  of  the  disease  the  diet  should  be  of 
the  most  nutritious  kind,  easy  of  digestion  ;  milk  is  to  be  preferred.  The 
exhaustion  and  emaciation  that  render  convalescence  so  tedious  must  be 
combated  from  the  onset  by  a  nutritious  and  generous  diet.  The  thirst 
which  is  so  tormenting  may  be  relieved  by  allowing  the  patient  to  drink  as 
much  ice  or  seltzer  water  as  he  desires.  If  constipation  exist  it  must  be 
overcome  by  promptly  acting  cathartics, — a  calomel  purge  is  to  be  pre- 
ferred. It  is  well  to  administer  a  turpentine  enema  to  aid  the  action  of 
the  calomel.  A  free  catharsis  must  be  early  obtained.  The  condition  of 
the  bladder  must  be  carefully  attended  to  throughout  the  disease.  If  the 
patient  does  not  evacuate  it  at  the  proper  intervals,  recourse  must  be  had 
to  the  catheter.     Sometimes  cystitis  has  resulted  from  neglect  of  this. 

As  with  all  severe  forms  of  disease,  various  plans  of  treatment  have 
been  adopted.  The  plan  of  general  blood-letting  and  depletion  has  no 
doubt  raised  the  death  rate.     In  no  case  is  blood-letting  indicated  or  al- 


EPIDEMIC    CEREBRO-SPIXAL   MENINGITIS.  693 

]owal)le  in  this  disease  any  more  than  in  typhoid  fever  or  diphtheria.  The 
internal  and  external  use  of  calomel  in  its  treatment,  although  it  has  been 
extensively  employed,  is  not  sustained  by  the  result  of  experience.  Kor  has 
iodide  of  potassium  the  reputation  which  it  once  had  for  promoting  the 
absorption  of  inflammatory  products.  Quinine,  if  useful  at  all,  is  only  so 
at  the  very  onset,  and  if  used  then  it  should  be  administered  in  large  doses. 
It  has  no  antipyretic  joower  in  this  disease. 

The  medicinal  agents  which  are  generally  accepted  as  most  useful  in 
the  treatment  of  this  disease  are  the  narcotics  :  among  these  opium  stands 
first  in  the  list ;  administered  hypodermically,  it  not  only  j)romptly  re- 
licA^es  the  pain  in  the  head,  the  restlessness,  jactitation,  insomnia,  delirium 
and  convulsions,  but  it  likewise  increases  the  arterial  tension.  This  drug 
should  be  given  until  the  desired  effect  is  produced,  namely,  complete  re- 
lief ;  there  must  be  no  hesitation  in  the  administration  of  large  doses  if 
required,  for  there  is  a  remarkable  tolerance  of  the  drug  in  this  disease. 
It  may  be  combined  with  atrojoia.  Bromide  of  potassium  is  regarded  by 
some  as  especially  indicated  in  this  disease,  and  it  has  been  given  quite  ex- 
tensively with  apparent  benefit,  esjDecially  in  children. 

In  my  experience  oj^ium,  hypodermically,  is  superior  to  all  other  rem- 
edies ;  it  should  be  administered  early,  in  full  doses,  and  the  patient 
should  be  kept  in  a  semi-comatose  state  until  the  stage  of  effusion  is  reached, 
after  which  it  should  be  given  in  small  doses.  When  cerebral  symj^toms 
are  violent,  cannabis  indica  '  may  be  cautiously  administered.  Chloral  hy- 
drate is  contraindicated,  and  ether  and  chloroform  inhalations  should  not 
be  resorted  to  unless  neurotics  have  failed  to  relieve  convulsions  or  pain. 
Ergot  is  recommended  by  many  on  the  ground  that  by  its  action  on  the 
vaso-motor  system  it  produces  cerebral  and  sjiinal  anemia.  It  is  pro- 
posed to  give  the  ergot  until  dizziness  is  produced.  Experience,  however, 
does  not  sustain  the  theory. 

When  symptoms  of  great  exhaustion  are  present,  stimulants  are  de- 
manded ;  decreasing  restlessness  and  a  continued  fall  of  temperature  are 
some  of  the  signs  that  indicate  that  stimulants  are  acting  remedially. 
The  rules  and  methods  of  stimulation  are  the  same  as  in  typhoid  fever.  When 
cerebro-spinal  fever  is  long  continued  and  there  is  reason  to  believe  that 
there  is  an  abundant  serous  effusion,  iodide  of  potassium  in  large  doses 
may  be  of  service. 

Cold  applications  to  the  head  and  spine,  by  means  of  evaporating  lotions, 
sprays,  or  ice-bags,  are  regarded  by  some  as  a  most  important  adjuvant  to 
its  treatment.  In  all  cases  their  use  demands  great  caution,  and  in  this 
country  the  profession  favors  the  application  of  heat  rather  than  cold  to 
the  spine,  in  the  form  of  hot-water  douches  or  hot-water  bags.  Many  are 
in  favor  of  first  blistering  the  region  over  the  spine  from  occiput  to  loins, 
and  then  covering  the  parts  with  a  poultice.  Blisters  at  the  nape  of  the 
neck  are  of  service  in  most  cases  after  the  acute  stage  is  passed.  In  sthenic 
cases  leeches  may  be  applied  over  the  temples  and  mastoid  processes  ; 
they  diminish  the  headache  at  the  beginning  of  the  disease.     The  extremi- 

■•  Maniikopf. 


694  ACUTE    GBNEEAL   DISEASES. 

ties  must  never  be  allowed  to  get  cold,  and  warm  flannel  is  to  be  continu- 
ally wrapped  about  the  legs  and  body.  Mustard  foot-baths,  stimulating 
enemata,  and  the  external  use  of  turiDcntine  are  indicated  when  the  simple 
means  fail  to  accomplish  the  desired  result.  Cold  baths  do  harm.  As  soon 
as  convalescence  shall  have  been  established,  a  tonic  plan  is  to  be  adopted. 
The  vegetable  bitters,  arsenic  and  iron  are  to  be  used.  In  some  cases  elec- 
tricity may  be  employed  with  benefit. 

SEPTICEMIA. 

Septicaemia  is  a  constitutional  disease  due  to  the  absorption  into  the 
blood  of  a  septic  material  which  has  its  origin  in  decomposing  animal  mat- 
ter. This  material  is  supposed  to  act  on  the  blood  as  a  ferment,  and  so 
render  it  incapable  of  performing  its  physiological  functions.  As  pyaemia  is 
called  "purulent"  infection,  so  septicaemia  maybe  denominated  "putrid" 
infection.  The  disease  is  closely  allied  to  "surgical "  or  "  traumatic  fever." 

Morbid  Anatomy. — The  changes  in  the  blood  in  septicaemia  are  similar  to 
those  which  occur  in  fevers.  It  is  darker  than  normal,  coagulates  less  read- 
ily, and  tends  to  rapid  decomposition.  This  loss  of  coagulating  power 
has  been  supposed  to  be  due  to  the  destruction,  by  the  septic  poison,  of  the 
white  blood  corpuscles,  which  contain  the  main  factors  for  producing 
a  clot.  Bacteria  and  micrococci  are  said  to  abound  in  the  blood  in  septi- 
caemia ;  other  observers  deny  their  presence. 

The  spleen  is  enlarged  and  often  softened.  The  heart,  kidney  and  liver 
exhibit  more  or  less  cloudy  swelling.  The  mucous  membrane  of  the  stom- 
ach and  intestines  is  congested  and  oedematous,  and  the  agminated  and  sol- 
itary glands  are  prominent.  Enteritis  is  not  frequent.  In  severe  cases 
ecchymotic  spots  are  found  in  the  intestinal  tract. 

The  serous  membranes  may  be  inflamed,  but  generally  they  are  only 
ecchymotic.  There  is  always  more  or  less  lymjahangitis  present.  It  seems 
evident  that  the  septic  poison  is  absorbed  chiefly  through  the  lymphatic 
vessels. 

.  Etiology. — The  nature  of  the  septic  poison  that  is  the  product  of  the 
decomposing  animal  tissues  is  still  a  matter  of  dispute.  Some  claim  that  it 
is  a  chemical  substance,  formed  in  a  wounded  part,  which  a'^ts  as  a  ferment 
in  the  blood  and  produces  the  septic  symptoms.  Others  rej^ard  the  bacteria 
which  are  present  as  themselves  the  sole  cause  of  the  septic  infection. 
Several  pathologists  have  attempted  to  find  the  true  poiscaous  principle, 
and  have  isolated — from  decomposing  fluids — what  they  call  "  sepsin,"  but 
yet  they  are  unable  to  prove  that  this  alone  is  poisonous,  for  decomposing 
fluids  are  still  found  to  be  noxious  after  the  removal  of  the  sepsin.  It 
has  been  observed  that  the  blood  of  an  animal  with  septicemia  produces 
greater  disturbances  and  graver  results  when  injected  into  a  healthy  animal 
than  decomposed  fluid. 

Dr.  Sanderson,  who  says  "  that  the  agency  of  bacteria  is  essential  to 
the  production  of  the  septic  poison,"  also  says  that  '-'they  are  incapable 
of  producing  the  poison  in  a  healthy  organism."     After  considering  the 


SEPTICEMIA. 


695 


various  theories  wliich  have  been  advanced,  it  seems  most  probable  that 
there  is  no  one  body  which  causes  the  septic  infection,  but  the  combina- 
tion of  a  number  of  poisonous  substances  which  produce  changes  analogous 
to  those  caused  by  fermentation,  and  that  the  j)oison  is  absorbed  chiefly  by 
the  lymphatics,  and  only  by  the  blood-vessels  in  exceptional  cases,  as  when 
their  walls  have  undergone  degenerative  changes. 

Decomposing  tissues  which  cause  septicsemia  may  be  in  the  body,  on  the 
surface  of  the  body,  or  outside  of  the  body. 

L  Thus,  a  decomposing  placenta  in  utero,  sloughing  ulcers  in  typhoid 
fever,  necrotic  processes  in  chronic  phthisis,  diphtheritic  sloughs,  ulcera- 
tive endocarditis,  abscess  and  gangrene  of  the  lung, — these  are  some  of  the 
internal  conditions  which  may  induce  septicsemia. 

II.  Wounds,  gangrene,  decomposing  membranes,  or  the  suppuration  and 
necrosis  in  small-pox,  any  ill-conditioned  wound,  especially  if  lacerated  and 
contused,  may  cause  septicaemia. 

III.  Dissecting  wounds  and  post-mortem  manipulation  of  those  who 
have  died  of  infection,  even  without  a  surface  abrasion,  may  induce  sep- 
ticaBmia.  The  respiratory  and  the  gastro-intestinal  tracts  are  sometimes 
the  mode  of  entrance  of  the  infection. 

Symptoms. — The  symptoms  of  septicaemia  will  vary  with  the  amount  of 
the  septic  material  introduced  into  the  system  and  the  length  of  the  in- 
fection ;  a  slight  infection  will  produce  fewer  and  less  grave  symptoms 
than  one  more  extensive ;  hence  the  symptoms  will  vary  : — sometimes 
urgent,  sometimes  so  mild 
as  to  be  overlooked.  In 
a  well-marked  case,  after  a 
rigor,  or  feeling  of  chilli- 
ness, but  rarely  a  distinct 
chill,  there  is  a  rapid  rise 
in  temperature  ;  105"'  or 
107°  F.  may  be  reached 
within  the  first  twenty- 
four  hours.  There  is  no 
typical  range  to  the  tem- 
perature. The  pulse  is 
rapid  (120  to  140),  feeble 
and  thread-like.  The 
mouth,  tongue,  and  sur- 
face of  the  body  become 
hot  and  dry.  If  sweats 
occur  they  are  very  slight, 
and    only   present  during       ^  .     t>      ^  •    ^^^'^^\    ,■      ■    .u    ■ 

■J     i-  o  Temperature  Record  m  a  cat^e  of  Septicaemia,  followmn:  an 

the  initial  stage,  and  can  Amputation. 

hardly  be  confounded  with  the  profuse  sweats  of  pyaemia.  Vomiting 
is  not  infrequent.  The  nervous  symptoms  are  always  well  marked. 
The  expression  of  countenance  is  dull  and  apathetic,  the  patient  lying  in  a 
listless  condition,  generally  free  from  pain.     There  is  restlessness  and  low. 


696  ACUTE    GENEKAL   DISEASES. 

muttering  delirium.  The  respirations  are  feeble,  labored,  and  hurried. 
The  skin  may  be  slightly  jaundiced.  Diarrhoea  is  present  in  about  50  per 
cent,  of  all  cases,  and  in  nearly  all  severe  cases.  The  urine  is  scanty,  high 
colored,  of  high  specific  gravity,  and  contains  urates  and  often  albumen. 

In  mild  cases  the  symptoms  may  remit,  and  complete  recovery  be 
established  within  a  couple  of  days.  This  happens  when  the  septic  cause 
is  discovered  and  removed.  In  severe  cases  death  may  occur  within 
twenty-four  or  seventy-two  hours,  the  patient  dying  in  comjalete  collapse. 
Typhoid  symptoms,  a  dry  tongue,  rise  in  temperature,  diarrhoea,  and  mut- 
tering delirium,  following  an  abortion  or  child-birth,  should  always  excite 
suspicion.  Septicemia  often  gives  rise  to  pysemia,  or  is  combined  with 
it,  which  is  shown  by  the  initial  chill  being  severe  or  often  repeated,  and 
by  the  occurrence  of  profuse  sweatings 

Differential  Diagnosis. — Septicaemia  may  be  confounded  with  pycemia, 
typhoid  and  typhus  fever. 

PycBinia  is  ushered  in  by  a  distinct  chill  ;  septicaemia  by  slight  shivering 
or  mild  rigors  only.  In  pysemia  the  chills  recur ;  in  septicasmia  there  is 
but  one — the  initiatory — chill.  In  pysemia  there  are  profuse  sweats  which 
recu7^ ;  in  septicaemia  there  are  slight,  if  any,  sweatings,  and  they  are 
never  recurrent.  In  pygemia  the  temperature  gradually  rises  to  102°  to 
104°  F.;  in  septicaemia  it  is  high  at  the  onset,  i.  e.,  105°'  to  107°  F.  The 
skin  is  of  a  dark,  leaden  yellow,  jaundiced  hue  in  pyaemia,  while  the  dis- 
coloration of  the  skin  is  never  so  marked  in  septicaemia.  There  is  a  sweet 
"  sickish  "  odor  to  the  breath  in  pyaemia,  absent  in  septicaemia.  Pyaemia 
develops  slowly,  septicaemia  rapidly.  In  pyaemia  the  heart  impulse  is  less 
forceful  than  in  septicaemia.  Finally,  itifarctions,  thrombi  and  multiple 
abscesses  develop  in  pyaemia  and  are  its  distinguishing  objective  evidence, 
while  they  never  occur  in  simple  septicsemia. 

Prognosis. — This,  in  most  instances,  depends  upon  the  extent  of  the 
poisoning,  "  when  the  symptoms  of  the  disease  are  well  marked  the  prog- 
nosis is  bad."  The  possibility  of  the  removal  of  the  source  of  the  infection, 
and  the  length  of  time  that  the  decomposing  mass  has  been  in  contact  with 
the  living  tissues,  influence  the  prognosis.  Its  duration  is  from  two  days 
to  two  months.  Death  occurs  from  asthenia,  exhaustion,  or  rapidly  from 
overwhelming  of  the  system  with  the  materies  morbi.  Collapse  is  nearly 
always  the  precursor  of  dissolution. 

Treatment. — The  first  thing  to  be  accomplished  in  the  treatment  of  this 
condition  is  the  discovery  and,  when  possible,  the  removal  of  the  cause. 
Antiseptics  should  always  be  used  at  the  seat  of  the  infection.  The  bowels 
must  be  freely  acted  upon  by  salines  throughout  the  whole  course  of  the 
disease.  The  tonic,  stimulant  and  antipyretic  plan  laid  down  for  the  treat- 
ment of  pyaemia  should  be  employed  here.  Quinine,  salicylic  acid,  and 
brandy  are  the  three  drugs  on  which  we  place  our  reliance.  Tanner 
recommends  quinine  and  nitric  acid.  The  diet  must  be  as  nourishing  as 
possible. 

Billroth's  treatment  is  cooling  drinks,  a  fever  diet,  morphine  at  night 
to  secure  sleep,  from  six  to  ten  grains  of  quinine  during  the  afternoon  ] 


PYEMIA. 


697 


the  induction  of  profuse  perspiration  when  the  skin  is  dry,  by  warm  baths, 
afterward  wrapping  the  patient  in  blankets. 


PYEMIA. 

Pyaemia  is  an  infectious  disease  caused  by  the  introduction  into  the 
blood  of  a  miasm  which  arises  from  decomposing  pus  or  its  constituents, 
attended  by  tlie  formation  of  infarctions,  metastatic  abscesses  and  diffuse 
local  inflammation.  Many  authors  make  no  distinction  between  septicaemia 
and  pyaemia. 

Morbid  Anatomy. — The  blood  in  pyaemia  is  characterized  by  a  tendency 
to  coagulate  spontaneously  wherever  there  is  slowing  of  the  blood-current. 
Colonies  of  micrococci  are  very  frequently  found  in  the  blood  and  on  the 
walls  of  the  vessels  ; '  venous  thrombosis  and  embolism  are  essential  feat- 
ures-of  this  disease.  The  thrombi  are  usually  near  the  seat  of  the  pus  ab- 
sorption ;  these  emboli  have  a  specific  action  on  certain  organs,  stamped  as 
they  are  with  the  peculiar  py^emic  infection.  When  these  emboli  become 
lodged  in  the  small  arteries  of  different  organs  they  lead  to  the  development 
of  infarctions  which  terminate  in  the  formation  of  abscesses. 

"  Metastatic  abscesses,"  the  result  of  suppuration  of  a  pyaemic  in- 
farction, caused  by  venous  thrombosis  and  embolism,  may  form  in  the 
lungs,  liver,  kidneys,  spleen,  muscles,  heart  and  brain. '^  In  the  lungs 
there  is  usually  more  or  less 
pneumonic  inflammation  about 
the  abscesses.  Even  patches  of 
gangrene  may  be  found  near 
them.  In  the  kidney  the  tu- 
bules and  vessels  are  found 
crowded  with  micrococci. 

The  spleen  is  swollen  and 
shows  more  or  less  parenchyma- 
tous degeneration,  according  to 
the  amount  of  fever.  Gener- 
ally will  be  found,  scattered 
through  the  organ,  a  few  firm 
wedge-shaped  nodules  with 
their  apices  inward,  or  their 
interior  partly  broken  down 
into  pus.  Metastatic  abscesses 
vary  in  size  from  a  pea  to  a 
large  walnut.  When  multiple 
abscesses  are  found  scattered 
through  the  various  viscera, 
softened  puriform  and  decom- 
posing thrombi  are  rarely  found 
in  the  veins  ;  but  when  the  abscesses  are  few  the  reverse  is  the  case. 


Fig.  155. 
Pyiemia. 
Metastatic  Pyaemic  Abscesses  of  the  Lung. 


The 


1  Weigi'rt  states  that  rnnall  thrombi  are  often  formed,  solely  of  bacteria. 

*  Recklinghausen  says  that  these  abscesses  depend  on  "  extra-vascular  accretions  offhnrji.^ 


698  ACUTE   GENERAL  DISEASES. 

joints,  the  serous  membranes  of  the  body,  and  the  connective-tissue  of 
various  parts  are  often  involved. 

Pleurisy,  pericarditis,  and  peritonitis  of  pyjemic  origin  are  frequent  and 
always  fibrino-purulent  in  character.  I  have  known  the  pleural  cavity  to 
fill  with  pus  twenty-four  hours  after  the  first  evidences  of  pysemic  suppu- 
rative pleurisy.  Suppurative  arthritis  is  a  rare  complication.  Lymphangi- 
tis is  usually  established  in  the  neighborhood  of  the  injury  or  source  of  in- 
fection. 

Ulcerative  endocarditis  with  the  presence  of  large  quantities  of  bacteria  is 
not  infrequent.  Pyaemic  pan-ophthalmia  with  sloughing  of  the  cornea  is  of 
rare  occurrence.  In  some  cases  nearly  all  the  tissues  and  serous  and  mucous 
membranes  exhibit  deep  post-mortem  staining;  the  gastric  and  intestinal 
mucous  membrane  being  swollen  and  congested,  the  solitary  glands  and 
Peyer's  patches  prominent.  Ulcers  may  form  at  points  along  the  intestine. 
The  skin  always  shows  more  or  less  jaundice.  Suppurative  cellulitis  often 
occurs.  Occasionally  there  are  cases  of  py83mia,  or  conditions  closely  re- 
sembling pygemia,  where  there  are  no  recognizable  pathological  lesions. 

Etiology. — Eecent  observations  and  experiments  seem  to  show— ^rs^, 
that  pus  with  micrococci  causes  suppurative  pyemic  inflammation  ;  sec- 
ond, that  the  micrococci  alone  can  establish  a  similar  inflammation  ;  and 
third,  that  without  micrococci  pus  is  inert.  Many  regard  the  pysemic  and 
septicsemic  poison  as  identical,  and  pyaemia  as  nothing  but  a  metastatic 
septicaemia,  claiming  that  pyemia  is  invariably  associated  with  more  or 
less  septicaemia,  and  therefore  have  advised  the  use  of  the  term  septicc 
pyaemia.' 

The  principal  theories  in  regard  to  its  nature  are  :  1st.  That  pus  is  ab- 
sorbed and  acts  as  a  poison.  2d.  That  a  chemical  substance  is  evolved 
from  decomposing  pus  which  enters  the  system  and  acts  as  a  poison.  3d. 
That  microscopic  organisms,  finding  their  way  into  the  blood  and  tissues, 
there  multiply  and  infect.  Suppuration  of  bone  is  a  very  frequent  cause 
of  a  pJilehitis  which  leads  to  pyaemic  infection.  Thus  a  blow  on  the  head 
of  one  saturated  with  alcohol  is  followed  by  a  phlebitis  in  some  of  the 
diploic  veins  ;  as  a  result,  thrombi  are  formed,  which  break  up  into  emboli 
and  thus  lead  to  pyaemic  infarction  and  abscess.  Suppuration  of  the  eye 
or  middle  ear  has  led  to  the  same  results. 

Cellulitis,  carbuncle,  erysipelas,  '' malignant  pustule,"  and  dissecting 
wounds  often  produce  pyaemia.  Endometritis  or  lacerations  about  the 
genital  tract  are  fruitful  sources  of  pyaemia  in  the  puerperal  state.  As 
regards  the  question  of  pyaemic  contagion,  nothing  definite  can  be  stated. 
From  a  surgical  standpoint  it  has  been  proven  that  certain  atmospheric 
conditions  and  surroundings,  such  as  want  of  cleanliness,  will  cause  wounds 
to  take  on  an  unhealthy  action,  and  then  pyemia  will  result ;  but  it  has 

'^Holmes'  Sys.  Surr/.,'Vol.  v.  Sanderson  claims  that  "pysemic  poison  multiplies  in  the  organism." 
Whether  the  poison  becomes  more  infective  or  virulent  as  time  elapses  or  as  it  is  developed  from  new 
foci,  is  a  mooted  que^^tion.  Panum  chiimed  that  "  there  is,  in  putrefying  fluids,  a  specific  chemical  sul>- 
stance  soluble  in  water  and  which,  when  introduced  into  the  blood,  causes  the  symptoms  of  putrid  or 
septic  infection."  Others  claim  that  pytemia  is  due  to  a  peculiar  miasm  which  lias  a  specific  action 
similar  to  the  exanthemata,  and  which  may  be  introduced  through  the  lungs,  mucous  membranes,  and 
through  abraded  surfaces. 


PYEMIA. 


699 


never  been  shown  that  pyaemia  can  be  contracted  as  small-pox  or  scarlatina 
can. 

Symptoms. — Pygemia  is  ushered  in  by  well-marked  symptoms.  First, 
there  is  a  chill  or  decided  rigor  followed  by  a  gradual  rise  of  temperature 
to  101°  or  104°  F.,  the  rise  of  temperature  being  proportional  to  the  phe- 
nomena of  the  chill.  The  chills  of  pygemia  occur  irregularly,  rarely  at 
night,  and  are  followed,  after  the  first  two  or  three,  by  profuse  and  exhaust- 
ing sweats,  which  only  afford  marked  relief  for  a  time,  the  skin  soon  be- 
coming hot  and  dry.  An  irritability  of  the  nervous  system  has  been 
noticed  as  preceding  the  occurrence  of  these  chills.  During  the  chill  the 
temperature  will  be  higher  than  in  the  sweating  stage,  the  thermometer 
often  showing  a  temperature  of  103°  or  105° 
F.,  or  108°  F.,  which  often  suddenly  falls 
below  the  normal,  soon  to  rise  again. '  The 
heart  power  is  notably  and  early  diminished. 
The  pulse  is  frequent,  120  to  140,  small  and 
often  intermittent ;  it  does  not  vaiy  with 
the  range  of  temperature.  The  conjunc- 
tivaB  and  skin  assume  a  sallow  tinge  ;  later 
they  may  become  markedly  jaundiced.  The 
breath  has  a  peculiarly  sweet,  sickish  odor. 
The  tongue  is  at  first  covered  with  a  white 
fur;  later  it  becomes  glazed,  dry,  brown, 
and  fissured.  Sordes  collect  on  the  teeth. 
Anorexia  is  marked  from  the  onset.  The 
patient  complains  of  great  thirst.  The 
bowels  are  usually  relaxed.  The  copious 
diarrhoeal  discharges,  with  the  attendant 
nausea  and  vomiting,  soon  bring  about  a 
condition  of  asthenia.  The  mind  remains 
clear  up  to  the  time  of  great  exhaustion 
and  the  appearance  of  multiple  abscesses  in 
some  central  organ  or  organs ;  then  the  patient  becomes  dull,  apathetic, 
and  often  slightly  delirious.  The  respirations  are  hurried  and  shallow, 
and  are  always  more  accelerated  just  before  a  chill  or  sweat.  As  death  ap- 
proaches, delirium  occurs,  the  pulse  becoming  more  feeble  and  intermittent, 
reaching  at  times  150  or  170,  or  200  ;  the  face  has  a  yellowish,  leaden  hue, 
and  finally  the  patient  passes  into  a.  comatose  state  and  dies. 

When  the  internal  organs  are  involved  the  local  signs  of  multiple  abscesses 
will  be  present.  The  physical  signs  of  pyasmic  pulmonic  infarctions  are  at 
first  obscure,  for  the  foci  are  so  small  and  so  scattered  through  the  lung 
that  percussion  fails  to  detect  them.  Usually  the  evidences  of  a  severe 
bronchial  catarrh  accompanied  by  a  cough,  with  frothy,  blood-stained, 
watery  expectoration,  are  followed  by  the  physical  signs  of  lobular  pneu- 
monia. 


Fig.  156. 
Temperature  Record  in  a  case  of  Pyaemia. 


1  This  intermittent  type  of  fever  is  peculiar  to  tliia  disease.  Billroih  says  statistics  favor  the  idea  that 
recurrent  chills  depend  on  new  inflammations,  having  their  chief  source  in  repeated  purulent  infections 
about  the  wound. 


700  ACUTE    GE]S"EEAL   DISEASES. 

The  kidney  changes  are  marked  by  albuminuria  and  hsematuria,  together 
with  the  i:)resence  of  epithelial  and  gelatinous  casts.  The  amount  of  urea 
is  always  increased.  The  changes  in  the  liver  and  spleen  cause  abdominal 
tenderness,  accompanied  by  a  marked  increase  in  these  organs  as  shown  by 
percussion.  In  pygemia  there  is  generally  more  or  less  jaundice.  The  signs 
of  arthritis,  pleuritis,  peritonitis  and  cellulitis  can  be  early  recognized,  and 
should  be  looked  for  in  severe  cases  after  the  second  or  third  day. 

Chronic  pycBniia  is  met  with  among  the  robust,  in  whom  the  infection  is 
moderate,  and  not  often  repeated.  The  abscesses  are  confined  to  the  cellu- 
lar tissue  and  followed  by  suppuration  in  the  Joints,  marked  debility  and 
muscular  weakness.  Weeks,  or  even  months,  may  elapse  before  death  or 
recovery  takes  place  in  this  class  of  cases. 

Differential  Diagnosis. — The  diagnostic  points  of  pyemia  are,  irregularly 
Tecurring  chills  and  sweats,  great  variations  in  temperature,  with  the  signs 
■of  multiple  abscess  in  the  -internal  organs.  It  may  be  mistaken  for  septi- 
cceniia,  iniermittent  (malarial) /ever,  acute  yellow  atropliy  of  the  liver,  acute 
articular  rheumatism,  typhus  and  typhoid  fever.  The  diagnosis  between 
pyaemia  and  septicaemia  has  already  been  considered  under  septicgemia. 

The  paroxysms  in  intermittent  fever  are  regular  in  their  development 
and  time  of  occurrence  ;  they  are  not  so  in  pygemia.  The  temperature  in 
intermittent  fever  ranges  higher  than  in  pyaemia.  There  is  slight,  if  any, 
jaundice  in  malarial  fever,  while  deep  hematogenous  jaundice  is  common 
in  pyaemia.  The  history  of  the  case,  together  with  the  presence  or  absence 
of  small  points  of  local  infection,  helps  to  differentiate  between  the  two  dis- 
eases. The  sweet,  nauseating  breath,  marked  muscular  prostration,  and 
dull  expression  of  the  face,  are  noted  in  pyaemia  and  not  in  intermittent 
fever. 

The  points  of  differential  diagnosis  between  pyaemia,  yellow  atrophy  of 
the  liver,  rheumatism,  and  typhoid  fever  are  found  in  the  history  of  these 
affections. 

Prognosis. — In  pyasmia  the  prognosis  is  always  unfavorable.  Some  deny 
the  possibility  of  recovery  in  a  well-marked  case  ;  still  recovery  is  possible 
in  cases  that  are  mild  at  the  onset  and  slow  in  their  development,  in  which 
the  chills  are  not  often  repeated,  the  intermissions  between  the  exacerba- 
tions of  fgver  are  long,  loss  of  strength  is  not  rapid,  and  the  tongue  re- 
mains moist.  Thus  we  see  that  the  prognosis  depends  entirely  on  the  course 
of  the  disease.  The  duration  of  pyaemia  varies  :  it  is  usually  acute,  lasting 
from  two  to  ten  days,  often  subacute,  lasting  from  two  to  four  weeks,  and 
rarely  chronic,  when  it  may  run  on  for  months.  The  duration  of  puer- 
peral pyasmi  a  is  usually  about  one  week.  If  death  occurs  in  four  or  eight 
days,  it  is  due  to  the  intensity  of  the  pyaemic  poison.  If  later,  it  depends 
upon  the  exhaustion  incident  to  the  formation  of  abscesses  and  the  occur- 
rence of  complications.  The  earlier  the  symptoms  of  multiple  abscesses 
appear  the  more  hopeless  the  case. 

It  must  be  remembered  that  pyaemic  patients  differ  in  their  power  of 
eliminating  poison  ;  hence  in  some  cases  the  system  will  be  at  once  over- 
whelmed, while  in  others  the  shock  will  be  recovered  from.     Every  day 


ERYSIPELAS.  701 

after  the  eighth  that  the  patient  survives  increase-;  his  chance  of  recov- 
ery. 

Treatment. — The  treatment  of  pyaemia  may  be  divided  into  the  prophy- 
laxis, and  the  treatment  of  the  developed  disease.  Its  prophylactic  treat- 
ment is  by  far  the  most  important  :  it  consists  in  avoiding  everything 
that  may  favor  the  development  of  the  disease,  the  details  of  Avhich  are 
included  under  the  general  management  of  surgical  operations,  and  the 
treatment  of  wounds.  The  history  of  these  antiseptic  methods  comes 
within  the  domain  of  surgery  rather  than  medicine.  Obstetricians  cannot 
be  too  careful  in  these  matters.'  Cleanliness,  good  ventilation,  sunlight 
and  quiet  are  important  prophylactic  measures.  There  are  undoubtedly 
certain  atmospheric  conditions  which  influence  the  development  of  pysemic 
marasmus  and  are  always  to  be  considered. 

Pysemic  poison,  if  eliminated  at  all,  is  eliminated  by  the  intestinal 
tract  and  not  by  the  skin  or  kidneys,  and  treatment  should  be  directed 
to  aid  this  elimination.^  With  the  idea  of  neutralizing  the  pysemic  poison 
after  it  has  gained  access  into  the  body,  or  counteracting  its  effects,  a  long 
list  of  antiseptics  have  been  employed.  The  sulphites  and  hyposulphites 
of  sodium,  calcium,  and  magnesium  ;  carbolic  and  salicylic  acids,  the  oil 
of  turpentine,  and  many  like  agents,  are  still  under  trial.  Quinine  is  the 
drug  which  is  most  extensively  employed,  for  its  antiseptic  and  also  for  its 
stimulant  and  antipyretic  powers. 

The  most  important  thing  in  the  treatment  of  pyaemia  is  to  support  the 
patient ;  and,  with  this  end  in  view,  the  largest  possible  amount  of  nour- 
ishment and  stimulants  should  be  administered.  There  is  no  disease  in 
which  so  large  an  amount  of  stimulants  can  be  administered  with  benefit 
as  in  pyaemia.  The  indications  for  their  administration  are  the  same  as 
in  the  essential  fevers.  If  life  can  be  prolonged,  in  mild  cases,  until  the 
violence  of  the  infection  is  passed,  recovery  is  possible. 

ERYSIPELAS. 

Erysipelas  is  an  acute  constitutional  disease  with  local  manifestations, 
which  are  first  developed  in  most  cases  about  wounds,  but  may  apjDcar 
primarily  in  previously  healthy  parts. 

Although  it  cannot  be  stated  with  certainty  that  erysipelas  is*never  idio- 
pathic in  its  genesis,  its  unquestionably  contagious  nature  when  once  de- 
veloped, from  whatever  source  it  may  have  arisen,  leads  me  to  class  it 
under  infectious  diseaees,  and  to  consider  it  a  connecting  link  between  the 
general  and  local  affections. 

Morbid  Anatomy. — The  changes  in  internal  organs  and  the  blood  are 
in  no  way  characteristic.  Early  in  the  disease  the  fibrin  and  white  cells 
are  increased,  but  the  blood  rapidly  assumes  the  condition  found  in  other 
acute  febrile  diseases,  and  becomes  thm  and  fluid,  or  dark  and  pitchy,  does 

'  An  interesting  proof  of  this  is  shown  in  the  case  I'elated  by  Dr.  Teale  :  Three  gentlemen  who  aided 
him  in  dissecting  a  subject  who  died  of  hernia,  attended  the  same  day  five  midwifery  cases  in  all.  Four 
of  these  cases  died  of  puerperal  fever,  while  no  other  cases  of  it  occurred  in  their  extensive  practice. 

2  Billroth  says  diarrhcea  is  a  severe  complication  which  quickly  induces  collapse. 


702  ACUTE    GEN"ERAL    DISEASES. 

not  coagulate  readily,  and  stains  the  heart  and  vessels.  The  local  mani- 
festations  may  affect  any  surface,  as  the  mucous  and  serous  membranes  or 
lining  membrane  of  the  blood-vessels  and  lymphatics,  but  are  most  charac- 
teristically displayed  in  the  skin. 

They  are  essentially  inflammatory.  Early  there  is  hypersemia,  followed 
by  exudation  of  lymph  and  cells,  which  gives  the  part  a  bright  red  color  and 
causes  some  swelling  and  induration.  This  inflammation  is  peculiar  in  its 
tendency  to  become  diffuse,  and  in  its  antagonism  to  reparative  processes. 
When  it  attacks  a  wound  already  partly  united  the  adhesions  are  speedily 
resolved  and  the  wound  is  reopened.  On  the  unbroken  skin  it  is  not 
limited  by  inflammatory  products,  but  extends  by  continuity,  and  may 
from  a  small  primary  focus,  involve  the  head,  an  entire  limb,  or  the  whole 
body.     The  intensity  of  the  inflammation  is  very  inconstant. 

In  most  cases  it  involves  only  the  skin,  and  is  hardly  more  than  a  simple 
erythema.  In  some,  and  generally  where  the  skin  is  lax,  there  is  well- 
marked  and  more  or  less  extensive  oedema.  In  more  severe  cases  there  is 
often  suppuration,  which  is  generally  a  diffuse  infiltration,  but  may  be  cir- 
cumscribed. 

The  inflammation  may  terminate  in  resolution,  vesication,  abscess,  or 
gangrene.  The  former  is  the  usual  ending.  The  hypersemia  subsides,  the 
infiltration  is  absorbed,  and  the  process  terminates  in  desquamation. 
When  vesication  occurs  previous  to  resolution,  the  cuticle  is  raised  by  se- 
rous effusion,  and  when  thrown  off  leaves  healthy  skin  or  superficial  ulcera- 
tion. Abscess  and  gangrene  present  the  same  pathological  changes  as  under 
other  conditions. 

Erysipelas  is  not  always  limited  to  the  skin,  but  often  involves  deeper 
parts.  It  is  somewhat  doubtful,  however,  whether  the  inflammations  of 
the  pleura,  pericardium  and  peritoneum,  which  often  complicate  severe 
attacks  of  the  disease,  are  the  result  of  direct  extension  of  inflammation  or 
are  due  to  the  systemic  poison. 

When  meningitis  complicates  erysipelas  of  the  scalp,  or  laryngitis  and 
oedema  giottidis  accompany  the  inflammation  of  tlie  neck,  the  relation  is 
probably  one  of  continuity,  but  the  peri-  and  endocarditis  which  are  occa- 
sionally present  in  a  similar  erysipelatous  condition,  together  with  the 
implication  of  the  veins  and  evidences  of  nephritic  complications,  point 
to  a  more  general  etiological  basis  for  such  conditions. 

The  lymphatics  are  generally  implicated,  and  their  course  can  be  traced 
by  red  lines  running  from  the  inflamed  area  to  the  adjacent  glands,  which 
are  enlarged  and  indurated.  Indeed,  some  authors  believe  that  the  primary 
seat  of  the  inflammation  is  often  in  this  system.  If  the  veins  are  in- 
volved, a  phlebitis  may  result  in  infarction,  or  more  rarely  in  pyaemia. 

Following  an  attack  of  erysipelas  there  remains  some  thickening  and  in- 
duration of  the  skin,  which  may  become  permanent  after  repeated  attacks.  ^ 

The  tissues  in  the  inflamed  area  and  the  lymph-spaces  and  channels 
connected  with  them  are  filled  with  bacteria,  whose  relation  to  the  inflam 
mation  is  not  definitely  determined. 

^  Virchow. 


ERYSIPELAS. 


703 


Etiology.— All  the  causes  of  general  debility,  as  indulgence  in  drink  and 
anti-hygienic  conditions,  predisjDOse  to  erysipelas.  In  a  large  proportion  of 
cases  it  is  preceded  by  some  abrasion  of  the  surface  or  a  distinct  wound, 
and  is  then  considered  traumatic. 

Some  individuals  show  a  constitutional  predisposition  to  the  disease,  and 
certain  unknown  atmospheric  conditions  favor  its  dissemination. 

It  is  fully  determined  not  only  that  erysipelas,  once  developed,  is  highly 
contagious  and  spreads  rapidly  among  surgical  patients  and  puerperal 
women,  but  that  the  disease  is,  in  such  cases,  the  result  of  a  specific  con- 
tagion which  may  render  buildings,  clothing,  and  the  persons  of  attendants 
infectious  centres.     The  nature  of  this  contagion  is  entirely  unknown. 

Inoculation  of  the  bacteria  which  fill  the  inflamed  tissues  produces  ery- 
sipelatous inflammation.  It  is  not  proven,  however,  that  they  are  the  sole 
cause  or  vehicle  of  infection.  Traumatic  erysipelas  is  generally,  if  not 
invariably,  due  to  such  a  specific  contagion.  It  is  not  equally  certain  that 
idiopathic  erysipelas  is  always  primarily  a  constitutional  disease,  although 
it  is  generally  so  considered.  In  its  contagiousness,  period  of  incubation, 
and  evidences  of  constitutional  disturbance  preceding  the  local  inflamma- 
tion, and  in  the  fact  that  it  can  be  propagated  by  inoculation,  it  is  allied  to 
the  purely  contagious  diseases. 

On  the  other  hand,  contagious  properties  do  not  prove  a  specific  origin. 
The  constitutional   condition  may  be  fully  accounted   for   by  the  local 


Fig.  157. 
Temperature  Record  in  a  case  of  Facial  Erysipelas. 


affection,  as  in  simple  traumatic  fever,  and  each  attack  renders  the  patient 
more  liable  to  another. 

Therefore  while  erysipelas  is  more  commonly  the  result  of  direct  con- 


704  ACUTE    GEXEEAL   DISEASES. 

tagion,  I  believe  that  in  some  cases  it  may  be  primarily  a  local,  non-specific 
disease  which  becomes  contagious  in  its  development,  in  the  same  sense  as 
pneumonia  is  a  local  disease,  and  may  be  due  to  exposure  or  direct  irrita- 
tion under  favoring  constitutional  conditions. 

Symptoms. — The  symptoms  of  erysipelas  are  constitutional  and  local. 

Both  traumatic  and  idiopathic  erysipelas  have  a  period  of  latency  of  from 
two  days  to  a  week  or  more,  during  whj«n  there  will  be  some  fever,  pos- 
sibly of  a  remitting  type,  with  slight  chills,  headache  and  malaise.  As  the 
local  symptoms  appear  the  fever  increases,  and  is  marked  by  decided  even- 
ing exacerbations.  It  seldom  passes  106°  F.,  and  the  morning  remission 
may  be  two  or  three  degrees,  and  be  attended  by  sweating.  The  fever  is 
accompanied  by  a  rapid  pulse,  coated  tongue,  nausea,  anorexia,  and  dis- 
ordered bowels.  In  some  sthenic  cases  the  attack  is  sudden  and  attended 
by  severe  chills  and  a  rapid  rise  of  temperature.  The  duration  of  the  fever 
is  very  varied. 

When  the  inflammation  is  localized  and  recovery  occurs,  generally  from 
the  fifth  to  the  tenth  day  there  is  a  rapid  decline  in  the  fever  and  dis- 
appearance of  all  unfavorable  symptoms.  The  temperature  may  even  be- 
come subnormal  and  continue  so  during  early  convalescence.  When  the 
local  condition  is  progressive,  however,  the  fever  continues  at  104°  or  105° 
P.  for  two,  three  or  more  weeks.  ^  In  these  cases  the  fall  in  temperature 
is  commonly  more  gradual  and  convalescence  more  prolonged. 

In  children  and  nervous  patients  a  mild  delirium  may  be  present  with- 
out any  meningeal  complications,  or  in  sthenic  cases  it  may  become  perma- 
nent and  violent. 

When  the  course  of  the  disease  is  unfavorable  it  assumes  a  typhoid  char- 
acter, the  temperature  rises  rapidly,  the  pulse  is  frequent  and  feeble  or 
irregular,  the  delirium  becomes  low  and  muttering,  and  passes  into  coma 
which  ends  in  death.  Sudden  extension  of  the  inflammation,  or  relapses 
when  convalescence  is  apparently  established,  are  frequent  and  are  marked 
by  a  rapid  rise  of  temperature,  corresponding  with  the  extent  of  new  tis- 
sue involved.  Final  recovery  may  thus  be  delayed  for  weeks,  during  which 
there  will  be  periods  of  normal  or  subnormal  temperature. 

The  urine  is  always  scanty  and  high-colored.  It  contains  an  excess  of 
urea  and  often  a  small  amount  of  albumen. 

I'his  course  of  the  fever  is  often  greatly  modified  by  complications. 

The  local  symptoms  are  equally  variable.  Traumatic  erysipelas  begins 
as  a  diffuse  rose  or  bright  red  blush  about  the  point  of  injury,  in  which  a 
white  line  follows  the  finger  as  it  is  lightly  drawn  across  the  surface. 
This  is  generally  preceded  for  a  day  or  two  by  some  enlargement  and  ten- 
derness of  the  adjacent  lymphatic  glands.  In  uncomplicated  cases  there 
are  no  further  changes,  but  the  inflammation  subsides  and  is  followed  by 
flaky  desquamation. 

Idiopathic  erysipelas  is  most  commonly  facial,  starting  from  either  the 
nose,  eyelid  or  ear.     It  may  begin  either  in  the  skin  or  areolar  tissue,  and 

1  In  a  case  where  the  inflammation  involved  by  degrees  the  entire  surface  from  a  wound  on  the  head  to 
the  toes,  the  temperature  was  between  103°-104°  for  over  four  weeks. 


ERYSIPELAS.  705 

is  attended  by  more  or  less  oedema.  The  part  is  first  swollen  and  second- 
arily the  characteristic  blush  appears.  The  jmrt  becomes  enlarged,  hot 
and  painful,  and  the  swelling  may  extend  so  as  to  close  the  eyes  and  involve 
the  whole  head  and  neck  to  such  an  extent  as  to  greatly  disfigure  the 
patient.  In  from  six  to  twelve  days  the  color  becomes  darker,  the  swell- 
ing recedes  and  the  cuticle  peeling  off  leaves  a  slightly  reddened  surface 
which  slowly  regains  its  normal  color. 

When  the  disease  is  "  erratic  "  it  extends  more  or  less  rajaidly  from  its 
primary  seat,  where  the  inflammation  slowly  ceases  as  it  advances  else- 
where, so  that  it  may  be  present  in  all  stages  from  the  first  faint  blush  to 
desquamation. 

When  the  disease  assumes  a  phlegmonous  or  suppurative  form,  the  pus, 
if  diffuse,  gives  a  peculiar  boggy  sensation  on  palpation,  but  if  circum- 
scribed it  has  the  usual  appearance  of  an  abscess. 

Ap]3roaching  gangrene  is  indicated  by  an  intense  burning  j^ain,  and  the 
parts  become  livid  and  finally  black  and  crackling. 

Erysipelas  may  be  com|)licated  by  meningitis,  which  will  be  indicated  by 
its  usual  symptoms  somewhat  modified  by  the  preexisting  fever.  Peri- 
carditis and  pleurisy  are  at  times  recognized  by  dyspnoea,  or  often  only  by 
their  physical  signs. 

Differential  Diagnosis. — When  erysipelas  attacks  n  joint  it  may  be  mis- 
taken for  a  short  time  for  acute  articular  rheumatism,  but  the  peculiar 
deep  rose  color  and  the  rapidity  with  which  the  inflammation  extends  will 
speedily  distinguish  it.  Similar  symptoms  with  the  oedema  will  also  dif- 
ferentiate the  disease  from  simple  erythema.  High  febrile  movement 
lasting  twenty-four  to  forty-eight  hours,  and  attended  by  pain,  swelling  and 
tenderness  of  the  lymphatics,  has  been  considered  diagnostic  of  develop- 
ing erysipelas. 

Other  questions  of  differential  diagnosis  belong  entirely  to  surgery. 

Prognosis. — Traumatic  erysipelas  is  a  very  unfortunate  complication  in 
surgical  injuries.  It  arrests  all  reiDarative  action  and  adds  largely  to  the 
gravity  of  the  previous  condition. 

Idiopathic  erysipelas,  when  it  attacks  the  face  and  head,  is  a  dangerous 
and  uncertain  disease  under  any  circumstances,  and  is  especially  so  in 
aged  people.  Many  patients  suffer  from  a  simple  erysipelas  of  the  face  at 
almost  regular  intervals  without  serious  discomfort,  but  there  is  always 
danger  that  the  meninges  will  become  involved  and  the  disease  at  once 
assume  a  most  serious  aspect. 

Death  may  result  from  the  overpowering  effects  of  the  poison,  from  the 
complications,  or  from  exhaustion  due  to  suppuration,  gangrene,  or  a  pro- 
longed course  of  the  disease.  CEdema  of  the  glottis  from  extension  of 
inflammation  may  cause  sudden  death.  The  disease  is  especially  fatal  in 
chronic  alcoholism,  Bright's  and  gout,  and  in  patients  over  sixty.  Eecur- 
rent  attacks  indicate  a  debilitated  condition  and  are  apt  to  be  of  increasing 
severity. 

Treatment. — In  common  with  other  miasmatic-contagious  diseases,  great 
care  should  be  taken  to  avoid  extension  of  the  disease,  and  as  we  are  unable  to 
45 


706  ACUTE    GESTEEAL   DISEASES. 

control  the  poisonous  emanations,  complete  isolation  of  such  patients 
affords  the  only  sure  means  of  prophylaxis. 

In  mild  cases  local  treatment  is  unnecessary,  and  it  is  doubtful  if  it  ever 
restricts  the  inflammation.  Cold  dressings  with  mildly  astringent  and 
anodyne  lotions  are  the  most  grateful  to  the  patient  and  as  efficacious  as 
any.  More  powerful  astringents  and  distinct  caustics,  as  iodine  and  a 
saturated  solution  of  nitrate  of  silver,  or  even  the  actual  cautery  have  been 
employed  with  a  view  to  cut  short  the  inflammation  or  to  prevent  its 
spreading. 

Erysipelatous  inflammation  often  improves  in  five  or  six  days  under  such 
treatment,  or  halts  at  a  line  where  iodine  or  silver  has  been  employed  ; 
but  it  quite  as  frequently,  when  extending,  is  not  perceptibly  restricted  by 
such  boundaries.  A  saturated  solution  of  silver  may  be  applied,  however, 
two  or  three  times  in  twenty-four  hours.  Subcutaneous  injections  of 
carbolic  acid  in  surgical  erysipelas  have  seemed  to  give  more  appreciable 
and  better  results  than  any  other  local  treatment.  If  oedematous  swellings 
are  excessive,  minute  punctures  will  afford  marked  relief.  Hot  applications 
and  poultices  are  to  be  used  only  when  suppuration  or  gangrene  is  present. 
We  have  no  means  of  neutralizing  the  poison  of  erysipelas,  and  internal 
treatment  is  confined  to  general  tonic  measures.  Concentrated  nutriment 
should  be  administered  frequently  in  small  quantities,  and  stimulants  em- 
ployed as  in  other  acute  febrile  conditions.  The  bowels  and  kidneys  should 
be  kept  active  by  cathartics  and  simple  diuretics.  Various  remedies  have 
been  employed,  but  the  tincture  ferri  chloridi  seems  to  be  generally  ac- 
cepted as  the  most  useful  drug,  and  is  even  considered  to  have  specific  effects 
in  erysipelas. 

Quinine  and  other  tonics  may  be  employed  with  advantage. 

The  bromides  and  chloral  are  preferable  as  soporifics  to  opium  or  hyos- 
cyamus. 

ACUTE   MILIARY   TUBERCULOSIS. 

Acute  miliary  tuberculosis  is  an  acute  general  disease  of  an  infectious 
nature  and  non-inoculable.  In  nearly  every  instance  it  is  secondary  to, 
and  a  part  of,  a  more  chronic  tuberculous  process,  of  which  the  symp- 
toms, in  some  cases,  are  of  so  passive  a  nature  as  to  escape  notice,  while 
the  manifestations  of  the  more  acute  process  alone  attract  attention.  More 
frequently  the  preceding  chronic  condition  and  the  acute  disease  appear 
as  a  part  of  a  general  tubercular  process.  It  is  only  when  it  occurs  with- 
out previous  tubercular  infection  that  it  can  be  considered  a  distinct  dis- 
ease. The  question  whether  it  is,  strictly  speaking,  primary,  awaits  its 
answer  in  an  accepted  definition  of  tubercle  and  a  demonstration  of  its 
etiology. 

Morbid  Anatomy. — While  acute  miliary  tuberculosis  is  not  a  local  affec- 
tion and  is  to  be  carefully  distinguished  from  acute  phthisis,  its  pathologi- 
cal changes  are  more  abundant  and  far  more  frequently  found  in  the  lungs 
than  in  any  other  organ.  They  are  also  generally  present  and  may  be 
principally  located  in  the   pia  mater  (acute  hydrocephalus)  intestines, 


ACUTE   MILIARY   TUBERCULOSIS.  707 

lymph  glands,  serous  membranes,  and,  rarely,  liver,  spleen  and  brain.  The 
characteristic  lesion  of  acute  miliary  tuberculosis  consists  of  an  irrui^tion 
of  delicate,  gray,  translucent  miliary  granules,  varying  in  size  from  a  pin's 
head  to  a  poppy-seed.  They  are  quite  evenly  distributed  throughout  the 
affected  organs  and  show  little  tendency  to  coalesce. 

In  the  early  stages  affected  lungs  show  little  change  from  the  normal, 
aside  from  the  presence  of  the  tubercle  granules.  Later  they  become 
slightly  hypergemic  and  oedematous,  with  some  infiltration  about  the 
granules  of  an  amorphous  matter.  Although  the  air  cells  may  become 
partially  filled  with  epithelium,  pus-cells  and  fibrin,  hej)atization  is  of 
rare  occurrence.  The  pleura  is  studded  with  similar  tubercular  granula- 
tions, and  they  are  also  present  more  or  less  abundantly  in  the  peritoneum 
and  the  various  glands  and  organs  throughout  the  body.  They  can  be 
recognized  in  some  cases  in  the  choroid.  In  the  pia  mater  they  occupy 
the  perivascular  lymph  spaces.  Histologically  a  gray  miliary  tubercle  con- 
sists of-lymphoid  and  epithelioid  elements  enclosed  in  a  fine  reticulum  re- 
sembling coagulated  fibrin.  One  or  more  masses  of  protoplasm  containing 
several  nuclei  with  bright  nucleoli  and  varying  in  size  from  1-500  to  1-200 
inch — the  so-called  ''giant  cells" — are  generally  present  in  each  tubercle, 
but  are  not  found  in  the  tubercles  of  the  pia  mater,  and  cannot,  therefore, 
be  regarded  as  essential  elements  of  miliary  tubercule. 

All  tubercle  manifests  a  strong  tendency  to  undergo  caseous  degeneration, 
but  in  acute  miliary  tuberculosis  the  patient  usually  succumbs  to  the  dis- 
ease before  any  such  change  occurs.  In  the  present  unsettled  state  of  the 
pathology  of  tubercle  it  is  impossible  to  formulate  any  accepted  theory  as 
to  the  nature  of  the  pathological  processes  or  the  origin  of  the  histological 
elements  in  acute  miliary  tuberculosis.  The  evident  etiological  relation  of 
caseous  foci,  plastic  inflammations  of  serous  membranes,  and  primary 
tubercle  to  acute  tuberculosis,  and  the  fact  that  miliary  tubercles  are  dis- 
tributed by  the  lymphatics,  lead  me  to  the  belief  that  the  pathological 
processes  are  essentially  inflammatory  in  their  nature,  and  result  in  a  neo- 
plastic growth. 

Etiology. — The  predisposing  causes  are  very  prominent  in  the  etiology 
of  acute  miliary  tuberculosis,  and  it  is  very  doubtful  if  it  ever  occurs 
when  they  are  not  present.  Most  prominent  of  these  is  the  undefined  con- 
dition so  universally  recognized  as  the  strumous  diathesis.  However  much 
authorities  may  differ  as  to  the  ultimate  cause  of  tubercle,  the  special 
dangers  to  which  persons  of  this  diathesis  are  exposed  are  uniformly  ad- 
mitted. Caseous  foci  as  found  in  chronic  phthisis,  inspissated  abscess, 
caries  of  bone,  or  caseous  glands  are  to  be  placed  in  the  class  of  predispos- 
ing or  exciting  causes,  according  as  we  accept  or  deny  the  specific  nature 
of  the  ultimate  cause  of  tubercle. 

If  the  term  tubercle  is  limited  to  that  tissue  in  whose  development  the 
tubercular  bacillus,  or  any  specific  element  is  the  primary  etiological  factor, 
then  caseous  matter  becomes  simply  a  predisposing  cause  as  furnishing  a 
favorable  soil  for  the  development  of,  and  a  means  of  transportation  for 
the  bacillus.     If,  however,  tubercle  is  defined  upon  an  histological  basis 


708 


ACUTE    GENEKAL   DISEASES. 


and  not  from  its  etiology,  I  think  I  am  justified  in  saying  that  while  the 
tubercular  bacillus  may  be,  and  undoubtedly  is,  one  cause  of  tubercle  and 
possibly  of  acute  miliary  tuberculosis,  in  whose  development  and  distribu- 
tion throughout  the  body  caseous  matter  plays  an  important  part,  on  the 
other  hand  caseous  deposits  per  se  and  other  irritants  may  also  become  ex- 
citing causes  of  the  peculiar  tuberculous  inflammation  and  neoplastic 
growth. 

The  process  of  infection  appears  to  be  one  of  metastasis  in  which  the 
irritating  elements  are  distributed  from  infectious  foci,  especially  of  primary 
tubercle,  caseous  matter,  or  the  products  of  inflammation  in  serous  mem- 
branes. The  channels  through  which  this  distribution  occurs  are  probably 
the  lymphatics.  The  location  of  miliary  tubercle  in  the  perivascular 
lyrnph  spaces,  however,  does  not  preclude  the  possibility  that  the  blood 
may  also  transmit  the  infection. i 

Symptoms. — When  acute  miliary  tuberculosis  complicates  the  last  stage 
of  phthisis  its  symptoms  are  so  modified  that  it  is  not  easily  recognized, 
more  especially  as  the  tubercular  deposit  does  not  materially  afl'ect  the 
physical  signs.  In  such  a  case  a  sudden  and  decided  increase  in  the  fever, 
and  marked  aggravation  of  the  dyspnoea  will  be  the  most  characteristic 
symptoms,  and,  occurring  in  connection  with  unchanged  iDhysical  signs, 
may  lead  to  a  corresponding  diagnosis.  When  the  disease  attacks  an  indi- 
vidual in  apparent  health  the  symptoms  are  well  marked. 

It  is  generally  ushered  in  by  repeated  chills,  a  rather  rapid  rise  in  tem- 


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Fig.  158. 
Temperature  Eecord  in  a  case  of  Acute  Miliary  Tuberculosis. 

perature  and  pulse  rate,  and  the  other  symptoms  of  an  acute  general  dis- 
ease, accompanied  by  rapid  respiration  and  a  short,  dry  cough.     The  tem- 

1  Ponflck  found  tubercle  in  the  wall  of  the  thoracic  duct  in  a  case  of  general  miliary  tuberculosis,  and 
this  is  adduced  as  a  proof  that  the  blood  becomes  an  infective  fluid. 


ACUTE   MILIARY   TUBERCULOSIS.  709 

perature  ranges  from  103°  to  106°  or  107°  F.,  with  irregular,  but  marked 
remissions,  and  is  more  frequently  high  in  the  morning  and  low  in  the  even- 
ing than  in  any  other  acute  affection.  The  pulse  is  soft,  small,  and  com- 
pressible, varying  from  120  to  150  per  minute,  but  in  no  constant  or  definite 
ratio  to  the  temperature.  The  respirations  are  from  50  to  60  per  minute, 
and  later  the  dyspnosa  becomes  intense.  The  persistent  sharp,  hard  cough 
is  rarely  accompanied  by  expectoration  ;  when  present,  the  expectoration 
consists  of  viscid  mucus,  occasionally  blood-streaked.  The  skin  is  pale  and 
cyanotic;  there  is  anorexia,  rapid  emaciation,  and  diarrhoea,  as  a  rule;  the 
lips  and  tongue  become  dry  and  covered  with  brown  crusts  ;  the  patient  is 
dull  and  semi-comatose,  and  at  night  delirious,  presenting  all  the  symjDtoms 
of  the  typhoid  state.     The  spleen  is  generally  slightly  enlarged. 

The  j)atient  may  survive  for  five  or  six  weeks,  but  more  frequently  suc- 
cumbs within  two  or  three.  As  death  approaches  the  pulse  rapidly  grows 
weaker  and  more  frequent,  the  cough  ceases,  the  temperature  falls,  or,  if 
already  low,  suddenly  rises,  the  cyanosis  deepens  and  death  occurs  from 
pulmonary  oedema  and  asphyxia. 

Physical  Signs. — In  most  cases  the  physical  signs  are  entirely  negative. 
Percussion  may  show  points  of  slight  dulness,  surrounded  by  ex*"ra  reso- 
nant areas,  and  auscultation  occasionally  reveals  moderate  bronchial  catarrh, 
with  fine  moist  rales,  but  they  are  not  characteristic.  A  soft  friction  sound 
may  be  produced  by  a  roughened  nodular  pleura. 

Differential  Diagnosis. — The  symptoms  of  acute  miliary  tuberculosis  are 
in  many  cases  so  exactly  those  of  typhoid  fever  that  a  differential  diagnosis 
is  impossible. 

The  fever  curve  of  typlioid  fever  is  regular  and  typical  ;  that  of  acute 
miliary  tuberculosis  is  irregular  and  not  characteristic.  Typhoid  presents 
a  distinctive  rasli  not  found  in  tuberculosis  ;  and  the  pea-soup  discharges 
with  gurgling  and  tenderness  in  the  right  iliac  fossa  of  typhoid  are  seldom 
present  in  acute  tuberculosis.  In  typhoid  the  bronchitis  follows  the  dis- 
tinct initiatory  symptoms,  and  its  physical  signs  are  more  prominent  than 
the  cough  and  dyspnoea,  while  in  acute  tuberculosis  the  hard,  persistent 
cough  and  intense  dyspnoea  which  precede  or  attend  the  development  of 
the  fever  are  accompanied  by  few,  if  any,  physical  signs  of  bronchitis. 
Large  doses  of  quinine  reduce  the  temperature  of  tyiDhoid  from  2°  to  3°  F., 
but  have  little  effect  upon  that  of  acute  miliary  tuberculosis,  and,  finally, 
recovery  is  the  rule  in  typhoid  and  would  tend  to  invalidate  a  diagnosis  of 
acute  miliary  tuberculosis.  Pneumonia  and  acute  diffuse  iroticliitis  in 
their  early  stages  may  simulate  acute  miliary  tuberculosis,  but  the  rapidly 
developing  physical  signs  and  the  absence  of  the  constitutional  symptoms 
of  an  acute  wasting  disease  render  an  early  diagnosis  possible. 

Prognosis. — The  prognosis  must  be  almost  absolutely  unfavorable.  The 
duration  of  the  disease  is  from  a  few  days  to  six  or  seven  weeks,  with  an 
average  of  three  weeks.  The  more  general  the  infection,  the  more  violent 
the  fever  and  the  nervous  symptoms,  the  sooner  is  a  fatal  termination  to 
be  expected.  When  complicating  phthisis,  its  course  is  very  rapid.  As- 
phyxia from  pulmonary  oedema,  asthenia,  cerebral  anaemia  and  collapse  are 


710  ACUTE   GENERAL  DISEASES. 

the  principal  causes  of  death,  but  in  about  one-third  of  the  cases  it  occurs 
from  implication  of  the  meninges. 

Treatment. — The  only  indications  for  treatment  which  afford  any  hope  of 
attaining  favorable  results  are  in  the  way  of  prophylaxis,  and  are  largely 
included  in  the  treatment  of  the  predisposing  diathesis.  In  treating  scrofu- 
lous patients,  acute  miliary  tuberculosis  should  be  remembered  as  among 
the  impending  dangers.  Caseous  matter,  wherever  situated,  should  be  re- 
moved when  the  attending  danger  is  not  great,  and  absorption  of  those 
masses  which  cannot  be  reached,  and  of  the  products  of  inflammation  in 
serous  membranes  should  be  assisted  by  all  the  usual  means.  More  defi- 
nite knowledge  of  the  etiological  relation  of  the  tubercle  bacillus  may  afford 
other  indications  for  prophylaxis. 

When  the  tubercular  deposit  has  once  taken  place,  treatment  is  confined 
to  the  reduction  of  temperature  and  supporting  the  patient.  For  the  first, 
quinine  is  of  little  avail.  It  is  sometimes  used  as  long  as  recurring  chills 
are  present,  but  is  of  doubtful  value  as  the  chills  are  probably  due  to  new 
deposits  of  tubercles.  Cold  will  be  found  more  useful  in  reducing  tempera- 
ture, and  may  be  used  in  baths,  packs,  or  by  sj)onging.  Stimulants  and 
highly  nutritious  food  fulfil  the  second  indication,  and  must  be  used  as  in 
other  wasting  diseases.  Morphia  must  be  used  for  the  relief  of  the  cough, 
and  for  the  dyspnoea  quebracho  may  afford  temporary  relief. 


TYPHUS    FEVEE. 

Typhus  fever  is  a  contagious  disease,  which  usually  prevails  epidem- 
ically. Although  it  has  many  phenomena  in  common  with  miasmatic-con- 
tagious fevers,  and  was  at  one  time  classed  with  typhoid  fever,  to-day  it  is 
regarded  as  a  distinct  type  of  fever,  dependent  upon  a  specific  poison  with 
certain  pathological  and  etiological  phenomena,  which  distinguish  it  from 
all  other  forms  of  disease.  It  has  received  a  great  variety  of  names,  such 
as  sJiip  fever,  hospital  fever,  jail  fever,  camp  fever,  petechial  fever,  putrid 
fever,  Irish  ague,  hrain  fever,  spotted  fever ,  continued  fever ,  typhus  fever, 
petechial  and  exanthematous  typfius. ' 

Morbid  Anatomy. — Those  pathological  lesions  which  are  common  to  ty- 
phus and  typhoid  fever  will  be  first  considered,  and  as  the  line  of  distinc- 
tion between  them  is  drawn  it  will  be  noticed  that,  in  many  respects,  the 
difference  is  one  of  degree,  rather  than  of  kind. 

The  changes  in  the  blood  are  as  follows  :  it  is  darker  in  color  than  nor- 
mal, and  when  drawn  from  the  body  during  life  coagulates  imperfectly  or 
not  at  all  ;  if  a  clot  is  formed  it  is  of  the  consistency  of  putty.  The  fibrin- 
factors  are  diminished,  or  the  blood  loses  its  coagulating  power  to  a  greater 
or  less  extent.  At  first  the  red  globules  are  increased  in  number,  but  as 
the  disease  progresses  they  diminish  ;  the  salts  of  the  blood  are  also  changed, 
and  urea  and  ammonia  are  present  in  excess ;  by  some  the  latter  is  sup- 

1  The  Germans  describe  an  abdominal  and  cerebral  typhus.  Their  abdominal  typhus  corresponds  to 
our  typhoid  fever  and  their  cerebral  typhus  is  our  typhus  fever. 


TYPHUS   FEVEK.  711 

posed  to  be  produced  by  the  decomposition  of  the  former.  The  blood  of  a 
typhus  fever  patient,  when  drawn  from  the  body,  rapidly  undergoes  am- 
moniacal  decomposition.  When  the  blood  is  examined  microscopical!}^, 
many  of  the  red  globules  will  be  seen  to  have  lost  their  normal  outline, 
and  their  edges  to  have  become  serrated  and  irregular.  In  some  instances 
they  will  be  found  to  have  undergone  degeneration  ;  their  coloring  matter 
will  then  ]oass  through  the  walls  of  the  blood-vessels  and  stain  more  or  less 
deeply  the  tissues  and  effusions  which  may  have  taken  place  in  the  serous 
cavities.  These  blood-changes  are  very  similar  to  those  which  take  place 
in  the  miasmatic-contagious  fevers — they  differ  in  degree  only. 

Parenchymatous  Degenerations. — There  is  the  same  tendency  to  par- 
enchymatous degenerations  of  the  different  organs  and  tissues  of  the  body 
in  typhus  as  in  typhoid.  Usually  the  body  is  not  very  much  emaciated  ; 
it  undergoes  decomposition  rapidly  after  death.  In  severe  cases  decom- 
position apparently  commences  before  death.  The  muscles  are  usually  of 
a  brownish  color,  dry,  presenting  an  infiltration  of  fine  granules  in  the 
primitive  fibres  ;  sometimes  hemorrhages  take  place  into  them.  The 
liver  and  spleen  undergo  degenerative  changes  similar  to  those  described 
as  occurring  in  typhoid,  but  they  are  not  so  extensive  nor  are  they  so  con- 
stant. One  may  make  very  many  autopsies  on  persons  dying  of  typhus 
fever,  without  finding  any  softening,  or  only  a  very  moderate  softening,  and 
enlargement  of  the  spleen,  while  blood  extravasations  are  not  uncommon. 
In  severe  cases  the  cortical  portion  of  the  kidneys  is  swollen,  opaque  and 
more  or  less  fatty,  according  to  the  duration  and  severity  of  the  disease. 
The  primary  enlargement  of  the  kidneys  is  mamly  due  to  a  cloudy  swelling 
of  the  epithelium  of  the  renal  tubes. 

This  tendency  to  cloudy  swelling  and  granular  fatty  degeneration,  the 
so-called  '^  vitreous  degeneration  of  Zenker,"  which  occurs  in  the  vol- 
untary muscles  and  the  kidneys,  also  occurs  in  the  muscular  tissue  of 
the  heart.  If  the  fever  is  protracted,  the  cardiac  walls  become  flaccid,  of 
a  brownish  color,  and  parenchymatous  changes  are  found  similar  to  those 
which  occur  in  typhoid  fever,  though  less  marked.  There  is  often  a  con- 
siderable amount  of  serum  in  the  pericardium.  Pultaceous  clots  are  found 
in  the  heart  cavities,  and  thrombi  are  found  firmly  adherent  to  the  walls 
of  the  larger  veins.  There  is  the  same  tendency  to  ulceration  of  the 
mucous  membrane  of  the  mouth  and  larynx  as  in  typhoid  fever.  In  ty- 
phus fever  the  ulcers  are  deeper,  involving  more  extensively  the  submucous 
tissue.  Splenization  of  the  lungs  also  occurs,  in  typhus  as  in  typhoid 
fever.  Hypostatic  congestion  of  the  lungs  and  pulmonary  oedema  are  as 
common  as  in  typhoid ;  some  claim  that  they  are  found  much  oftener. 
Thus  far  I  have  noticed  only  these  lesions  which  occur  both  in  typhus 
and  in  typhoid  fever.  I  now  come  to  those  which  are  found  only  in 
typhus. 

Brain. — Although  there  is  nothing  in  the  appearance  of  the  brain  which 
is  characteristic  of  this  fever,  yet  it  is  very  unlike  that  met  with  in  ty- 
phoid fever.  In  the  latter  disease  it  usually  presents  an  anaemic  appear- 
ance.    In  all  cases  of  typhus  the  cerebral  vessels  will  be  found  more  or  less 


712  ACUTE    GE]!fEEAL   DISEASES. 

congested.  In  some  epidemics  all  the  sinuses  and  blood-vessels  of  the  brain 
will  be  found  engorged  with  dark  blood,  so  that  when  the  calvarium  is  re- 
moved the  vessels  will  stand  out  upon  its  surface.  In  other  epidemics,  in- 
stead of  iinding  intense  congestion,  there  will  be  more  or  less  extensive  se- 
rous effusion  into  the  meshes  of  the  pia  mater  :  the  quantity  of  the  effusion 
varies  from  one  to  eight  or  ten  ounces,  and  it  is  most  abundant  upon  the  con- 
vexity, although  it  takes  place  to  a  limited  extent  into  the  ventricles.  When- 
ever there  is  a  large  amount  of  fluid  effusion  there  will  be  little  cereDral 
congestion.  The  fluid  effusion  is  usually  clear  ;  if  it  is  turbid  one  may 
be  certain  that  the  fever  is  complicated  by  meningitis.  The  arachnoid 
loses  its  natural  glistening  appearance,  and  in  many  instances  one  will  find 
the  membrane  dotted  over  with  yellow  or  yellowish-white  spots.  The 
brain  undergoes  little  or  no  change  unless  the  fluid  effusion  is  abundant, 
when  by  its  pressure  the  sulci  are  deepened  and  the  convolutions  are 
sharpened. 

Abdominal  Lesions. — In  typhus  and  typhoid  fever,  the  lesions  found  in 
the  abdominal  cavity  widely  differ.  The  real  pathological  distinction  is 
in  the  presence  or  absence  of  intestinal  changes.  These  are  present  in  ty- 
phoid and  absent  in  typhus.  In  tyijhus  fever  there  are  no  changes  which 
show  a  tendency  to  ulceration  of  the  intestinal  glands,  except  those  which 
are  produced  by  congestion,  such  as  are  frequently  seen  in  scarlet  fever  and 
measles,  where  the  Peyerian  patches  present  the  shaven-beard  appearance  ; 
while  in  typhoid  fever,  either  ulceration  of  the  intestinal  glands  will  be  pres- 
ent, or  the  glands  will  present  the  apjDearance  which  just  precedes  ulceration. 
At  the  post-mortem  examination,  if  ulceration  of  the  agrainated  and  sol- 
itary glands  is  found,  one  may  be  certain  the  patient  died  of  typhoid  fever. 
The  presence  or  absence  of  intestinal  changes  settles  the  question  as  to 
whether  the  fever  is  typhus  or  typhoid. ' 

Complications. — Although  the  complications  which  occur  in  the  course 
of  typhus  fever  are  in  no  way  peculiar  to  it,  yet  they  are  of  such  frequent 
occurrence,  and  are  developed  during  its  active  progress,  and  modify  its 
phenomena  to  such  a  degree,  that  it  is  necessary  that  they  should  be  taken 
into  account  in  the  study  of  its  pathological  lesions.  These  complications 
will  vary  according  to  the  peculiar  type  of  the  epidemic  which  is  prevail- 
ing. In  one  epidemic  the  complications  will  be  pulmonary,  in  an- 
other they  will  be  almost  exclusively  cerebral  and  spinal,  in  another  nearly 
all  will  be  glandular  in  character.  The  pulmonary  complications  are  bron- 
chitis, pneumonia,  pleurisy,  pulmonary  congestion,  and  oedema.  In  most 
cases  these  pulmonary  complications  are  developed  during  the  primary 
fever,  before  convalescence  commences.  Their  advent  is  always  insidious. 
An  extensive  capillary  bronchitis  may  develop  with  very  few  of  the  rational 
symptoms  of  bronchitis  until  within  a  short  time  previous  to  the  death  of 
the  patient ;  in  fact,  the  bronchitis  might  pass  unrecognized  but  for  the 
presence  of  its  physical  signs.  All  the  rational  symptoms  of  pneumonia 
may  also  be  absent  and  still  a  physical  examination  of  the  chest  may  reveal 

1  Lebert  states  that  rarely,  in  epidemics,  small  ulcers  of  Peyer's  patches  and  of  solitary  glands  and 
swelling  of  the  mesenteric  glands  have  been  seen.     (Ziemssen's  Encyc.) 


TYPHUS   FEVEE.  713 

a  whole  lung  in  a  state  of  pneumonic  consolidation.  The  pneumonia  which 
complicates  typhus  is  usually  hjrpostatic.  It  sometimes  leads  to  pulmonary 
gangrene.  At  most  of  the  autopsies  there  will  be  found  pulmonary  con- 
gestion and  oedema.  In  many  cases  when  these  are  associated  with  capil- 
lary bronchitis  or  pneumonia  they  are  the  immediate  cause  of  death.  Lar- 
yngitis is  often  associated  with  more  extensive  bronchitis  which  occurs 
during  the  active  part  of  the  fever. 

The  only  cerebro-spinal  complication  which  is  met  with  in  typhus  fever 
is  meningeal  inflammation.  As  has  been  stated,  in  a  large  majority  of 
autopsies  of  typhus  fever  serum  is  found  in  the  meshes  of  the  pia  mater, 
but  that  is  not  a  certain  sign  that  meningeal  inflammation  has  existed  prior 
to  death.  In  addition  to  the  subarachnoid  effusion,  there  must  be  an  ex- 
udation of  plastic  material  into  the  meshes  of  the  pia  mater,  causing  it 
to  become  thicker  than  normal.  When  such  appearances  are  found  it  shows 
that  the  case  has  been  complicated  by  meningitis. 

Glandular  Enlargements. — The  glandular  enlargements  and  inflam- 
mations which  occur  in  the  course  of  typhus  fever  are  peculiar  in  their 
character,  and  are  rarely  met  with  in  typhoid,  and  then  are  not  extensive  ; 
but  in  typhus  fever  the  superficial  glands — especially  those  about  the  neck, 
the  parotid  and  subling-ual— often  become  so  much  enlarged  and  inflamed 
as  to  interfere  with  deglutition,  and  not  infrequently  these  glandular  en- 
largements are  apparently  the  immediate  cause  of  death.'  The  inguinal 
glands  sometimes  become  so  enlarged  as  to  interfere  with  the  return  circu- 
lation, and,  as  the  consequence  of  this  interference,  swelling  of  the  lower 
extremities  may  be  developed.  The  bronchial  glands  are  nearly  always  en- 
larged and  softened.  There  is  a  swelling  of  the  lower  extremities  which 
depends  upon  a  different  cause.  It  may  occur  at  the  beginning  of  con- 
valescence;  then  the  limbs  will  present  very  nearly  the  same  appearance 
as  that  noticeable  in  the  condition  called  phlegmasia  dolens.  Under  such 
circumstances  phlebitis  might  be  suspected. 

It  has  been  stated  that  the  voluntary  muscles  undergo  a  peculiar  waxy  or 
vitreous  degeneration,  and  that  the  same  kind  of  degeneration  occurs  in 
the  muscular  tissue  of  the  heart.  When  this  does  occur  the  walls  of  the 
heart  become  very  flabby,  and  when  this  change  has  reached  a  certain  point 
there  is  developed  a  tendency  to  the  formation  of  clots  in  the  heart  cavities, 
and  a  slowing  of  the  general  circulation.  The  result  of  such  retarding  or 
obstruction  of  the  return  circulation  is  the  formation  of  thrombi  in  the 
superficial  veins,  which  interfere  with  the  venous  circulation,  and  a  swell- 
ing of  the  lower  extremities  follows  ;  this  closely  resembles  that  which  is 
seen  in  phlegmasia  dolens.  With  this  swelling  of  the  lower  extremities, 
suppuration  and  cellular  inflammation  may  occur,  which  often  result  in 
the  formation  of  quite  extensive  abscesses. '^ 

Diseases   of  the  organs  of  special  sense,  which  so  frequently  compli- 

'  Lebert  regards  enlargement  and  suppuration  of  the  parotid  as  a  very  dangerous  complication. 

2  It  is  an  established  fact  that  whenever  the  return  circulation  is  slowed  from  any  cause  in  any  disease 
where  there  is  great  feebleness  of  heart  power,  thrombi  are  liable  to  form  in  the  veins  of  the  lower 
extremities.  This  is  often  well  illustrated  in  the  later  stages  of  phthisis,  when  swelling  of  one  or  both 
lower  extremities  occurs  as  the  result  of  the  formation  of  venous  thrombi  in  the  superficial  veins. 


714  ACUTE    GENERAL   DISEASES. 

cate  typhoid,  rarely  occur  in  typhus  fever,  and  there  are  no  serious  or 
constant  complications  of  the  digestive  organs  ;  the  gastric  mucous  mem- 
brane is  sometimes  softened,  reddened  and  mammilated. 

Etiology, — At  the  present  day  this  fever  is  regarded  as  depending  upon  a 
specific  i)oison,  of  whose  exact  nature  we  are  ignorant.  AU  observers  agree 
that  in  the  majority,  if  not  in  all  instances,  it  is  the  product  of  contagion, 
and  that  the  contagion  only  emanates  from  the  bodies  of  those  who  are 
affected  with  the  fever.  Careful  clinical  observation  has  established  the 
fact  beyond  a  doubt  that  there  exists  a  specific  typhus  poison  which  can  be 
communicated  from  the  sick  to  the  healthy,  which  some  declare  is  never 
of  spontaneous  origin,  while  others  maintain  that  the  poison  may  be 
generated '^^e  novo,"  Some  have  strenuously  maintained  that  it  can  be 
developed  by  overcrowding  and  filth  ;  others,  who  have  seen  the  largest 
number  of  typhus  fever  cases  during  the  past  ten  years,  maintain  that  it  is 
at  least  very  doubtful  whether  typhus  fever  is  ever  of  spontaneous  origin. 
It  is  possible  to  develop  a  fever  from  overcrowding,  imperfect  ventilation, 
filth,  and  a  combination  of  causes  belonging  to  this  category,  but  such  a 
fever  is  not  typhus. 

The  results  of  my  investigation  of  the  origin  of  the  epidemic  of  typhus 
fever  which  prevailed  in  New  York,  from  July,  1861  to  1864,  have  led  me 
to  the  belief  that  typhus  poison  is  of  endemic  origin — in  other  words,  that 
there  are  certain  endemic  centres  ;  that  Ireland,  Italy,  and  Russia  are  the 
great  centres,  and  that,  whenever  it  occurs  in  other  localities,  it  has  been 
conveyed  from  these  endemic  centres  to  those  localities. '  The  histories  of 
those  cases  which  were  developed  within  the  limits  of  the  hospital,  showed 
that  a  residence  in  an  atmosphere  necessarily  more  or  less  tainted  with 
typhus  poison,  is  not  sufficient  to  develop  the  disease,  but  that  it  is  neces- 
sary for  the  subject  of  the  contagion  to  have  been  brought  in  contact  with 
an  infected  person,  or  within  the  atmosphere  immediately  impregnated 
with  his  exhalations.  The  fact  that  no  employee  in  the  hospital  who  was 
only  brought  in  contact  with  the  clothing  of  fever  patients  contracted  the 
disease,  as  well  as  the  absence  of  any  evidence  that  the  disease  was  propa- 
gated by  such  clothing,  goes  far  to  show  that  typhus  is  not  readily  propa- 

1  In  the  month  of  July,  1861,  fourteen  cases  of  typhus  fever  were  admitted  in  one  day  to  the  fever  wards 
of  Bellevue  Hospital,  of  which  wards  I  had  the  charge.  Previous  to  this  time,  for  several  years  (I  think 
for  more  than  ten  years),  there  had  been  no  case  of  typhus  fever  in  the  wards  of  the  hospital.  limme- 
mediately  commenced  investigations  in  order  to  ascertain  the  oris^iii  of  the  fever  in  these  cases.  I  found 
that  it  had  its  origin  in  the  upper  story  of  a  rear  tenement-house  in  Mulberry  Street,  in  the  most  filthy  por- 
tion of  the  city.  The  first  case  was  that  of  a  little  girl,  who  had  been  brought  into  the  house,  ten  days  be- 
fore she  sickened,  from  a  ship  which  had  come  from  Ireland,  and  which  had  cases  of  t}'phus  fever  on 
board.  Two  weeks  after  her  illness  commenced,  her  aunt,  the  only  other  occupant  of  the  apartments  (con- 
sisting of  a  room  and  dark  bed-room),  sickened  of  fever  and  died.  In  gradual  succession,  nearly  every 
family  residing  in  the  building  took  the  fever.  Becoming  frightened,  some  of  these  families  moved  into 
other  streets,  formed  the  nucleus  for  the  development  of  the  disease  in  the  different  localities  to  which 
they  removed,  and  it  soon  became  a  wide-spread  epidemic.  There  were  two  hundred  tj'phus  fever  patients 
at  one  time  in  the  hospital.  These  families  were  as  well  nourished  and  lived  in  as  well  ventilated  apart- 
ments as  thousands  of  their  class  in  other  parts  of  the  city.  The  only  difference  was  that  typhus  poison 
was  brought  to  them  in  the  person  of  the  little  girl,  and,  on  account  of  their  badly  ventilated  apartments 
and  their  utter  disregard  of  all  hygienic  laws,  they  furnished  a  fit  soil  for  the  reproduction  and  spread  of 
that  typhus  poison,  the  constant  and  unrestrained  intercourse  between  the  healthy  and  the  sick  being  the 
means  by  which  the  fever  was  spread.  I  found  unmistakable  evidence  that  persons  living  in  healthy  locali- 
ties, simply  by  visiting  friends  sick  with  the  fever,  contracted  the  disease. 


TYPHUS   FEVER.  715 

gated  by  fomites  alone,'  although  most  authorities  claim  that  it  can  be 
thus  propagated  ;  that  it  is  thus  that  ships,  barracks  and  jails  become  hot- 
beds of  it ;  that  the  poison  may  be  latent  and  held  in  garments,  especially 
those  that  are  dark  and  woolen.  The  certainty  with  which  every  unpro- 
tected person  who  was  brought  in  personal  contact  with  fever  patients  con- 
tracted the  disease,  proves  the  contagious  power  of  the  poison. 

The  distance  that  typhus  poison  can  be  transmitted  through  the  atmos- 
phere (from  the  manner  in  which  the  disease  was  contracted  by  some  of  the 
house  physicians),  would  seem  to  be  limited.  It  has  been  proved  by  actual 
expei'iment  that  the  contagious  distance  of  small-pox,  in  the  open  air,  does 
not  exceed  two  and  one-half  feet,  and  it  would  seem  that  the  contagious 
distance  of  typhus  fever  is  even  less.^  Typhus  poison  is  undoubtedly 
present  in  the  body  exhalations  and  the  expired  air  of  typhus  fever  patients; 
but  it  requires  a  concentration  of  the  poison  to  render  it  infectious.  Slight 
exposure  is  not  sufficient ;  it  requires  a  concentrated  j)oison  and  a  prolonged 
exposure.  The  more  numerous  the  typhus  fever  patients  are,  the  more  power- 
ful does  the  contagion  become  ;  yet  a  single  exposure  even  to  such  an  atmos- 
phere is  rarely  sufficient  to  develop  the  disease  in  an  individual  who  is  in 
good  health  at  the  time  of  the  exposure. 

The  length  of  the  period  of  incubation  varies.  It  usually  requires  about 
two  weeks  of  exposure  such  as  comes  to  one  who  is  around  those  sick  with 
the  fever.  Eepeatedly  have  I  noticed  this  fact  in  my  own  case.  I  have 
never  had  typhus  fever,  and  have  never  taken  special  care  to  avoid  infec- 
tion. My  immunity  is  probably  due  to  some  special  constitutional  idiosyn- 
crasy. I  have  noticed  that  whenever  I  enter  upon  a  typhus  fever  service  I 
do  not  experience  any  effects  from  the  exposure  to  typhus  poison  until  after 
about  two  weeks  ^  have  elapsed,  then  I  begin  to  suffer  from  a  peculiar  form 
of  headache  which  continues  for  about  two  weeks  ;  the  period  before  the 
commencement  of  the  headache  corresponds  to  the  period  of  incubation, 
and  the  period  of  headache  to  the  average  duration  of  the  disease. 

The  established  belief  is  that  typhus  fever  attacks  an  individual  but 
once,  and  that  those  who  have  had  typhoid  fever  are  to  a  certain  degree  pro- 
tected from  typhus.  Of  all  the  typhus  fever  patients  treated  in  Bellevue 
Hospital,  only  three  gave  histories  of  having  previously  had  the  disease. 
From  these  facts  one  may  reach  the  following  conclusions  : — 

First. — That  typhus  fever  is  due  to  a  specific  poison. 

» In  Quains  Dictionary  it  is  stated  that  It  is  "  not  carried  by  clothing  or  excreta,  and  free  dilution  with 
fresh  air  destroys  its  virulence." 

2  The  question  now  arises  :— can  this  poison  be  conveyed  in  the  clothing  ?  During  the  epidemic  to  which 
I  have  referred,  when  typhus  fever  patients  were  brought  into  the  hospital,  their  clothing  was  removed  in 
the  reception-room  and  afterward  washed  and  packed  away  in  a  lower  room  of  the  building.  Upon  a  most 
thorough  investigation  made  at  that  time,  I  found  that  not  a  single  person  contracted  the  disease  whose 
duty  it  was  to  wash  or  pack  away  the  clothing;  but  every  one  whose  duty  it  was  to  carry  the  fever  patients 
from  the  reception-room  to  the  hospital  ward  took  the  fever.  Every  physician  and  nurse  who  had  the  care 
of  typhus  fever  patients 'contracted  the  disease  ;  those  who  were  on  the  surgical  service  escaped.  Every 
clergyman  who  came  to  administer  spiritual  consolation  to  the  patients  in  the  fever  ward  fell  a  victim  to 
the  disease.  I  have  brought  forward  these  facts  to  show  that  duiing  this  epidemic  there  was  no  evidence 
that  the  disease  was  either  of  spontaneous  origin,  or  that  it  was  transmitted  from  the  sick  to  the  healthy, 
except  by  direct  personal  contagion. 

8  Lebert  puts  five  to  seven  days,  and  Murchison  says,  "  no  longer  than  twelve  days  '"  for  the  period  of 
incubation  ;  one  week  is  the  average  ;  some  patients  have  the  fever  one-half  to  two  hours  after  first  and 
second  exposure  (St.  Thorn.  IIos.  Eep.,  vol.  ii.). 


716  ACUTE    GENEEAL   DISEASES. 

Second. — That  this  poison  is  communicated  from  the  sick  to  the  healthy 
mainly  by  personal  contagion — that  is,  the  recipient  of  the  poison  must  be 
brought  in  contact  with  the  personal  exhalations  of  the  infected  person. 

Third. — That  where  there  is  free  ventilation,  personal  contagion  is  con- 
fined to  narrow  limits. 

Fourth. — That  the  evidences  of  the  spontaneous  origin  of  typhus  are  not 
conclusive,  although  there  can  be  no  question  but  that  overcrowding  and 
bad  ventilation  favor  its  spread  and  increase  its  severity. 

Fifth. — Typhus  poison  passes  into  the  body  mainly  through  the  respired 
air.  Whether  it  can  be  taken  into  the  system  in  the  food  and  drink  is  still 
an  unsettled  question. 

Sixth. — Immunity  from  a  second  attack  is  enjoyed  after  the  first  in  a 
large  majority  of  cases.' 

Symptoms. — An  outline  of  the  phenomena  which  attend  the  development 
of  typhus  will  first  be  given  and  afterward  some  of  its  more  prominent 
symptoms  will  be  considered  in  detail. 

Its  advent  is  usually  sudden  ;  there  are  no  constant  premonitory  symp- 
toms. In  some  cases,  for  a  few  days,  there  may  be  a  feeling  of  indisposi- 
tion, perhaps  of  headache,  restlessness  at  night,  nausea,  loss  of  appetite, 
and  vertigo  ;  but  in  a  large  majority  of  cases  it  is  ushered  in  by  a  distinct 
chill.  This  differs  from  the  chill  of  pneumonia  or  that  of  malarial  fever, 
in  that  it  is  short,  sharp,  and  sudden.  It  may  amount  to  nothing  more 
than  a  chilly  sensation.  There  may  be  several  chilly  sensations  on  the  day 
of  attack  with  distinct  intervals  between  them.  Following  the  chill  there 
is  a  severe  and  steadily  increasing  headache  ;  it  is  frontal  and  increases  in 
intensity  from  hour  to  hour.  This  is  accompanied  by  a  more  or  less  severe 
pain  in  the  back  and  limbs,  especially  in  the  thighs.  The  headache  of 
typhus  is  more  constant  and  persistent  than  that  which  attends  the  devel- 
opment of  any  other  fever  ;  usually,  after  a  few  days  it  diminishes  in  inten- 
sity. Headache  is  associated  with  dulness  and  confusion  of  mind,  and  in 
the  case  of  children  with  vomiting.  A  sense  of  extreme  prostration  very 
soon  follows  the  ushering-in  chill. 

In  some  cases  the  patient  is  compelled,  within  twenty-four  hours  from 
the  commencement  of  his  sickness,  to  take  to  his  bed  from  muscular  weak, 
ness.  This  loss  of  muscular  power  will  sometimes  show  itself  by  the  un 
steady,  tottering  gait  of  the  patient,  and  is  more  marked  in  the  early  stage 
of  typhus  fever  than  it  is  in  any  other  disease.  At  one  time,  while  I  was 
making  my  visit  in  the  fever  ward,  my  house  physician,  who  was  sicken- 
ing from  typhus  fever,  staggered  and  fell  by  my  side  from  loss  of  muscular 
power.     He  died  on  the  eighth  day  of  the  disease. 

Within  the  first  twenty-four  hours  after  the  chill  the  temperature  may 
rise  as  high  as  105°  or  106°  F.,  although  at  the  same  time  the  patient 
may  complain  of  a  chilly  feeling,  and  will  draw  up  to  the  fire  or  cover 
himself  with  blankets.     It  is  a  peculiarity  of  this  fever  that,  during  the 

1  Lebert  say8  :  "  all  agree  that  the  disease  is  spread  by  a  typhus  germ.  Some  say  it  is  microsphere  , 
others  that  it  is  bacteria,  spiral  forms,  fungus,  eic,  etc.    It  must  either  be  organic  poison  or  organized 


TYPHUS   FEVEK.  717 

first  two  or  three  days  the  patient  experiences  a  sensation  of  coldness, 
while  the  thermometer  shows  the  temperature  to  range  at  105°  F.  or 
higher.  During  tlie  iirst  week  of  the  disease  the  temperature  remains  at 
104°  F.  or  105°  F.  There  will  be  morning  and  evening  variations,  most 
marked  at  noon  and  midnight ;  but  these  variations  follow  no  regular 
course,  as  in  typhoid  fever.  From  the  eighth  to  the  fourteenth  day  the 
temperature  is  liable 'to  sudden  depression.  Asa  rule,  the  temperature 
falls  between  the  eighth  and  fourteenth  days.  There  is,  without  doubt,  a 
day  of  crisis  in  this  disease.  Just  before  the  critical  fall  in  temperature 
there  may  be  an  abrupt  temporary  rise  of  3°  or  even  4°  F.  In  typical  cases, 
before  the  fourteenth  day  there  is  a  marked  decline,  and  often  a  sudden  fall 
in  temperature.  By  the  beginning  of  the  second  week  the  temperature 
ranges  at  its  highest.  If  there  is  a  sudden  rise  in  temperature  during  the 
second  week,  it  is  almost  certain  evidence  that  some  complication  exists. 

At  first  the  tongue  is  swollen  and  covered  with  a  white  coating.  It  pre- 
sents very  much  such  an  appearance  as  is  seen  in  many  nervous  affections. 
As  the  disease  progresses,  after  a  day  or  two  it  assumes  a  yellowish-brown 
color,  and  the  coating  becomes  thicker  ;  later  it  becomes  dry,  dark  and  fis- 
sured. Nausea  is  sometimes  present,  rarely  vomiting.  The  abdomen  is 
free  from  pain,  except  over  the  liver ;  the  bowels  are  constipated.  Some 
enlargement  of  the  spleen  can  usually  be  detected  quite  early. 

The  pulse  is  accelerated  from  the  very  beginning  of  the  fever,  ranging 
from  100  in  the  morning  to  110  or  130  in  the  evening  ;  the  acceleration  is 
greater  in  children  than  in  adults.  At  the  onset  of  the  fever  the  pulse  is 
full,  but  it  soon  becomes  soft  and  compressible,  and  finally  feeble.  It  is 
rarely  dicrotic.  It  is  only  in  the  severest  cases,  just  pi-ecediug  death,  that 
the  pulse  becomes  irregular  and  intermitting.  The  face  is  flushed,  the 
conjunctivas  injected,  the  expression  of  countenance  is  dull,  heavy,  and 
weary,  and  as  the  fever  progresses,  the  cheeks  assume  a  mahogany  color. 
The  sleep  is  disturbed,  and  when  the  patient  is  awake  his  mind  is  con- 
fused ;  in  very  severe  cases  delirium  is  very  early  present,  and  the  patient 
needs  careful  watching  at  night. 

Between  the  fifth  and  eighth,  usually  on  the  fifth,  day  of  the  disease,  an 
eruption  makes  its  appearance  upon  the  surface.  The  skin  is  extremely 
hot,  and  there  is  no  tendency  to  perspiration.  It  appears  first  upon  the 
sides  of  the  abdomen,  and  gradually  extends  over  the  whole  anterior  portion 
of  the  body,  except  the  face  and  palms  of  the  hands.  In  a  few  cases  it  first 
appears  on  the  back  of  the  hands  and  wrists.  It  is  more  marked  upon  the 
trunk  than  on  the  extremities.  At  first  the  eruption  consists  of  dirty  pink- 
colored  spots,  varying  in  size  from  a  mere  point  to  three  or  four  lines  in  di- 
ameter. These  spots  are  slightly  elevated  above  the  surface,  and  temporarily 
disappear  on  firm  pressure.  After  a  day  or  two  the  eruption  becomes  darker 
in  color,  and  assumes  a  purplish  hue.  It  is  no  longer  elevated  above  the  sur- 
face, does  not  entirely  disappear  on  firm  pressure,  and  the  spots  have  no  well- 
defined  margin.  Thiserujotion  is  made  up  of  irregular  spots,  varying  from 
a  point  to  two  or  three  lines  in  diameter,  either  isolated  or  grouped  to- 
gether in  patches,  presenting  a  very  irregular  outline  ;  in  children  it  often 


718  ACUTE    GENEEAL   DISEASES. 

resembles  the  eruption  of  measles.  When  the  eruption  is  abundant  it  im- 
parts to  the  skin  a  mottled  aspect,  which  has  giyen  rise  to  the  term  "  mul- 
berry rash  "  of  typhus.  Another  distinctive  peculiarity  is,  that  each  spot 
or  patch  remains  visible  from  its  first  appearance  until  convalescence  is 
established  or  death  occurs,  and  it  is  often  seen  upon  the  bodies  of  those 
who  have  died  of  typhus  fever. 

In  some  cases  of  typhus  there  are  only  a  few  spots  of  the  eruption,  while 
in  other  cases  they  are  very  abundant,  and  the  surface  of  the  body  -pve- 
sents  a  v/ell-marked  mottled  appearance.  In  a  certain  proportion  of 
cases,  after  the  eruption  which  I  have  just  described  has  been  visible  for  a 
few  days,  there  will  appear,  scattered  over  the  surface,  small  dark  spots, 
due  to  minute  subcutaneous  hemorrhagic  extravasation  ;  these  are  called 
petechias.  On  this  account  the  disease  \\2i&\iQQn(i2i\\Qdi petechial  typhus; 
but  these  petechige  are  by  no  means  distinctive  of  typhus,  for  they  are  also 
met  with  in  other  diseases.  The  majority  of  cases  of  typhus  which  one 
meets  will  have  no  eruption  except  the  "mulberry  rash."  When  the 
petechial  spots  are  present  they  indicate  a  severe  form  of  the  disease, 
and  more  extensive  blood-changes  than  usual.  This  mottling  or  marbling 
of  the  skin  begins  as  the  mulberry  rash  fades  ;  it  appears  once  for  all — 7iot 
in  crops — and  resembles  slightly  the  rose-rash  of  typhoid  fever.  It  is  the 
subcutaneous  eruption,  so-called. 

In  all  severe  cases,  at  the  close  of  the  first  week  the  headache,  which 
has  been  the  most  troublesome  symptom,  disappears,  and  delirium  comes 
on.  The  delirium  will  vary  in  character  and  severity  in  different  epidemics, 
being  much  more  violent  and  active  in  some  than  in  others.  Sometimes 
at  the  very  outset  of  the  disease  the  delirium  is  very  active,  the  patient 
shouts  and  talks  more  or  less  incoherently,  and  is  more  or  less  violent.  If 
not  restrained,  he  may  throw  himself  out  of  the  window.  This  period  of 
intense  nervous  excitement  may  last  two  or  three  days,  during  which  the 
countenance  becomes  livid,  the  conjunctivae  injected,  the  hands  tremulous, 
and  suddenly  the  patient  may  pass  into  a  state  of  apparent  coma.  It  is 
not  that  of  complete  coma,  for  the  patient  can  be  easily  aroused  ;  but  he 
lies  upon  his  back,  with  a  tendency  to  slip  down  in  bed,  picking  at  the  bed- 
clothes. The  mental  faculties,  the  special  senses,  are  all  blunted,  and  the 
patient  is  in  a  condition  of  stupor  for  three  or  four  days  preceding  the 
delirious  period,  and  sometimes,  when  the  delirium  is  not  active,  this 
stupor  lasts  till  the  end  of  the  disease.  It  is  not  a  state  of  unconscious- 
ness, although  one  of  apparent  coma,  for  the  mental  processes  are  going 
on  with  great  activity,  and  the  imagination  will  conjure  up  a  great  variety 
of  horrid  fancies,  and  the  visions  which  pass  before  the  patient  will  be  dis- 
tinctly remembered  after  recovery  has  taken  place. 

This  condition  has  been  called  "coma  vigil."  During  this  period  the 
experience  of  years  may  be  crowded  into  a  day  or  an  hour,  and  the  patient 
may  feel  that  he  has  lived  a  lifetime  while  in  this  state.  Those  who  have 
the  greatest  mental  power  and  possess  the  highest  culture  have  the  most 
distressing  fancies  during  this  somnolent  period.  If,  in  this  condition, 
there  is  a  tendency  toward  a  fatal  issue,  the  patient  will  pass  into  a  more 


TYPHUS   FEVER.  719 

complete  stupor  and  the  coma  will  become  more  and  more  profound  ;  the 
respiration  hecomes  less  and  less  frequent ;  the  pulse,  which  has  i-anged 
about  1:30  per  minute,  rises  to  140  or  150,  and  finally  becomes  imperceptible 
at  the  wrist ;  the  tongue,  rolled  into  a  round  mass,  becomes  brown  and  dry, 
so  that  the  patient  is  unable  to  protrude  it  from  the  mouth  ;  or,  if  he  pro- 
trude it,  he  does  not  withdraw  it  until  asked  to  close  his  mouth ;  sordes 
collect  upon  the  teeth  ;  the  conjunctivae  are  red,  and  the  eyes,  when  open, 
present  a  leaden  appearance.  The  face  has  a  dusky  pallor.  The  patient 
has  no  longer  power  to  move  his  body ;  he  lies  on  his  back  with  his  head 
thrown  back,  perhaps  is  only  able  to  make  slight  tremulous  motions  with 
his  hands.  There  may  now  be  some  intestinal  catarrh,  with  diarrhceal  dis- 
charges. The  urine  collects  in  the  bladder,  and,  if  not  removed  with  a 
catheter,  dribbles  away.  The  extremities  become  cold,  but  the  body  tem- 
perature remains  at  105°  F.,  or  it  may  rise  as  high  as  107°  or  108°  F.  In 
one  case  under  my  observation  it  rose  to  110°  F.  just  preceding  death,  while 
the  extremities  were  cold. 

If  the  case  is  tending  to  a  favorable  termination,  about  the  tenth  to  the 
fourteenth  day  of  the  fever  there  is  an  amelioration  of  all  the  symptoms. 
The  patient  falls  into  a  quiet  sleep,  from  which  he  awakes  conscious  and 
convalescing.  The  pulse  and  temperature  fall,  the  tongue  becomes  clean 
and  moist,  the  delirium  subsides,  and  there  is  a  desire  for  food.  After  two 
or  three  days  the  pulse  reaches  its  normal  standard  and  strength  gradually 
returns.  Critical  sweats,  diarrhoea,  and  large  flows  of  urine  are  not  infre- 
quent occurrences. 

This  is  an  outline  of  the  progress  of  the  disease  in  a  severe  case  of  typhus 
fever,  terminating  either  in  death  or  in  recovery.  In  a  mild  case  there  will 
be  no  delirium.  The  temijerature  may  not  rise  above  102°  F.  ;  the  tongue 
is  neither  brown  nor  dry.  There  is  no  great  acceleration  of  the  pulse, 
the  rate  never  being  over  120  per  minute,  and  that  only  for  a  very  short 
period.  During  the  entire  course  of  a  severe  or  mild  case,  there  is  no 
gastric  or  intestinal  disturbance,  no  diarrhoea,  no  distention  of  the  abdo- 
men, no  pain  in  the  right  iliac  fossa,  no  gurgling — in  a  word,  no  abdomi- 
nal symptoms.  In  mild  cases  the  erT-T^tion  is  never  very  abundant,  but 
it  appears  on  the  fifth  day,  and  remains  visible  until  convalescence  is 
established. 

Those  more  important  sym.ptoms  which  determine  the  character  of  the 
fever  will  be  considered  in  detail.  As  has  been  already  stated,  symptoms 
indicating  disturbance  of  the  nervous  system  are  among  the  earliest  and 
most  prominent.  Of  these,  headache  is  the  most  constant.  For  the  first 
week  or  ten  days  it  is  severe  and  persistent,  after  which  time  it  gradually 
abates  and  disappears  towards  the  close  of  the  second  week  ;  it  is  confined 
to  the  forehead  and  temples,  rarely  to  the  occiput. 

Delirium  comes  on  usually  about  the  eighth  day  ;  sometimes  it  is  pres- 
ent at  the  onset  of  the  disease.  At  whatever  period  it  may  be  developed, 
it  will  continue  until  the  termination  of  the  disease.  Delirium  is  preceded 
by  a  dull,  apathetic  state,  which  follows  the  abatement  of  the  headache. 
At  first  it  shows  itself  at  intervals  during  the  night,  or  lasts  all  night  to 


720  ACUTE    GENEKAL   DISEASES. 

disappear  during  the  day.  Its  character  varies  from  a  low,  muttering  form 
to  a  very  active  and  noisy  delirium.  Every  possible  variation  is  met  with 
during  an  epidemic  of  typhus  fever.'  Acute  delirium  is  more  liable  to  be 
present  with  the  intelligent  and  highly  cultured,  while  the  delirium  is  usu- 
ally low  and  muttering  in  character  in  the  case  of  the  aged  or  uncultured  : 
other  things  being  equal  the  intensity  of  the  fever  can  be  measured  by  the 
kind  and  amount  of  delirium. 

Stupor  or  somnoletice  in  some  degree  is  seldom  absent.  It  may  develop 
with  or  without  previous  delirium.  Usually,  as  the  case  progresses  toward 
a  fatal  termination  stupor  comes  on  ;  this  becomes  more  and  more  profound 
as  the  disease  advances.  The  patient  often  lies  for  hours  apparently  un- 
conscious, with  his  eyes  open  as  though  awake,  but  he  is  absolutely  indif- 
ferent to  all  that  is  going  on  around  him.  This  is  another  condition  to 
which  the  term  ^'  coma  vigil "  has  been  applied.  It  is  almost  invariably  fol- 
lowed by  a  fatal  termination.  Sometimes  coma  comes  on  suddenly,  without 
any  antecedent  somnolence ;  under  such  circumstances  the  urine  will  be 
found  loaded  with  albumen. 

Loss  of  muscular  strength  is  an  early  and  striking  symptom.  In  the 
majority  of  cases  it  is  present  from  the  very  first  day  of  the  fever.  In  many 
cases,  as  the  fever  progresses,  the  loss  of  muscular  power  is  so  great  that 
the  patient  is  unable  to  turn  in  bed  ;  the  prostration  always  increases  as 
the  disease  advances.  In  some  cases  there  is  little  loss  of  strength  during 
the  first  week,  but  the  prostration  comes  on  suddenly  during  the  second 
week. 

In  addition  to  the  general  loss  of  rauscular  power,  in  certain  cases  there 
is  paralysis  of  some  muscles,  such  as  the  sphincter  ani  and  the  muscles  of 
the  bladder,  so  that  the  urine  and  faeces  are  discharged  involuntarily.  Dys- 
phagia, partial  or  complete  aphonia,  and  inability  to  protrude  the  tongue, 
are  common  symptoms.  Muscular  tremor  is  an  indication  of  very  great 
muscular  prostration,  and  is  usually  met  with  in  the  aged  and  infirm  and 
in  those  who  have  been  addicted  to  the  use  of  intoxicating  drinks.  Muscu- 
lar spasms  and  subsultus  tendinum  are  present  to  a  greater  or  less  degree 
in  all  severe  cases  ;  the  tendons  of  the  wrist  are  most  frequently  affected. 
One  form  of  these  spasmodic  movements  is  manifested  by  the  patient's  pick- 
ing or  fumbling  the  bed-clothes  ;  another  by  obstinate  hiccough.  Trismus, 
strabismus,  and  in  rare  cases  opisthotonos,  have  occurred.  All  these  symp- 
toms must  be  regarded  as  grave.  Emaciation  is  never  a  marked  symptom. 
It  is  rarely  present  to  any  great  degree  before  the  third  week  of  the  fever. '^ 

Temperature. — During  the  first  week  of  typhus  fever  there  are  no  such 
marked  typical  variations  in  temperature  as  are  met  with  in  typhoid — none 
that  will  enable  one  to  make  a  diagnosis.  Usually  the  temperature  rises 
rapidly  from  the  very  onset  of  the  fever,  and  in  cases  of  average  severity 

1  The  incoherent,  nonsensical  muttering  is  beyond  the  control  of  the  patient,  who  is  himself  aware  of 
its  disjointed  and  erratic  character. 

2  The  eyes  at  first  are  suffused  ;  later  the  conjunctiva  becomes  dry.  The  pupils  are  contracted  and  are 
insensible  to  light  in  many  cases.  Vertigo,  dizziness,  noises  in  the  head,  partial  and  even  complete  deaf- 
ness are  observed.  Coryza,  epistaxis,  slight  hypersesthesia,  and,  finally,  general  anaesthesia,  are  infrequenr: 
symptoms. 


TYPHUS  FEVER. 


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attains  its  maximum  from  the  third  to  the  sixth  day.  At  this  period  the 
evening  temperature  will  range 
between  103°  F.  and  106°  F.  In 
severe  cases,  the  maximum  tem- 
perature is  not  reached  until  the 
eighth  or  tenth  day.  Before  the 
temperature  reaches  its  maximum, 
the  morning  and  evening  varia- 
tions are  slight,  about  1°  or  1^°  F. 
After  the  temperature  has  reached 
its  maximum  for  several  days  there 
will  be  little  change,  but  at  some 
time,  usually  between  the  seventh 
and  tenth  days,  there  will  be  a 
slight  remission  until  the  twelfth  p,g  j^g 

or  fourteenth  day,  when  it  rapidly  Temperature  Kecord  m  a  Case  of  Severe  Typhus  Fever, 
„,,.,.,  L^     L   X.  ■  ending  in  Recovery. 

tails,  m  typical  cases  that  termi- 
nate in  recovery,  to  its  normal  standard.     Any  sudden  rise  or  fall  (except 
in  crisis)  indicates  a  complication.     Occasionally  an  elevation  of  two  or 
more  degrees  precedes  the  fall.     This  sudden  fall  about  the  fourteenth  day 
is  peculiar  to  typhus.     The  fall  may  amount  to  4°  or  5°  F. 

A  very  high  range  of  temperature  during  the  first  week  is  an  indica- 
tion that  severe  cerebral  symptoms  will  be  develoj)ed  during  the  second 
week  of  the  fever.  A  case  of  typhus  fever  may  terminate  fatally,  in  which 
the  temperature  at  no  time  has  exceeded  103°  F.  In  all  fatal  cases,  just 
-preceding  death  there  is  usually  a  rise  of  from  2°  to  5°  in  temperature. 
During  the  first  week  of  convalescence  the  temperature  often  remains  below 
the  normal  standard,  especially  in  the  morning. 

Pulse. — The  pulse  in  this  fever  is  usually  frequent,  soft,  easily  com- 
pressed, and  often  irregular.  The  heart  may  partake  of  the  general  muscular 
weakness,  so  that  the  first  sound  may  become  inaudible.  There  is  a  soft  sys- 
tolic C fever")  murmur  heard  over  the  heart.  In  the  severe  cases,  during 
the  first  week  the  pulse  may  reach  120  beats  per  minute,  after  which  time 
it  increases  in  frequency  and  feebleness  with  the  severity  of  the  general 
symptoms.  By  the  third  day  it  may  reach  120  beats  per  minute  ;  usually  in 
the  milder  case  it  does  not  exceed  on  that  day  100  beats  per  minute.  If 
during  the  first  week  it  continues  for  three  consecutive  days  so  frequent  as 
120  beats  per  minute,  it  indicates  danger.  The  rate  may  be  106  in  the 
morning  and  120  in  the  evening.  The  higher  the  temperature,  and  the 
more  frequent  the  pulse  during  the  first  week,  the  more  severe  will  be  the 
symptoms  during  the  second  week.  If  during  the  second  week  it  becomes 
small,  feeble  and  frequent,  perhaps  beating  140  or  150  per  minute,  the  case 
may  be  regarded  as  unfavorable.  Absence  of  pulsation  in  the  radial  artery 
for  several  days  has  been  observed,  and  is  explained  on  the  ground  of  embolic 
obstruction  of  the  medium-sized  vessels. 

During  the  first  week,  if  the  pulse  increases  in  frequency  the  temperature 
rises,  and  if  the  pulse  diminishes  in  frequency  the  temperature  falls  ;  but 
46 


72-i  ACUTE    GEKERAL    DISEASES. 

during  the  second  week  the  pulse  may  increase  in  frequency,  and  the 
temperature  fall,  or  it  may  diminish  in  frequency  and  the  temperature  rise. 
The  pulse  is  not  an  infallible  guide  as  to  the  condition  of  the  heart,  for 
sometimes  the  pulse  is  full  and  distinct,  while  the  heart  power  is  yery  feeble ; 
on  the  other  hand,  the  cardiac  pulse  may  appear  strong  and  the  sounds 
distinct,  and  yet  the  radial  pulse  may  be  im]3erce]otible.  In  most  fatal  cases, 
after  the  first  week  the  radial  pulse  becomes  imperceptible  for  several  days 
prior  to  death.  Although  in  most  severe  cases  there  is  a  rapid  pulse,  yet  a 
slow  pulse  does  not  necessarily  indicate  a  mild  attack.  In  some  severe  and 
fatal  cases  the  pulse  may  never  be  over  100. 

Eruption. — The  general  character  of  the  typhus  eruption  has  already 
been  described.  Its  appearance  is  preceded  and  accompanied  by  a  bright 
redness  of  the  whole  surface,  on  which  dark  red  spots  are  scattered,  giving 
the  skin  a  mottled  appearance  '' sub-cuticular  rash."  These  spots  have 
an  irregular  outline,  and  vary  in  size  from  a  point  to  three  or  four 
lines  in  diameter.  Sometimes  they  are  few  in  number,  but  more  com- 
monly they  are  numerous  ;  the  large  spots  are  formed  by  the  coalescence  of 
the  smaller  ones.  It  is  a  macular,  not  a  papular  eruption.  At  first  they 
have  a  dusky  pink  hue,  partially  or  wholly  disappearing  on  pressure,  and 
as  the  finger  passes  over  them  they  seem  to  be  slightly  elevated.  After  a 
day  or  two  they  assume  somewhat  of  a  brick-dust  color,  and  are  but  slightly 
changed  by  pressure  ;  then  the  color  of  the  spots  becomes  darker  in  hue, 
and  finally  they  are  not  affected  by  firm  pressure.  Another  peculiarity  is 
that  each  patch  or  cluster  remains  visible  from  its  first  appearance  until 
the  termination  of  the  disease.  The  eruption  may  appear  upon  any  por- 
tion of  the  body.  Usually,  it  first  makes  its  appearance  upon  the  trunk,  soon 
spreading  to  the  extremities  ;  very  rarely  is  it  seen  on  the  face.  When  the 
eruption  is  scanty,  it  is  limited  to  the  chest  and  abdomen.  In  some  pa- 
tients the  eruption,  though  well  developed,  is  not  prominently  marked; 
the  spots  are  pale 'and  undefined  ;  and  though  grouped  in  patches  are  so 
irregular  that  they  give  to  the  entire  surface  a  faint,  dingy  appearance. 
Blood-extravasations  into  the  centre  of  the  typhus  spots  may  occur  at  the 
end  of  the  second  week. 

Respiration. — Usually,  during  the  first  week  the  respirations  do  not  ex- 
ceed twenty  or  thirty  per  minute  ;  but  during  the  second  week  they  often 
run  up  to  forty  or  fifty  per  minute.  In  cases  where  there  is  great  prostra- 
tion accompanied  by  stupor,  the  respirations  sometimes  fall  to  eight  or  ten 
per  minute.  Under  such  circumstances  they  are  often  irregular  and  pufiing 
in  character.  Hypostatic  congestion  of  the  lungs,  if  extensive,  is  attended 
by  great  frequency  of  respiration  and  evidences  of  cyanosis.  The  occur- 
rence of  these  changes  in  respiration  ought  always  to  lead  to  careful  exam- 
ination of  the  chest. 

The  digestive  system  is  very  little  disturbed  in  typhus  fever.  Nausea  and 
vomiting  are  rare,  and  an  examination  of  the  abdomen  presents  nothing 
abnormal.  There  is  no  tympanitis  or  tenderness  on  pressure.  Spontane- 
ous diarrhoea  is  of  exceedingly  rare  occurrence  ;  the  bowels  are  generally 
constipated.     Intestinal  hemorrhage  is  of  rare  occurrence,  and  wheu  it  is 


TYPHUS   FEVEE.  723 

present  depends  either  upon  congestion  of  the  mucous  membrane  of 
the  colon  or  on  hemorrhoids,  which  accompany  an  engorged  portal  circu- 
lation. 

Urine. — The  urine  in  typhus  undergoes  important  changes.  The  quan- 
tity varies  somewhat  with  the  amount  of  fluid  taken  into  the  stomach  ; 
usually,  it  is  diminished  during  the  first  week  to  one-fourth  or  one-half  the 
normal  quantity.  In  the  advanced  stage  of  severe  cases  there  is  sometimes 
complete  suppression  of  urine,  but  more  frequently  the  quantity  of  urine 
increases  during  the  later  stages  of  the  fever.  The  reaction  is  first  acid,  later 
neutral  or  alkaline.  The  quantity  of  urea  excreted  in  twenty-four  hours 
during  the  first  few  days  of  the  fever  is  increased,  and  the  increase  is  in 
proportion  to  the  intensity  of  the  fever.  In  the  majority  of  cases  it  remains 
abnormally  increased  until  the  period  of  crisis  is  reached,  when  it  gradu- 
ally, or  in  some  instances  rapidly  falls  below  the  normal  standard.  Uric 
acid  is  similarly  increased.  The  chlorides  grow  less  and  less  till  the  second 
week,  when  they  disappear.  In  all  severe  cases,  during  the  first  week  of  the 
disease,  a  small  amount  of  albumen  is  found  in  the  urine  ;  when  the  quan- 
tity is  large  the  case  may  be  regarded  as  severe.  In  the  severe  cases  the 
urine  will  also  be  found  to  contain  vesical  and  renal  epithelium,  and  when 
the  quantity  of  albumen  is  large,  epithelial  and  fatty  casts  of  the  urinifer- 
ous  tubes  will  be  present  with  blood. 

In  this  connection  it  is  important  to  bear  in  mind  the  necessity  of  daily 
inquiry  into  the  expulsive  power  of  the  bladder.  When  there  is  little  cer- 
ebral disturbance,  the  urine  is  passed  without  difficulty ;  but  when  stupor 
and  a  tendency  to  coma  exist,  there  is  often  retention  or  an  involuntary 
dribbling  of  urine,  which  might  lead  one  to  think  that  there  was  no  ac- 
cumulation of  urine  in  the  bladder.  It  is  safe  to  inquire  at  least  once  a 
day  as  to  the  state  of  this  organ,  and  if  involuntary  discharges  of  urine 
occur,  the  contents  of  the  bladder  should  be  evacuated  by  means  of  a 
catheter.     Copious  sediments  form  in  the  urine  on  the  day  of  crisis. 

Differential  Diagnosis. — Before  the  appearance  of  the  eruption,  the  diag- 
nosis of  typhus  fever  is  always  difficult,  and  sometimes  impossible.  The 
diseases  with  which  it  is  most  liable  to  be  confounded  are  typhoid  fever, 
relapsing  fever,  measles,  pneumonia,  acute  Brighfs  disease,  meningitis, 
delirium  tremens,  and  some  of  the  other  acute  blood  diseases,  such  as 
erysipelas,  pycemia,  septiccemia,  etc. 

The  early  characteristic  symptoms  of  typhus  fever  are  chilliness,  pain  in 
the  back  and  limbs,  and  headache.  During  the  first  week  the  headache 
increases  in  severity  from  hour  to  hour,  and  is  accompanied  by  a  rapid  rise 
in  temperature.  These  symptoms  occurring  in  one  who  has  been  exposed 
to  typhus  poison  are  always  sufficient  for  a  diagnosis.  The  a23pearance  of 
the  eruption  settles  the  question.  On  account  of  the  similarity  in  appear- 
ance of  the  eruption  of  typhus  fever  and  that  of  measles  in  children,  the 
one  disease  is  sometimes  mistaken  for  the  other.  In  both  diseases  the  erup- 
tion may  appear  on  the  fifth  day,  but  the  eruption  of  measles  is  of  a  brighter 
tint  than  that  of  typhus  fever,  and  its  appearance  is  preceded  by  a  cough 
and  coryza,  which  are  not  present  in  typhus  fever. 


724  ACUTE    GENERAL   DISEASES. 

Meningitis. — The  differential  diagnosis  between  typhus  fever  and  cerebro- 
spinal meningitis  is  often  difficult.  Not  infrequently,  days  may  elapse  be- 
fore one  is  able  to  decide  whether  a  case  is  one  of  typhus  fever  or  of  cerebro- 
spinal meningitis.^  The  distinguishing  points  between  the  two  diseases 
are  as  follows  : — the  headache  of  meningitis,  at  the  outset  of  the  disease, 
is  much  more  distressing  than  that  of  typhus,  and  it  alternates  with  delir- 
ium. When  delirium  comes  on  in  typhus  fever,  the  pain  in  the  head  ceases. 
Vomiting  is  prominent  in  meningitis,  absent,  as  a  rule,  in  ty|)lius.  Photo- 
phobia and  contracted  pupils  are  among  the  early  symptoms  of  meningitis, 
and  the  patient  is  greatly  disturbed  by  noise,  while  in  typhus  fever  he  seems 
indifferent  to  both.  Dulling  and  blunting  of  all  the  senses  are  common 
in  typhus.  All  the  senses  are  abnormally  acute  at  the  onset  of  meningitis. 
Inequality  of  the  pupils,  strabismus,  ptosis,  and  paralysis  are  common  in 
meningitis  and  rare  in  typhus.  In  meningitis  the  countenance  is  pale  and 
expressive  of  pain,  wildness,  and  anxiety ;  in  typhus  fever  it  is  dusky, 
blank,  and  stupid.  Convulsions  are  an  early  symptom  in  meningitis  and 
rare  in  typhus.  Again,  in  meningitis  the  pulse  is  hard  and  wiry,  rapid 
and  irregular,  and  at  the  last  intermitting ;  while  in  typhus  fever  it  is 
rapid  at  the  onset  of  the  disease,  easily  compressed,  full  and  bounding. 
Lastly,  the  eruption  of  typhus  fever  is  characteristic.  If  an  eruption  is 
present  in  meningitis,  it  has  no  regularity  in  its  development  ;  it  may  ap- 
pear within  twenty-four  hours  after  the  development  of  the  first  symptom 
of  the  disease,  or  it  may  be  postponed  for  several  days.  It  does  not  appear 
on  the  fifth  or  sixth  day  of  the  disease  with  the  uniform  regularity  of  the 
typhus  eruption.  Petechias  may  be  present  in  meningitis  as  well  as  in 
typhus  fever,  but  they  are  not  characteristic  of  either  disease.  The  tem- 
perature rises  rapidly  in  typhus,  and  reaches  a  higher  range,  e.  g.,  104°  to 
106°  in  twenty-four  to  forty-eight  hours  ;  while  in  meningitis  the  average 
temperature  on  the  second  and  third  days — indeed,  during  its  entire  course — 
is  102°,  often  loioer.  Eigidity  of  the  muscles  of  the  neck  is  not  always 
positive  evidence  of  meningitis,  for  it  sometimes  occurs  in  typhus  fever. 
The  ataxia,  muscular  prostration,  aiid  character  of  the  tongue  in  typhus 
are  also  points  that  greatly  aid  in  distinguishing  it  from  cerebro-spinal 
fever. 

Pneumonia. — Sometimes  a  latent  pneumonia  with  typhoid  symptoms  is 
mistaken  for  typhus  fever  ;  especially  is  this  the  case  when  the  latter  is  pre- 
vailing. I  frequently  saw  cases  where  such  a  mistake  had  been  made,  while 
in  charge  of  the  typhus  fever  patients  on  Blackwell's  Island,  during  the 
epidemic  to  which  reference  has  been  made.  In  these  cases  there  will  be 
active  typhoid  symptoms,  e.  g.,  dry  tongue,  delirium,  high  temperature,  etc. 
The  countenance  in  this  pneumonia,  although  the  cheeks  may  have  a  pur- 
plish hue,  does  not  exhibit  that  dull,  heavy  expression  so  commonly  seen 
in  typhus.    Although  there  may  be  delirium  in  both  instances,  the  delirium 

1  To  show  how  difficult  is  the  diagnosis  between  these  two  affections,  a  circumstance  ma}'  be  men- 
tioned which  occurred  in  Bellevue  Hospital .  A  patient  was  brought  into  the  hospital  directly  from  a 
ship,  and  the  diagnosis  of  cerebro-spinal  meningitis  was  made  by  several  of  the  attending  stafE ;  but  at 
the  autopsy  there  were  found  none  of  the  lesions  of  meningitis  ;  all  the  changes  corresponded  to  those 
found  at  the  autopsies  of  patients  djdng  of  typhus  fever. 


TYPHUS   FEVER.  725 

in  the  former  disease  is  of  a  milder  type  than  the  latter.  The  characteristic 
pneumonic  expectoration  is  not  usually  present  in  these  cases  ;  so  that  in 
making  the  differential  diagnosis  this  symptom  cannot  be  relied  upon. 
The  physical  signs  of  pulmonic  consolidation  will  lead  one  to  diagnosticate 
pneumonia,  and  unless  the  typhus  eruption  is  present,  this  will  be  sufficient 
for  a  diagnosis.  If  pulmonary  consolidation  is  a  complication  of  typhus 
fever,  it  will  not  be  developed  until  after  the  sixth  day  of  the  fever,  the 
time  when  the  eruption  should  have  appeared.  If  no  eruption  is  present, 
the  pneumonic  consolidation  may  be  regarded  as  the  primary  affection,  and 
the  symptoms  which  simulated  those  of  typhus  fever  may  be  regarded  as 
secondary. 

Delirium  Tremens. — The  delirium  of  alcoholism  may  sometimes  so 
closely  resemble  that  of  typhus  fever  that  the  one  may  be  mistaken  for 
the  other.  Typhus  fever  patients  have  been  placed  in  the  cells  under  the 
supj)osition  that  they  had  delirium  tremens.  If  the  delirium  tremens  is 
uncomplicated  by  pneumonia,  the  temperature  will  suffice  for  the  differen- 
tial diagnosis,  for  in  delirium  tremens  the  temperature  is  rarely  above  100° 
P.  There  may  be  a  rapid  pulse  in  delirium  tremens,  and  often  the  joatient 
has  a  brown,  dry  tongue,  and  other  typhoid  symptoms  ;  but  there  is  only 
a  slight  rise  in  temperature  ;  besides,  there  is  no  eruption.  The  attack  is 
not  ushered  in  by  headache,  but  by  an  inability  to  sleep  ;  and  the  circum- 
stances which  precede  and  give  rise  to  such  an  attack  will  establish  beyond 
a  doubt  the  true  nature  of  the  attack. 

Acute  Bright' s  Disease.— It  is  not  surprising  that  acute  uraemia  should 
be  mistaken  for  typhus  fever.  The  brown,  dry  tongue,  the  tendency  to 
stupor,  the  contracted  pupil,  the  low,  muttering  delirium,  and  all  the  phe- 
nomena of  the  typhoid  state,  as  well  as  the  albuminous  urine,  belong  to  both 
diseases ;  but  the  temperature  is  not  raised  in  uraemia  as  it  is  in  typhus 
fever,  and  the  oedema  which  is  always  present  in  acute  uraemia  is  absent  in 
typhus  fever. 

Erysipelas,  pycemia,  septiccemia,  and  all  similar  acute  Mood  diseases  are 
often  attended  by  many  of  the  symptoms  which  attend  the  development  of 
typhus  fever.  In  pyaemia  and  septicaemia  there  are  irregular  chills,  followed 
by  fever  and  profnse  sweats,  with  evidences  of  septic  and  pygemic  poison- 
ing; in  erysipelas,  there  are  evidences  of  a  localized  phlegmon.  It  should 
not  be  forgotten  that  erysipelas  is  sometimes  ushered  in  by  all  the  phe- 
nomena that  attend  the  ushering-in  of  typhus  fever  ;  this  is  before  the  local 
inflammation  shows  itself.  In  such  cases  it  is  impossible  to  make  a  differ- 
ential diagnosis  until  the  local  phenomena  which  characterize  erysipelas 
show  themselves,  or  until  the  typhus  eruption  appears.  In  many  of  the 
acute  infectious  diseases  one  is  compelled  to  wait  until  the  time  for  the  ap- 
pearance of  the  eruption  before  typhus  fever  can  be  excluded.  When  ty- 
phus fever  is  prevailing  and  the  physician  is  watchful  for  its  appearance, 
there  will  usually  be  little  difficulty  in  diagnosis.  Sometimes  typhoid,  ty- 
phus and  relapsing  fever  prevail  at  the  same  time  in  the  same  locality. 

The  importance  of  early  forming  a  correct  differential  diagnosis  between 
typhus  and  typhoid  fever  cannot  be  over-estimated  ;  and  to  accomplish 


736       •  ACUTE   GENERAL   DISEASES. 

■     .A 

this,  the  prominent  symptoms  of  each  will  be  reviewed  and  compared. 
The  first  point  to  be  considered  in  the  differential  diagnosis  of  these  two 
diseases  is,  that  typhus  fever  is  sudden  in  its  advent,  while  typhoid  fever 
comes  on  insidiously,  and  is  slowly  developed.  In  the  majority  of  cases  of 
the  former  disease  there  is  a  chill  at  the  commencement,  and  severe  pain 
in  the  head,  whereas  in  the  latter  there  is  only  a  chilliness,  some  aching  in 
the  limbs,  and  a  slight  headache.  Muscular  prostration  and  progressive 
muscular  weakness  appear  earlier,  and  are  much  more  marked  in  typhus 
than  in  typhoid. 

The  ranges  of  temperature  in  the  two  forms  of  fever  differ  greatly. 
Typhoid  fever  commences,  on  the  first  day,  with  a  slight  rise  of  tem- 
perature, which  continues,  with  morning  remissions  and  evening  exacer- 
bations, until  the  end  of  the  first  week,  when  it  has  reached  its  highest 
point ;  during  the  second  week  it  remains  at  about  the  same  height, 
with  only  slight  variations  ;  during  the  third  week  there  are  more  marked 
morning  remissions  ;  and  by  the  end  of  the  fourth  week  the  temperature 
has  reached  its  normal  standard,  by  intermittent  periods.  In  typhus 
fever,  the  temperature  rises  rapidly,  and  before  tJie  end  of  the  second  day 
reaches  104°  F.  or  105°  F.  Whatever  degree  is  reached  on  the  third 
day  may  be  regarded  as  the  maximum  temperature  ;  after  this  time 
there  are  slight,  irregular  variations  until  the  tenth  or  twelfth  day,  when 
the  temperature  begins  to  fall,  and  rapidly  reaches  the  normal  standard. 
In  typhoid  there  is  great  emaciation  ;  in  typhus  it  is  slight,  but  the 
exhaustion  and  muscular  prostration  are  far  greater  than  in  typhoid.  The 
eruptions  of  these  two  foi-ms  of  fever  differ  very  markedly.  In  typhus  it 
makes  its  appearance  upon  the  fifth  or  sixth  day  ;  while  the  eruption  of 
typhoid  fever  makes  its  appearance  between  the  seventh  and  ninth  days. 
The  eruption  of  typhus  fever  appears  upon  the  arms  and  chest,  and  more 
or  less  over  the  entire  body  ;  whereas  the  eruption  of  typhoid  appears  upon 
the  chest  and  abdomen,  very  rarely  upon  the  extremities  ;  sometimes  it 
appears  upon  the  loins  when  it  cannot  be  found  on  any  other  part  of  the 
body.  As  a  rule,  the  spots  in  typhus  are  numerous,  while  in  typhoid  they 
are  not  very  abundant.  In  typhus  fever,  the  spots  at  first  are  small, 
slightly  elevated,  of  a  dark  pinkish  hue,  and  disappear  only  on  firm  press- 
ure. As  the  disease  advances  they  become  darker,  and  finally  are  not 
affected  by  firm  pressure,  and  remain  visible  from  the  time  of  their  appear- 
ance until  death  occurs  or  convalescence  is  established.  In  typhoid  fever 
each  spot  is  rose-colored,  slightly  elevated,  and  disappears  on  slight  press- 
ure. Each  spot  remains  visible  for  three  days  and  then  disappears,  to  be 
followed  by  another  crop.  Usually  the  eruption  is  visible  about  two 
weeks,  and  when  it  disappears  it  leaves  the  skin  unstained,  whereas  in  ty- 
phus the  eruption  leaves  a  stain  upon  the  surface.  There  is  a  mottling  of 
the  surface  in  typhus  fever,  the  mulberry  rash,  which  is  not  seen  in 
typhoid. 

The  brain  symptoms  in  these  two  diseases  also  differ.  In  typhus 
fever  they  appear  early,  and  the  headache  and  delirium  are  more  intense 
than  in   typhoid.     Delirium  in  typhoid  more  commonly  appears   at  the 


TYPHUS    FEVER.  737 

end  of  tlie  second  or  during  the  third  week  of  the  disease  ;  whereas  in 
typhus  it  appears  early,  and  before  the  end  of  the  second  week  has  disap- 
peared if  recovery  is  to  take  place.  As  a  rule,  in  typhus  fever  constipation 
is  present,  and  a  mild  cathartic  must  be  given  to  move  the  bowels  ;  whereas 
in  typhoid  fever  the  pea-soup  diarrhoea  is  a  prominent  symptom.  Tym- 
panitic distention  of  the  abdomen,  gurgling  and  tenderness  in  the  right 
iliac  fossa,  and  intestinal  hemorrhage,  are  all  phenomena  of  typhoid  fever, 
but  are  never  present  in  typhus  fever.  Epistaxis  is  frequent  in  typhoid 
and  not  in  typhus  fever.  In  typhus  fever  convalescence  will  usually  be 
established  before  the  end  of  the  second  week  ;  it  may  occur  at  any  time 
between  the  eighth  and  fourteenth  days.  The  average  duration  of  typhus 
fever  is  fourteen  days,  whereas  the  average  duration  of  typhoid  fever  is 
from  twenty-one  to  thirty  days.  Typhus  fever  is  contagious,  typhoid  fever 
is  non-contagious.'  Typhus  fever  is  generally  epidemic ;  typhoid  fever  is 
always  endemic.  In  regard  to  the  protection  which  one  attack  of  typhus 
fever  furnishes  against  a  second  attack,  it  very  markedly  differs  from  ty- 
phoid fever.  One  may  have  typhoid  fever  whenever  the  system  has  been 
exposed  to  the  typhoid  poison  ;  but  one  attack  of  typhus  is  almost  a  cer- 
tain protection  against  a  second  attack. 

Prognosis. — The  prognosis  in  this  disease  is  always  grave,  and  no  opinion, 
as  to  its  termination,  can  be  given  until  every  point  in  each  case  has 
been  considered,  such  as  the  age  of  the  patient,  the  character  of  the  epi- 
demic, and  the  tendency  to  certain  complications.  In  all  eiDidemics  the 
majority  of  cases  will  recover.  The  ratio  of  mortality,  as  given  by  differ- 
ent writers,  varies  from  one  death  in  five  to  one  death  in  sixteen  cases.*  The 
surroundings  of  each  patient  should  be  carefully  noted,  also  the  hygienic 
influences  which  he  is  under,  and  his  habits  of  life  should  be  taken  into 
account.  With  the  intemperate  the  disease  is  likely  to  prove  fatal.  Some 
of  the  circumstances  which  increase  the  danger  in  any  particular  case  are 
a  debilitated  condition  of  the  patient  from  advanced  age,  intemperate  hab- 
its, privation,  and  previous  disease ;  mental  depression,  presentiment  of 
death,  overcrowding  and  bad  ventilation  ;  a  gouty  diathesis  is  always  dan- 
gerous. 

Death  may  occur  in  typhus  fever  from  three  general  causes  :  first, 
from  coma,  the  result  of  overwhelming  the  system  with  typhus  poison. 
The  patient  does  not  die  from  the  effect  of  a  prolonged  high  temperature, 
nor  from  any  complication,  but  dies  as  patients  die  in  acute  ureemia,  be- 
cause the  system  is  overwhelmed  by  the  typhus  poison,  and  the  functions 
of  organic  life  are  arrested  by  its  action  on  the  nerve-centres. 

'  When  the  pathological  lesions  are  studied  and  the  manner  in  which  death  occurs  in  these  two  forms 
of  fever  is  considered,  it  can  readily  be  seen  how  widely  they  differ.  The  characteristic  pathological 
lesions  of  typhoid  fever  are  the  changes  which  take  place  in  the  intestinal  glands,  such  as  ulceration  or 
tendency  to  ulceration.  In  all  cases  these  characteristic  lesions  are  present.  Suppose  a  case  of  what  has 
been  called  typhoid  fever  is  followed  to  the  dead-house,  and  ulceration  or  evidences  of  a  tendency  to  ulcer- 
ation of  Peyer's  patches  are  not  discovered,  then  it  is  certain  a  mistake  in  diagnosis  has  been  made.  If, 
on  the  other  hand,  in  a  case  of  supposed  typhus  fever  is  found  ulceration  of  Peyer's  patches,  it  is  equally 
certain  that  a  mistake  has  been  made,  and  that  a  case  of  typhoid,  and  not  typhus  fever  has  been  treated. 
The  parenchymatous  changes  which  are  common  to  both  diseases  have  already  been  sufficiently  con 
eidered. 

*  Griesinger  and  Murchison  state  "  that  in  cariixm  epidemics  fhQ  mortality  runs  as  high  as  40  to  50  per 
cent."  An  average  epidemic  shows  about  15  per  cent,  of  deaths  ;  a  mild  one,  about  6  to  8  per  cent. 


72S  ACUTE    GENERAL   DISEASES. 

Death  may  occur,  secondly,  from  syncope,  due  to  heart  failure,  whethej* 
the  heart  failure  is  the  result  of  the  prolonged  high  temperature,  or  the 
direct  action  of  the  typhus  poison.  A  continued  temperature  of  105° 
or  106°  F.  is  very  liable  to  be  followed  by  fatal  syncope  from  failure  of 
heart  power,  although  the  evidences  of  parenchymatous  degeneration  of 
the  heart  may  not  be  present.  Death  may  occur,  thirdly,  from  complica- 
tions. Although  they  do  not  properly  belong  to  the  primary  disease,  yet 
they  so  modify  it  that  they  enter  very  largely  into  its  history.  In  a  large 
number  of  cases  which  terminate  fatally,  death  is  due  to  some  one  of 
these  complications.  In  some  epidemics  they  are  all  pulmonary ;  in  others 
they  are  all  cerebral.  The  advent  of  pulmonary  complications  is  always 
insidious ;  the  cough  and  expectoration  which  usually  attend  pulmonary 
diseases  are  either  absent,  or  so  slight  as  not  to  attract  the  attention  of 
the  physician.  Eapid  breathing  and  lividity  of  the  face  are  often  the  first 
obvious  indications  of  extensive  disease  of  the  lungs.  When  these  symp- 
toms are  present,  a  careful  physical  examination  of  the  chest  should  be 
made. 

Bronchitis  may  come  on  at  any  period  during  the  fever,  and  it  may 
continue  after  the  fever  has  subsided.  So  long  as  it  is  confined  to  the 
larger  tubes  there  is  little  danger,  but  som.etimes  suddenly  and  insidiously 
it  extends  into  the  smaller  tubes,  and  is  complicated  with  pulmonary  con- 
gestion and  oedema.  Under  such  circumstances  it  may  be  the  direct  cause 
of  death.  The  pneumonia  which  complicates  typhus  fever  is  lolular  in 
character,  and  is  frequently  preceded  or  accompanied  by  bronchitis.  It 
has  a  tendency  to  terminate  in  abscess  or  gangrene.  During  life  it  is  not 
always  possible  to  distinguish  it  from  hypostatic  congestion.  If,  however, 
the  dulness  on  percussion  is  confined  to  one  lung,  if  the  respiration  is 
bronchial,  the  diagnosis  of  pneumonia  is  readily  established.  The  seat  of 
pneumonia  is  generally  at  the  upper  portion  of  the  lung.  Pleurisy 
(serous  or  purulent)  may  occur. 

Laryngitis  is  sometimes  a  very  serious  complication  of  typhus.  The 
common  form  is  that  of  acute  oedema  glottidis.  Its  occurrence  is  readily 
recognized  by  the  signs  of  laryngeal  obstruction  which  attend  its  develop- 
ment. "Whenever  there  is  extensive  swelling  of  the  glands  about  the  neck, 
with  great  tumefaction  of  the  mucous  membrane  of  the  pharynx,  one 
must  be  on  his  guard  for  the  occurrence  of  this  comjDlication. 

On  account  of  the  extensive  blood-changes  whiqh  sometimes  occur  in 
severe  cases  of  typhus  fever,  the  blood  readily  escapes  through  the  walls 
of  the  vessels,  giving  rise  to  extensive  hemorrhages  from  the  mucous  sur- 
faces, nose,  gums,  bowels,  the  genito-urinary  tract,  vagina,  etc.,  and  into 
the  cellular  tissue.  The  occurrence  of  the  hemorrhages  is  peculiar  to 
certain  epidemics,  and  when  they  occur  it  is  during  the  first  week  of  the 
fever. 

Meningitis  is  probably  the  only  cerebral  complication  which  will  be  met 
with  in  this  fever.  This  occurs  more  frequently  in  children  than  in  adults, 
and  is  not  present  in  every  epidemic.  The  cerebral  symptoms  which  are 
such  constant  attendants  upon  typhus  fever  do  not  depend  upon  menin- 


TYPHUS   FEVEK.  729 

geal  inflammation  ;  they  belong  to  the  natural  history  of  the  disease.  If, 
during  the  course  of  the  fever,  there  is  a  deep-seated  jiain  in  the  head,  with 
restlessness,  which  shows  itself  by  constant  attempts  to  get  out  of  bed,  with 
photophobia,  contracted  pupils,  and  flushing  of  the  face  and  eyes,  followed 
by  somnolence  gradually  lapsing  into  coma,  it  is  almost  certain  that  men- 
ingitis is  occurring  as  a  complication.  This  is  most  liable  to  occur  during 
the  second,  week  of  the  fever.  The  characteristic  symptom  which  marks 
its  development  is  the  constant  attempt  on  the  part  of  the  patient  to 
get  out  of  bed.  He  is  so  persistent  in  this  that  unless  watched  with  the 
greatest  care  he  will  be  found  upon  the  floor,  vainly  attempting  to  rise. 
The  patient  has  more  muscular  power  than  before  the  occurrence  of  the 
meningeal  complication,  for  he  will  perform  acts  which  previously  he  was 
wholly  unable  to  execute.  Usually  the  delirium  lasts  two  days,  then  the 
patient  gradually  passes  into  a  state  of  coma  from  which  he  cannot  be 
aroused  ;  his  respirations  may  not  be  more  than  eight  or  ten  per  minute. 
Dilatation  of  the  pupils,  and  an  intermitting  and  almost  imperceptible 
pulse,  immediately  precede  death. 

I  regard  most  of  the  Tcidney  changes  as  a  part  of  the  history  of  the  fever 
rather  than  as  complications,  although  in  some  few  instances  croupous 
nephritis  occurs,  and  must  be  included  in  the  list  of  complications.  Its 
occurrence  in  the  course  of  typhus  fever  is  indicated  by  the  almost  entire 
suppression  of  urine,  and  by  the  presence  of  albumen  and  exudative  and 
blood  casts  in  the  urine. 

Glandular  swellings  are  also  occasional  complications  of  typhus  fever, 
and  sometimes  may  be  of  a  very  serious  nature,  for  they  may  so  interfere 
with  deglutition  and  respiration  as  to  destroy  life.  The  parotid,  the  sub- 
maxillary, axillary  and  mammary  glands  may  enlarge  and  suppurate.  These 
swellings  usually  appear  immediately  after  ihe  crisis  of  the  primary  fever. 
They  often  enlarge  with  great  rapidity,  and  in  some  instances  terminate 
in  extensive  suppuration. 

Bed-sores  are  rather  infrequent.  Gangrene,  necrosis,  cancrum  oris,  sup- 
purative cellulitis,  purulent  arteritis — all  have  occurred  in  various  epidem- 
ics, and  render  the  prognosis  unfavorable.  If  menstruation  occur  in  a 
female  with  typhus,  the  bleeding  is  commonly  very  profuse  and  may  cause 
death  from  acute  anaemia. 

Duration. — The  average  duration  of  the  fever  is  thirteen  or  fourteen 
days.  Usually  the  day  of  crisis  is  between  the  tenth  and  sixteenth  days. 
It  is  of  shorter  duration  in  the  young  than  in  the  old,  in  children 
than  in  adults.'  Relapses  are  extremely  rare  in  this  fever.  I  have  met 
with  a  second  and  third  attack  of  the  fever  in  the  same  individual,  but  I 
have  never  met  with  a  true  relapse.  Typhus  fever  varies  very  slightly  in 
its  general  character  and  different  cases.  A  number  of  different  varieties, 
depending  upon  the  mildness  or  severity  of  the  disease,  the  prominence 
of  certain  symptoms,  the  presence  of  comjDlications,  and  the  circum- 
stances under  which  fever  appears,  have  been  described,  but  the  general 

'  In  .'jOO  cases  ending  in  recovery,  thirteen  and  a  half  days  was  tbe  average  ;  and  in  100  fatal  cases,  the 
duration  was  fourteen  and  a  half  days.— Murchison. 


730  ■  ACUTE   GE]SfEEAL   DISEASES. 

description  already  given    includes   that   of   (so-called)    "  varieties "   of 
typhus/ 

The  individual  symptoms  and  signs  which  render  the  prognosis  unfavor- 
able are  as  follows : 

A  pulse  continuing  a  number  of  days  at  more  than  120  per  minute, 
becoming  at  times  intermittent  and  irregular,  bespeaks  an  unfavorable 
prognosis.  A  hurried  and  difficult  respiration,  with  turgidity  of  the  face, 
due  either  to  cerebral  or  pulmonary  oedema,  renders  the  prognosis  unfavor- 
able. 

Delirium  which  is  very  active  and  accompanied  by  great  muscular  pros- 
tration, as  indicated  by  subsultus,  slipping  down  in  bed,  and  accompanied 
by  that  condition  known  as  "coma  vigil,"  lasting  for  a  number  of  days,  is 
almost  a  certain  indication  of  a  fatal  termination. 

The  "  pin-hole  pupil, ^'  mentioned  by  old  writers,  is  an  unfavorable  omen. 
It  does  not  necessarily  indicate  the  presence  of  meningitis,  as  was  once 
supposed.  Great  muscular  prostration  at  the  very  onset  of  the  disease 
renders  the  prognosis  unfavorable. 

Sudden  fading  of  the  eruption,  and  a  widely  expanded  pupil  may  be 
regarded  as  unfavorable  signs.  Marked  impairment  of  the  special  senses, 
accompanied  by  very  great  rapidity  of  the  pulse,  is  an  element  of  unfavor- 
able prognosis. 

The  darker  and  more  abundant  the  eruption,  especially  if  accompanied 
by  petechial  spots,  the  more  unfavorable  the  prognosis.  In  children  the 
eruption  is  lighter  in  color  than  it  is  in  adults,  presenting  an  appearance 
similar  to  the  typhoid  eruption.  In  adults  where  there  is  dark  mottling  of 
the  surface  confined  to  the  extremities,  with  evidences  of  blood  extravasa- 
tion, indicated  by  the  presence  of  petechise,  the  prognosis  is  unfavorable, 
but  the  case  is  by  no  means  hopeless. 

A  dry,  brown,  retracted,  tremulous  tongue  is  seen  only  in  severe  cases. 
A  long-continued  high  temperature  is  always  an  unfavorable  symptom. 
Great  diminution  in  the  quantity  of  urine  is  an  unfavorable  symptom,  as 
also  is  the  presence  of  casts  and  albumen  in  the  urine.  Eetention  of  urine 
is  a  more  unfavorable  symptom  than  incontinence  ;  convulsions  and  coma 
are  liable  to  follow  such  retention.  It  is  to  be  remembered  that  in  typhus 
fever,  more  than  in  any  other  disease,  patients  pass  into  an  apparently 
hopeless  condition,  and  afterward  rally  and  recover.  A  patient  who  seems 
to  be  overwhelmed  with  the  poison,  who  has  "coma  vigil,"  "pin-hole 
pupils,"  rolling  of  the  tongue,  and  a  feeble,  irregular,  and  intermitting 
pulse,  may  recover,  although  these  symptoms  warrant  an  unfavorable 
prognosis  ;  but  "coma  vigil  "  more  than  any  single  symptom  indicates  an 
unfavorable  prognosis. 

The  fii'st  indication  of  recovery  is  a  diminution  in  the  frequency  of  the 
pulse.  The  pulse  may  have  been  130,  but  on  the  tenth,  twelfth,  or  four- 
teenth day  it  begins   to   diminish  in  frequency.      The  tongue  has  been 

1  TVMw^'Sic^e^CfJW  is  that  form  where  death  occurs  in  three  or  four  days,  after  the  most  intense  febrile 
movement  and  constitutional  disturbance.  Headaches  and  a  feeling  of  malaise,  etc.,  during  an  epidemic 
give  rise  to  what  many  call  "  abortive  "  typhus.  Walking  typhus  is  that  form  where  the  patient  is  not  con- 
fined to  his  bed  until  the  second  week. 


TYPHUS  FEVBE.  731 

brown  and  dry,  subsultusand  delirium  may  iiave  been  present,  even  "  coma 
vigil  "  may  have  manifested  itself;  there  has  been  great  muscular  pros- 
tration ;  the  patient,  attempting  to  rise  from  the  bed,  may  have  fallen  ujDon 
the  floor  ;  now,  the  pulse  begins  to  get  slower,  the  patient  falls  into  a  re- 
freshing sleep  and  awakes  perfectly  conscious  ;  his  countenance  is  changed 
from  the  dusky  hue  to  an  almost  natural  appearance,  and  he  desires  food. 
In  other  words,  within  twenty-four  hours  an  entire  change  comes  over  the 
patient,  and  that  change  is  first  indicated  by  a  diminution  in  the  frequency 
of  the  pulse,  accompanied  by  a  fall  in  temperature.  The  fall  in  tenxpeva.- 
ture  is  not  extreme  ;  j)erhaps  a  fall  of  two  degrees  is  first  noticed.  In  my 
experience,  there  is  an  attempt  at  convalescence  upon  the  eighth  day  of  the 
fever.  Especially  in  those  cases  that  recover,  a  slight  fall  in  temperature 
will  be  noticed  on  this  (the  eighth  day),  although  the  temperature  may 
again  rise ;  upon  the  twelfth  or  fourteenth  day  there  is  a  distinct  fall  in 
temperature  and  diminution  in  the  frequency  of  the  pulse  that  is  indicative 
of  convalescence.  The  mode  of  recovery  in  typhus  and  typhoid  is,  perhaps, 
the  most  distinguishing  clinical  feature.  In  typhus  recovery  is  rapid,  in 
typhoid  it  is  markedly  slow. 

Of  all  the  conditions  which  influence  the  prognosis  in  typhus  fever,  age 
and  the  habits  of  the  patient  have  as  great,  if  not  greater,  influence  than 
any  other.  I  am  convinced  of  this  from  an  experience  in  the  care  of  typhus 
fever  patients  which  dates  back  almost  to  the  very  commencement  of  my 
study  of  medicine,  for  very  early  did  I  have  the  care  of  a  typhus  fever  ward. 
In  children,  typhus  fever  is  a  very  simple  form  of  disease.  The  rate  of 
mortality  is  very  low.  I  remember  having  the  care  of  sixty  children  with 
typhus  fever,  and  among  these  only  one  death  occurred.  This  is  as  low  a 
rate  of  mortality  as  one  can  expect  in  measles.  Under  the  fifteenth  year 
of  life  the  rate  is  very  low,  viz.,  two  or  three  per  cent.  From  twenty  to 
thirty  the  rate  is  fifteen  per  cent.,  with  advancing  years  the  disease  is  more 
fatal.  When  the  patient  has  passed  the  middle  period  of  life,  there  is  great 
danger  from  typhus  fever.  So  with  the  intemperate,  and  those  who  have 
livid  amid  unfavorable  hygienic  surroundings.  The  bright,  educated  and 
cultured,  those  whose  brains  are  active,  are  less  likely  to  recover  than  the 
stupid  and  uneducated. 

Treatment. — The  more  prominent  measures  which  have  been  and  are  now 
employed  in  the  management  of  typhus  fever  are  in  many  respects  similar 
to  those  proposed  for  the  management  of  typhoid  fever  patients,  yet  the 
treatment  of  these  two  diseases  differs  in  certain  essential  particulars. 
When  the  symptoms  are  mild,  very  simple  measures  are  all  that  is  required. 
Of  these,  confinement  to  bed,  cooling  drinks,  mild  aperients,  a  milk  diet, 
and  free  ventilation  are  the  chief,  and,  indeed,  the  only  means  required. 
It  is  also  important  to  observe  the  same  rules  in  regard  to  the  arrangement 
of  the  sick-room  which  are  recommended  in  the  case  of  typhoid  fever 
patients.  The  more  perfect  the  ventilation,  the  greater  the  amount  of 
fresh  air  around  the  patient,  the  better  his  chances  for  recovery.  The 
majority  of  cases  of  typhus  fever  are  ushered  in  by  active  and  severe 
symptoms,  such  as  would  tempt  one  to  adopt  a  vigorous  plan  of  treatment. 


732  ACUTE    GE]SrERAL   DISEASES. 

symptoms  which  at  one  time  were  thought  to  indicate  the  employment  of 
heroic  antiphlogistic  measures. 

Writers  usually  consider  its  treatment  under  two  heads — the  preventive 
and  curative.  I  prefer  to  use  the  terms  ^jrophylactic  and  remedial,  for  I 
question  our  ability  to  cure  this  disease. 

Much  can  be  done  to  prevent  its  development,  and  this  will  constitute  an 
important  part  in  its  management.  How,  then,  can  the  development  of 
typhus  fever  be  prevented  ?  Medical  skill  cannot  prevent  the  importa- 
tion of  the  disease  into  localities  where  it  is  not  indigenous,  for  this  is  con- 
trolled by  state  and  national  authority.  Consequently  typhus  fever  will 
probably  continue  to  be  imported  into  districts  where  it  does  not  originate. 
For  examj)le,  we  shall  occasionally  see  the  disease  in  all  our  large  cities  ;  it 
may  appear  in  any  commercial  seaport,  and  from  there  it  may  be  carried 
into  the  interior.  Yet  much  can  be  done  to  prevent  its  spread  after  it  is 
imported,  and  to  prevent  its  development  as  an  epidemic  when  it  is  carried 
into  any  locality  in  the  interior. 

It  is  important  that  the  first  cases  of  typhus  fever  which  are  developed 
in  any  locality  should  be  closely  watched.  They  should  be  immediately 
quarantined.  The  dwelling  in  which  the  fever  has  broken  out  should  be 
depopulated — that  is,  in  a  tenement-house  in  which  the  fever  has  made 
its  appearance,  all  the  families  should  be  removed,  and  the  house  should 
be  thoroughly  disinfected.  The  disinfection  must  be  thorough,  not  for  a  few 
hours,  but  for  one  or  two  days,  and  afterward  the  house  should  remain 
open  for  the  free  circulation  of  air  for  a  considerable  length  of  time  before 
persons  should  be  allowed  again  to  inhabit  the  rooms.  If  typhus  fever 
occur  in  the  dwellings  of  the  wealthy,  their  houses  must  be  quarantined. 
All  persons  must  be  prevented  from  visiting  them,  and  all  persons  within 
the  dwelling  must  be  prevented  from  going  abroad.  After  the  sick  have 
recovered,  there  mnst  be  the  same  thorough  disinfection  as  in  the  tene- 
ment-house. Usually,  in  epidemics  of  typhus  fever  there  are  certain  foci 
from  which  the  disease  spreads.  Perhaps  the  points  from  which  the  con- 
tagion more  especially  emanates  are  within  an  area  of  half  a  square  mile, 
and  yet  the  disease  may  have  been  prevailing  for  two,  three,  or  even  four 
months.  Under  such  circumstances  it  is  possible  to  prevent  the  spread  of 
the  fever  by  the  means  Just  indicated. 

As  far  as  its  management  in  hospitals  is  concerned,  I  would  say  :  never 
undertake  it  within  brick  or  stone  enclosures.  If  possible,  patients  should 
be  placed  in  broad  pavilions  or  tents,  so  that  the  largest  possible  amount  of 
fresh  air  shall  be  in  circulation  about  them.  It  is  not  sufficient  to  have 
free  ventilation  in  the  ordinary  acceptation  of  that  term.  The  opening  of 
a  window  will  not  accomplish  the  desired  result.  Eemove  all  the  windows 
in  a  room,  regardless  of  the  cold,  and  cover  the  patients  with  a  sufficient 
number  of  blankets  to  keep  them  warm.  Allow  fresh  air  to  surround  them. 
When  typhus  fever  manifests  itself,  it  can  readily  be  understood  how  im- 
portant it  is  that  the  guardians  of  the  poor  should  not  only  enforce  cleanli- 
ness, but  that  they  should  feed  the  poor  better  than  at  other  times.  If 
cleanliness  is  observed,  the  dwellings  thoroughly  disinfected,  and  the  poor 


TYPHUS   FEVEE.  733 

well  fed,  the  most  virulent  epidemic  can  soon  be  stayed.  The  effects  pro- 
duced by  such  measures  are  sometimes  wonderful.  In  the  year  ISGl,  at  the 
commencement  of  the  epidemic  (as  has  been  stated),  the  first  case  occurred 
in  a  tenement-house  in  a  down-town  street,  in  New  York  City  ;  it  was  six 
weeks  before  it  spread  from  that  locality.  The  spread  of  the  fever  should 
have  been  stopped  at  that  point ;  but  veiy  little  attention  was  paid  to  it, 
and  it  began  to  spread  from  one  point  to  another,  until  some  six  or  seven 
thousand  cases  were  developed.  Many  prominent  citizens  sickened  with 
the  fever  and  died.  This  epidemic  could  have  been  prevented  had  measures 
been  taken  early  to  prevent  the  spread  of  the  disease.  It  seemed  to  me  that 
the  authorities  of  New  York  City  were  responsible  for  a  large  proportion  of 
the  deaths  which  occurred  during  the  prevalence  of  that  epidemic. 

Medicinal  treatment  is  powerless  either  to  arrest  the  progress  or  shorten 
the  duration  of  this  fever,  but  it  can  undoubtedly  save  lives  that  would 
otherwise  be  lost,  and  hasten  convalescence.  The  first  point  under  this 
head  relates  to  neutralizing  the  poison.  I  have  found  no  medicinal  agent 
which  can  neutralize  or  destroy  typhus  poison,  or  which  has  power  to 
arrest  the  progress  or  shorten  the  duration  of  this  fever.  Different  agents 
have  been  proposed  for  the  accomplishment  of  this  result,  according 
to  the  views  held  in  regard  to  the  nature  of  the  typhus  poison  and  its 
effects  upon  the  system.  At  one  time  the  mineral  acids  were  supposed  to 
possess  this  power,  and  were  administered  for  that  purpose,  but  have  now 
fallen  into  disuse.'  The  internal  use  of  carbolic  acid,  chlorine  water, 
creasote,  and,  more  recently,  salicylic  acid  has  been  recommended  for  the 
same  purpose.  The  inhalation  of  oxygen  gas  has  also  been  thought  to  be 
of  service  in  arresting  the  blood-changes,  and  thus  preventing  the  poison 
from  having  its  customary  effect  upon  the  system.  By  the  stimulation 
which  it  produces,  the  patient  may  be  brought  out  of  an  apparent  state  of 
coma,  and  revive  in  a  marked  degree ;  but  the  relief  is  only  temporary. 
For  a  time  the  patient  may  improve,  his  consciousness  return,  and  his  ap- 
pearance indicate  that  convalescence  is  established ;  but  his  unfavorable 
symptoms  will  return,  and  it  will  become  quite  evident  that  the  oxygen 
has  not  neutralized  the  typhus  poison. 

Fresh  air  is  the  only  thing  which  I  have  found  to  have  power  to  neutral- 
ize the  poison  of  typhus  fever.  It  certainly  possesses  this  power  when  ex- 
ternal to  the  body.  For  example  :  place  a  patient  sick  with  typhus  fever 
in  a  well  ventilated  board  pavilion,  or  in  a  tent,  where  an  abundance  of 
fresh  air  can  circulate  about  him,  and  it  is  almost  impossible  for  him  to 
communicate  the  disease  to  a  healthy  person.  Again,  place  a  patient  in 
a  closed  room,  perhaps  twelve  by  fourteen  feet  square,  let  a  healthy  person 
remain  with  him  a  single  night — probably  a  much  shorter  time  will  be 
sufficient — and  the  latter  will  be  almost  certain  to  contract  the  disease. 
Why  is  the  disease  more  readily  communicated  in  the  one  case  than  in  the 
other  ?  Certainly  the  fresh  air  which  circulated  about  the  typhus  fever 
patient  must  have  prevented  contagion.    Fresh  air,  when  inhaled,  produces 

1  Though  a  very  recent  work  (Wikon  on  Fevers)  says  nitro-miiriatic  acid,  alternating  with  turpentine  is 
preferred  in  the  United  States,  and  that  mineral  acids  occupy  the  highest  rank. 


734  ACUTE   GENERAL   DISEASES. 

to  a  greater  or  less  extent  the  same  effect.  How  do  we  know  this  ?  As  a 
clinical  fact,  I  have  seen  a  typhus  fever  patient,  who  was  apparently  over- 
whelmed by  the  poison — who  within  forty-eight  hours  from  the  commence- 
ment of  the  attack  was  m  a  state  of  coma,  with  high  temperature,  a  rapid 
pulse,  etc.,  and  all  symptoms  indicating  that  he  was  fast  succumbing  to 
the  disease — when  brought  from  a  crowded  tenement  house  and  placed  in 
a  tent  where  he  could  inhale  plenty  of  fresh  air,  within  four  or  five  hours 
from  the  time  of  admission  begin  to  rally,  and  go  on  to  recovery.  Fresh 
air  was  the  only  remedial  agent  employed. 

If  fresh  air  does  not  neutralize  the  poison,  it  certainly  has  some  effect  in 
eliminating  the  poison,  and  thus  mitigating  the  severity  of  the  fever,  and, 
perhaps,  shortening  its  duration.  It  may  be  regarded  as  a  I'emedial  agent, 
for  it  certainly  is  of  greater  value  than  any  so-called  remedial  agent  at  our 
command.  To  accomplish  the  best  results,  place  three  or  four  patients  in 
a  tent  twenty  feet  square ;  the  fly  of  the  tent  should  be  thrown  up,  and  if 
the  weather  is  cold,  the  patients  should  be  well  covered  with  blankets.  By 
this  means  all  the  advantages  of  free  ventilation  will  be  insured.  The 
question  arises:  what  therapeutical  agents  can  be  employed  with  advantage 
in  order  to  accomplish  the  desired  results  ? 

It  is  of  the  greatest  importance  to  reduce  temperature  and  to  sustain 
heart-power.  The  former  is  of  as  great  importance  in  typhus  as  in  typhoid 
fever,  and  the  same  rules  should  govern  one  with  regard  to  the  agents  to  be 
employed,  and  the  mode  of  their  employment.  As  in  the  management  of 
typhoid,  so  in  this  fever,  we  have  two  antipyretic  agents,  namely,  the  sul- 
phate of  quinine  and  the  application  of  cold  to  the  surface.  These  agents 
may  be  employed  separately  or  in  conjunction.  The  temperature  rise& 
more  quickly  in  typhus  than  in  typhoid,  after  it  has  been  reduced  by  tha. 
cold  bath,  and  all  through  the  early  part  of  the  fever  one  will  be  obliged 
to  resort  to  the  bath  much  more  frequently  than  in  typhoid. 

The  rules  for  the  administration  of  the  baths  in  typhus  fever  diffei 
somewhat  from  those  that  obtain  in  typhoid.  In  typhus  fever,  as  soon  ah 
the  temperature  of  the  patient  rises  to  104°  F.,  he  must  be  placed  in  a 
bath  the  temperature  of  which  is  about  ten  degrees  below  that  of  the 
patient ;  gradually,  by  the  addition  of  ice  or  ice-water,  bring  the  tem- 
perature of  the  bath  down  to  68°  or  70°  F.  He  must  be  kept  in  the  bath 
until  his  temperature  falls  to  101°  or  102°  F.,  then  taken  out,  quickly 
dried  and  placed  in  bed.  For  some  time  after  the  removal  from  the  bath, 
the  axillary  temperature  will  continue  to  fall,  as  the  trunk  parts  with  heat 
to  the  extremities.  As  soon  as  the  temperature  rises  again  to  104°  F.,  the 
patient  must  receive  another  bath.  If  he  suffers  with  intense  pain  in  the 
head,  or  is  actively  delirious  during  the  bath,  ice-bags  may  often  be  applied 
to  the  head  with  benefit.  If  the  cold  baths  do  not  readily  reduce  the  pa- 
tient's temperature,  or  if  the  fall  is  of  short  duration,  antipyretic  doses  of 
quinine  must  be  administered,  according  to  the  rules  given  for  its  adminis- 
tration in  the  treatment  of  typhoid  fever.  As  soon  as  the  first  week  of  the 
disease  is  past,  having  kept  the  patient's  temperature  below  103°  F.,  it  will 
not  usually  be  necessary  or  advisable  to  continue  the  baths.     In  most  cases 


TYPHUS   FEVEE.  735 

antipyretic  doses  of  quinine  will  be  found  sufficient  to  keep  down  the  tem- 
perature. 

Now,  if  not  before,  there  will  be  evidence  of  heart  failure,  and  the  question 
presents  itself  :  shall  alcoholic  stimulants  be  administered  ?  The  history 
of  alcoholic  stimulants  in  the  treatment  of  typhus  fever  dates  back  to  the 
teachings  of  Graves  and  Stokes,  since  which  time  until  quite  recently  they 
have  constituted  an  important  element  in  the  treatment  of  this  fever,  re- 
ceiving the  approval  of  almost  the  entire  profession.  Even  at  the  present 
day  the  rule  is  to  administer  alcohol  in  large  quantities  in  fever.  Most 
writers  have  regarded  a  frequent  feeble  pulse,  with  feeble  cardiac  impulse, 
even  though  cerebral  symptoms  may  be  present,  as  certainly  indicating  the 
administration  of  alcoholic  stimulants.  The  directions  were,  to  com- 
mence their  administration  early,  and  in  sufficient  quantities  to  control 
the  pulse.  It  was  thought  that  the  earlier  their  administration  was  com- 
menced, the  better  the  chance  for  recovery,  as  the  failure  of  heart-power, 
which  makes  its  appearance  in  the  later  stages  of  typhus,  would  be  pre- 
vented. No  limit  was  given  as  to  the  quantity  to  be  administered.  The  ob- 
ject to  be  accomplished  was  to  control  the  pulse.  This  could  in  most  cases 
be  done  for  a  time,  but  as  the  disease  advanced,  and  the  patient  became 
more  and  more  overwhelmed  by  the  typhus  poison,  alcohol  lost  the  power 
of  giving  force  to  the  pulse.  Under  such  circumstances,  the  rule  was  to 
give  it  ad  libitum,  for  alcohol  was  regarded  as  the  only  agent  by  which  the 
life  of  the  patient  could  be  saved.  After  carefully  studying  for  two  years 
the  action  of  alcohol  on  typhus  fever  patients,  I  became  convinced  that 
in  some  patients,  if  not  in  all,  those  who  were  severely  ill,  especially 
where  there  was  interference  with  the  function  of  the  kidneys,  its  bene- 
ficial effects  were  doubtful,  if  its  action  was  not  decidedly  injurious. 

That  stimulants  will  control  the  pulse  and  sustain  the  heart's  action  for 
a  time,  there  can  be  no  question  ;  but  I  found  that  in  all  severe  cases 
there  came  a  time  when  alcohol,  in  however  large  doses  it  was  given, 
ceased  to  have  power.  Besides,  it  must  be  remembered  that  large  quanti- 
ties of  alcohol  thus  administered  disturb  nutrition,  lessen  secretion,  pre- 
vent the  elimination  of  urea,  and  tend  to  induce  a  state  of  coma,  which 
cannot  readily  be  distinguished  from  that  induced  by  the  disease  itself,  all 
of  which  must  necessarily  greatly  increase  the  danger  of  a  fatal  termina- 
tion. ' 

>  During  the  prevalence  of  the  epidemic  of  typhus  fever  in  1864, 1  took  charge  of  the  fever-tents  on 
Blackwell's  Island,  with  the  intention  of  testing  the  effect  of  the  withdrawal  of  stimulants  in  the  treatment 
of  typhus  fever.  In  my  earlier  professional  life  I  was  thoroughly  imbued  with  the  idea  (for  I  was  almost 
bom  into  the  profession  from  a  typhus  fever  ward)  that  alcohol  was  a  necessity  in  the  treatment  of 
typhus.  My  house  physician,  Dr.  Engs,  who  took  ihe  immediate  care  of  the  fever-tents  under  my  direction, 
had  had  a  large  experience  in  the  treatment  of  typhus  fever  in  Bellevue  Hospital,  had  there  contracted  the 
disease,  and  believed  that  his  life  had  been  saved  by  the  free  use  of  stimulants.  As  we  assumed  the 
charge  of  the  tents  I  ordered  that  no  stimulants  or  medicines  should  be  administered  to  any  patient. 
The  cases,  as  they  were  brought  into  the  tents  from  the  city,  were  of  as  severe  a  type  as  any  we  had 
treated  in  Bellevue  Hospital  ;  some  were  in  a  state  of  coma,  with  an  imperceptible  radial  pulse,  and 
all  the  signs  of  speedy  dissolution— conditions  which  I  had  been  educated  to  regard  as  most  cer- 
tainly indicating  the  free  administration  of  stimulants.  The  rule  which  I  established  was  faithfully  car- 
ried out,  with  the  following  results  :  while  the  fever  was  in  Bellevue  the  ratio  of  mortality  was  one  death 
in  every  five  ;  and  in  the  tents  one  in  sixteen.  I  do  not  claim  that  the  great  diminution  in  the  ratio  of 
mortality  in  the  tents,  as  compared  with  that  of  Bellevue  Hospital,  was  due  to  the  non-administration  of 


^736  ACUTE    GEISTEEAL   DISEASES. 

Typhus  fever  patients  under  twenty-five  years  of  age  rarely  require,  or 
are  benefited  by,  alcohol,  unless  they  were  of  intemperate  habits  prior  to 
the  attack.  To  the  old  and  feeble  its  occasional  ad  minis  fcration  may  be  of 
great  benefit,  and  at  times  be  the  means  of  saving  life.  A  copious  dark 
eruption,  with  coldness  of  the  extremities,  especially  indicates  the  use  of 
alcohol.  As  a  rule,  delirium,  headache,  scanty  urine,  and  intense  surface 
heat  contraindicate  the  use  of  alcohol.  In  any  case  when  it  is  decided  to 
administer  spirits,  carefully  watch  the  effect  of  the  first  few  doses ;  the 
same  rules  govern  here  that  were  laid  down  for  the  administration  of  stimu- 
lants in  typhoid  fever.  It  is  impossible  to  give  any  positive  rule  as  regards 
the  quantity  of  stimulants  required  in  each  case.  It  is  very  rarely  neces- 
sary at  any  time  during  the  fever  to  give  more  than  eight  ounces  of  brandy 
during  twenty-four  hours.  If  this  amount  will  not  sustain  the  heai't- 
power,  I  am  confident  larger  quantities  will  fail  to  do  it,  and  also  that  such 
administration  has  hastened  the  fatal  issue.  As  soon  as  the  symptoms  on 
account  of  which  the  alcohol  may  have  been  resorted  to  are  relieved,  the 
quantity  must  be  reduced,  or  its  administration  altogether  stopped. 

I  do  not  altogether  condemn  the  use  of  stimulants  in  typhus  fever,  but 
I  do  so  as  regards  stimulants  as  a  "  plan  of  treatment  ;"  and  where  the 
patient  can  be  freely  exposed  to  fresh  air,  I  doubt  if  their  use  is  often  re- 
quired. To  diminish  the  frequency  of  the  pulse  cardiac  sedatives  have  been 
employed,  such  as  veratrum  viride,  aconite,  and  digitalis. 

The  rapid  pulse  in  typhus  fever,  after  the  first  onset  of  the  disease,  often 
is  not  due  to  the  high  temperature,  but  to  the  failure  of  heart-power ; 
when  such  is  the  case,  digitalis  should  be  employed.  Digitalis  diminishes 
the  frequency  of  the  pulse,  by  increasing  the  power  of  the  heart,  and  at  the 
same  time  it  increases  the  secretion  of  urine,  which  frequently  is  scanty, 
and  thus,  to  a  limited  extent,  it  becomes  an  eliminative.  From  four  to 
six  drachms  of  the  infusion  of  digitalis  may  often  be  given  with  benefit, 
during  twenty-four  hours.  If  the  heart-power  cannot  be  sustained  by  the 
moderate  use  of  stimulants  and  by  digitalis  (given  as  indicated),  no  more 
can  be  done  so  far  as  remedial  agents  are  concerned.  The  treatment  of  the 
special  symptoms  of  typhus  fever  require  only  a  passing  notice.  The  head- 
ache, when  intense,  is  best  relieved  by  cold  applications  in  the  form  of  ice- 
bags.  If  it  is  accompanied  by  intolerance  of  light,  a  blister  to  the  back  of 
the  neck  will  be  found  to  give  relief. 

Sleeplessness  in  any  stage  of  the  disease,  if  it  continues  for  two  or  three 
days,  must  be  relieved,  for  it  is  of  itself  sufiicient  to  cause  a  fatal  termina- 
tion. If  sleep  does  not  follow  the  application  of  cold  to  the  head,  opiates 
may  be  administered  in  full  doses.  I  have  seen  typhus  fever  patients  that 
had  not  slept  for  forty-eight  hours  drop  into  a  quiet  sleep  within  a  few 
hours  after  they  had  been  exposed  to  free  ventilation.  Great  care  should 
be  exercised  that  their  apartments  are  kept  perfectly  quiet  and  darkened. 

stimulants  in  the  one  case,  and  their  free  administration  in  the  other.  I  do,  however,  most  certainly 
affirm  that  my  experiments  in  the  tents  convinced  me  that  the  beneficial  effects  which  had  been  ascribed 
to  the  use  of  alcohol  in  typhus  fever  were  not  fairly  due  to  it.  Although  I  would  not  entirely  discard 
the  use  of  alcohol  in  the  treatment  of  typhus,  still  I  would  greatly  limit  its  use  and  give  it  only  as  an 
occasional  aid,  to  carry  a  patient  over  some  time  of  peculiar  danger  from  heart  failure. 


TYPHUS   FEVER.  737 

When  delirium  and  cerebral  symptoms  are  associated  with  sleeplessness, 
hydrate  of  chloral  may  be  carefully  employed.  Stupor  is  to  be  counter- 
acted by  promoting  the  action  of  all  the  excreting  organs,  applying  exter- 
nal stimulants,  and  administering  diffusible  stimulants,  the  most  service- 
able of  which  are  black  coffee,  musk,  and  camphor.  In  the  early  stage  of 
the  disease  the  cold  douche  may  be  employed. 

Two  remedies  have  been  recommended  for  the  coma  of  tyjahus,  namely  : 
Talerian  and  phosphorus  ;  neither  of  these  remedies  has  seemed  to  me  to 
be  efficacious.  When  there  are  evidences  of  great  prostration  in  connection 
with  any  of  these  special  symptoms  to  which  reference  has  been  made, 
the  moderate  administration  of  stimulants  may  be  resorted  to,  and  if  relief 
follows  the  first  few  doses  their  use  may  be  continued.  In  the  treatment 
of  the  complications  which  are  liable  to  occur  during  the  course  of  typhus 
fever,  one  must  be  guided  by  general  principles  and  by  the  symptoms 
in  each  individual  case,  it  being  always  remembered  that  the  primary  dis- 
ease has  a  tendency  to  induce  great  nervous  prostration  and  depi'ession,  and 
that  the  heart's  action  forbids  the  use  of  all  depleting  remedies,  and  indi- 
cates a  supporting  plan  of  treatment.  The  pulmonary  and  laryngeal  com- 
plications, as  well  as  erysipelas,  bed-sores  and  gangrene  are  to  be  managed 
in  the  same  manner  as  was  proposed  when  they  occur  as  complications  of 
typhoid  fever. 

The  diet  is  of  primary  importance.  Though  the  patient  refuse  all  nourish- 
ment, if  possible  he  must  be  required  or  even  compelled  to  take  it.  As  the 
digestive  powers  are  impaired,  great  care  is  required  in  selecting  and  admin- 
istering the  proper  nourishment,  and  it  must  be  given  at  stated  intervals, 
varying  from  one  to  two  hours.  Care  must  be  taken  not  to  overfeed — 
much  harm  may  be  done  in  this  way.  When  the  patient  clinches  his  teeth 
and  obstinately  refuses  all  food,  or  is  unable  to  swallow,  his  life  may 
sometimes  be  saved  by  pouring  liquid  nourishment  into  the  stomach  by 
means  of  a  long  tube  passed  thi-ough  the  nose.  Milk  best  serves  the  pur- 
pose as  an  article  of  diet.  It  may  be  given  ice-cold,  if  desired,  and  in  such 
quantities  as  the  stomach  can  receive  and  digest.  If  more  concentrated 
nutrition  is  desirable,  the  yolk  of  eggs  may  be  beaten  up  and  added  to  the 
milk. 

The  management  of  patients  during  convalescence  from  typhus  fever  is 
a  matter  of  very  great  importance.  As  soon  as  the  fever  ceases,  most  pa- 
tients convalesce  rapidly  unless  there  is  some  complication,  and  the  chief 
duty  of  the  physician  is  to  prevent  premature  exertion  and  exposure  tO' 
cold,  and  to  restrain  the  patient  in  the  gratification  of  an  inordinate  appe- 
tite. At  this  time  porter  or  ale  may  be  taken  with  benefit.  The  mineral 
acids,  Peruvian  bark,  and  iron  may  also  be  given  as  tonics  ;  these  are  par- 
ticularly called  for  when  the  pulse  is  slow  and  feeble.  It  is  important, 
to  guard  against  any  sudden  physical  effort  during  the  early  period  of  con- 
valescence, as  it  may  lead  to  coagulation  of  blood  in  the  veins.  An  opiate 
or  hydrate  of  chloral  is  sometimes  required  to  produce  sleep  during  convales- 
cence. In  all  cases  great  benefit  will  be  derived  from  a  temporary  change 
of  residence  and  daily  exercise  in  the  open  air. 
47 


738  ACUTE   GEJSTEEAL  DISEASES. 


EELAPSING    FEVER. 


This  has  been  called  famine  and  seven-day  fever,  synocha,  typhinia, 
mild  yelloiv  fever,  typhus  recurrens,  dynamic  fever.  The  French  call  it 
'^  Fievre  a  Eechute  ;  "  and  the  G-ermans,  "  Hungerpest." 

Relapsing  fever  is  no  new  form  of  disease.  It  was  described  more  than 
a  century  ago  by  Dr.  Kutty/  and  since  that  time  has  prevailed  as  an  epi- 
demic disease  in  most  of  the  countries  in  northern  Europe."  There  is  no 
reliable  history  of  its  occurrence  as  an  epidemic  in  this  country  until  1872- 
3,  when  an  epidemic  prevailed  in  New  York  City.  It  has  been  reported  that 
in  the  year  1844  a  vessel  landed  in  Philadelphia  passengers  ill  of  relapsing 
fever.  At  one  time,  while  typhus  fever  was  prevailing  in  Buffalo,  some  twelve 
or  fourteen  cases  of  relapsing  fever  were  reported  ;  but  it  is  altogether  prob- 
able that  they  were  cases  of  irregular  typhus  fever,  for  when  relapsing  fever 
has  been  introduced  into  a  locality  it  is  not  limited  to  one  or  two  dozen 
cases. 

Morbid  Anatomy. — In  this  disease  there  are  no  pathological  lesions  that 
are  characteristic.  There  are  changes  present  in  some  of  the  organs  which 
very  closely  resemble  those  met  with  in  typhus. 

Spleen. — In  the  majority  of  autopsies,  if  death  has  occurred  in  the  ac- 
tive period  of  the  disease,  the  spleen  will  be  found  increased  in  size,  its 
capsule  thickened,  smooth,  tense  and  slightly  clouded,  the  trabeculae  of  the 
organ  increased,  and  the  Malpighian  tufts  more  j)rominent  than  normal. 
In  some  cases  the  spleen  will  be  found  enlarged,  soft,  flabby,  and  even  dif- 
fluent. There  is  no  uniform  change  in  its  substance,  although  it  is  always 
increased  in  size  during  the  active  period  of  the  disease.  After  this  period 
has  passed,  it  will  be  found  diminished  in  size,  and  its  surface  will  pre- 
sent a  shrivelled  appearance,  with  the  capsule  rolled  into  folds.  Infarc- 
tions (not  embolic  in  origin)  are  often  found.  In  many  cases  a  number  of 
Tounded  or  irregular  miliary  masses,  of  a  dull  yellow  color,  will  be  found, 
containing  granular  detritus,  cell-elements,  and  free  nuclei. 

Liver. — During  the  active  period  of  the  fever,  the  liver  will  also  be  found 
enlarged.  The  gall-bladder  is  generally  distended  with  dark  yellow  and 
viscid  bile. 

Kidneys. — The  kidneys  are  increased  in  size,  the  increase  being  due  to 
congestion  of  the  cortical  substance.  There  is  a  granular  infiltration  of 
the  epithelium  of  the  uriniferous  tubes,  a  change  similar  to  that  noticed  in 
other  fevers.     Small  hemorrhages  stud  the  whole  organ  in  severe  cases. 

The  urine  often  presents  a  cloudy  appearance. 

Intestines. — Usually  enlargement  of  the  glandular  follicles  of  the  intes- 
tines will  be  found.  The  solitary  glands  are  more  commonly  affected,  but 
even  the  Peyerian  patches  may  present  the  ''shaven-beard"  appearance. 
The  mesenteric  glands  are  slightly  enlarged  in  severe  cases.  Their  appear- 
ance is  similar  to  that  noticed  in  typhus. 

1  John  Rutty,  "  A  Chronological  History  of,  etc.,  etc.,  in  Dublin,  from  1725  to  1765."    London,  1770. 

2  Accounts  in  Hippocratic  writings  leave  no  doubt  but  that  it  prevailed  3,000  years  ago  in  islands  off 
Thrace. 


EELAPSIKG   FEVEE.  739 

Mucous  Membranes. — In  the  majority  of  cases,  small  spots  of  blood- 
extravasation  will  be  found  upon  the  mucous  surfaces,  especially  the 
membranes  of  the  stomach  and  intestines,  and  they  may  be  found  on  the 
mucous  membrane  of  the  bronchial  tubes.  The  stomach  shows  small 
blood-extravasations  when  vomiting  has  been  severe  during  life,  or  when 
there  has  been  black  vomit.  These  spots  of  ecchymosis  are  perhaps  as  con- 
stant as  any  pathological  lesions  of  the  disease. 

Blood. — The  blood  coagulates  imperfectly,  as  in  typhus.  Spirilli  are 
discoverable,  oftentimes,  provided  death  occurs  in  an  active  stage.  The 
heart  presents  no  constant  changes.  In  some  cases  fine  granular  infiltration 
or  vitreous  degeneration  of  the  muscular  fibres  has  been  observed.  This 
same  granular  infiltration  is  also  sometimes  seen  in  the  voluntary  muscles. 
Coagula  are  rare.  ^  Diffuse  or  circumscribed  changes  in  the  marrow  of  the 
bones  occur,  according  to  Poufick.  The  lymphoid  elements  increase,  and 
large  cells,  filled  with  numerous  oil  globules,  appear  along  the  track  of 
vessels.     Necrotic  softening  of  the  marrow  has  been  seen  in  severe  cases. 

Etiology. — There  have  been  differences  of  opinion  and  much  discussion 
in  regard  to  the  etiology  of  this  disease.  At  the  present  time  it  seems  to 
be  the  unanimous  opinion  of  those  who  have  had  the  best  opportunities  for 
study,  that  it  is  a  contagious  disease,  and  that  it  is  a  distinct  type  of  fever. 
Although  it  presents  many  phenomena  which  ally  it  to  typhus,  and  many 
other  phenomena  which  ally  it  to  malarial  fever,  it  is  neither  typhus  nor 
malarial,  but  is  a  distinct  type  of  fever  having  a  distinct  poison. 

From  observations  which  have  been  made  upon  the  blood  of  patients 
suffering  from  this  fever,  distinct  organisms  which  have  the  power  of  de- 
veloping the  fever  are  thought  to  have  been  found.  This  parasitic  organ- 
ism [spirillum  Ohermeieri)  is  a  spiro-bacterium,  unlike  that  sometimes  found 
in  water  and  in  mucus  from  the  mouth.  But  Billroth  and  Manassein  have 
found  them  in  fluid  from  noma  and  in  a  cyst  of  the  antrum.  Several 
German  observers,  Cohnhein  among  them,  have  given  drawings  of  these 
organisms,  which  seem  to  be  little  spiral  lines  that  are  constantly  under- 
going a  twisting,  rotary,  rapid  motion,  and  these  observers  tell  us  that 
they  are  distinctive  of  this  form  of  disease,  and  are  always  present  during 
its  active  period.^  They  are  absent  in  the  interval  between  the  primary 
attack  and  the  relapse,  but  are  to  be  seen  as  soon  the  relapse  occurs.  With 
reference  to  these  animal  organisms,  and  others  which  are  claimed  to  be 
the  cause  of  fevers  and  other  infectious  diseases,  while  it  may  be  true  that 
distinct  forms  are  found  in  different  forms  of  fever,  I  question  very  much 
if  by  the  introduction  of  these  organisms  into  the  system  the  fever  can  be  de- 
veloped. In  relapsing  fever,  more  than  in  any  other,  have  these  organisms 
been  seen  and  studied,  and  yet  all  experimenters  have  failed  to  develop  the 
fever  from  them.  This  fact  gives  those  who  do  not  believe  that  living 
organisms  are  the  cause  of  infectious  diseases  a  very  strong  argument  ;  yet, 

'  Ponfick,  in  Virchow's  Archiv.,  B.  60,  p.  153,  1874,  states  that  the  cardiac  degeneration  may  be  so 
extensive  as  to  cause  death,  resembling  the  heart  of  phosphorus  poisoning. 

2  Vide  Centralblatt,  1873,  and  Virchow's  Archiv.,  Bd.  47.  Also  Obermeier's  article  in  Berliner  Klin. 
Wochen.,  No.  3.5,  1873.  It  is  from  two  to  si.^  times  as  long  as  a  red  blood  disc,  and  no  thicker  than  the 
finest  fibrin-fibril.    It  is  readily  destroyed  by  nearly  every  reagent. 


740  ACUTE   GENERAL   DISEASES. 

on  the  other  hand,  does  nothing  for  those  who  hold  the  chemical  theory  ol 
the  disease.' 

Clinical  experience  has  shown  that  relapsing  fever  is  a  contagious  disease, 
and  can  be  propagated  by  personal  contagion.  The  disease  is  not  neces- 
sarily accompanied  by  starvation,  for  it  is  developed  among  those  who 
are  well  fed  as  well  as  among  those  who  are  badly  nourished.  As  in  typhus 
fever,  there  is  a  connection  between  the  development  of  an  epidemic  of  this 
fever  and  imperfect  ventilation  and  bad  hygiene. 

I  had  never  seen  a  case  of  relapsing  fever  until  1870,  when  the  epidemic 
prevailed  in  New  York  City.  At  that  time  patients  were  brought  into  my 
wards  in  Bellevue  Hospital  with  a  fever  differing  from  typhus  fever  by  the 
absence  of  an  eruption ;  from  intermittent,  in  the  order  of  its  develop- 
ment, and  not  closely  resembling  remittent  fever.  It  seemed  to  me  an 
irregular  form  of  malarial  fever,  differing  from  any  with  which  I  was 
acquainted.  Eight  cases  were  brought  in.  From  these  my  house  phy- 
sician contracted  the  fever,  and  during  his  illness  I  reached  the  diagnosis  of 
relapsing  fever.  Subsequently  we  had  large  numbers  of  relapsing  fever 
patients,  and  a  hospital  was  established  for  their  reception  on  Hart's 
Island.  In  every  case  that  occurred  at  that  time,  where  the  origin  of  the 
fever  could  be  traced,  it  was  found  that  there  had  been  direct  exposure,  and 
it  was  established  beyond  doubt  that  the  first  cases  were  brought  from  Ire- 
land. The  contagious  character  of  the  affection  was  also  established  by 
the  fact  that  all  the  nurses  and  all  the  physicians  who  were  in  immediate 
attendance  upon  the  sick  contracted  the  fever.  If  a  patient  was  placed  in 
a  bed  previously  occupied  by  a  person  sick  with  relapsing  fever,  before  it 
had  been  cleaned,  he  was  almost  certain  to  contract  the  disease.  The  closer 
the  contiguity  the  more  certain  is  the  individual  to  contract  the  fever. 

At  the  time  of  this  epidemic  we  found  no  evidence  that  the  fever  was 
conveyed  by  clothing,  although  some  British  writers  have  claimed  that  it  can 
be  done.  When  our  patients  were  admitted  into  the  hospital,  their  clothing, 
as  it  was  removed,  was  simply  washed,  not  disinfected  in  any  special  manner, 
then  packed  away,  and  not  a  single  person  who  was  thus  brought  in  imme- 
diate contact  with  the  clothing  contracted  the  disease.  There  is  no  immu- 
nity from  a  second  attack.  The  period  of  incubation  ranges  between  five 
and  seven  days,  rarely  nine.^ 

Symptoms. — The  symptoms  which  usher  in  relapsing  fever  are  usually 
well  marked.  If  there  are  any  prodromes,  they  are  the  same  as  in  typhoid 
fever  {q.  v.). 

It  is  sudden  in  its  advent.  This  is  marked  by  a  severe  rigor  or  by  a  dis- 
tinct chill.  Accompanying  the  chill  there  is  frontal  headache,  vertigo,  pain 
in  the  limbs  and  joints,  more  or  less  pain  in  the  back,  nausea  and  not  in- 

1  Very  recently  spirilU  have  been  found  to  develop  in  blood  taken  from  relapsing  fever  patients, 
when,  on  first  withdrawal,  none  could  be  discovered.  Small,  rounded  bodies,  called  spores,  have  been 
found  in  the  blood  by  Albrecht,  and  from  these,  it  is  supposed,  that  spirilli  develop.  Cent.  f.  d.  Med. 
Wissenschaften,  May  22,  1880.  Dr.  Carter,  of  Bombay,  has  succeeded  in  reproducing  the  disease  by  in- 
oculation in  small  monkeys.     "Medico-Chir.  Trans.,"  p.  125,  1880. 

2  In  some  cases  the  fever  begins  a  few  hours  after  exposure.  Lebert  found  75  per  cent,  of  cases  to  have 
an  incubatory  period  within  seven  days,  and  of  these  more  than  one-half  sickened  within  three  days  after 
exposure. 


EELAPSING   FEVER.  74l 

frequently  vomiting.'  A  rapid  rise  in  temperature  follows  the  chill,  and 
with  the  pyrexia  the  headache  increases,  as  does  also  the  pain  in  the  limbs, 
especially  about  the  joints.  Sweats  may,  at  first,  follow  the  rigors.  There 
is  vomiting,  at  first  only  of  the  simple  contents  of  the  stomach,  afterwards 
of  yellowish  material.  This  may  be  followed  by  the  ejection  of  a  dark- 
colored  material,  which  very  closely  resembles  the  black  vomit  of  yellow 
fever.  In  this  disease  the  rise  in  temperature  is  always  rapid,  and  usually 
attains  its  highest  point  within  the  first  twenty-four  hours;  during  this 
time  it  may  rise  to  104°  F.,  or  even  as  high  as  109°  F.  From  this  time, 
for  two  or  three  days,  there  is  usually  very  little  variation.  With  tlie  occur- 
rence of  the  chill  aiid  fever  there  is  also  a  rapid  increase  in  the  frequency 
of  the  pulse.  In  uo  disease  does  the  pulse  so  quickly  become  rapid  as  in 
relapsing  fever.  It  is  not  uncommon  for  it  to  reach  140,  150,  or  even  160 
beats  per  minute  within  the  first  twenty-four  hours.  It  is  usually  small 
and  compressible,  sometimes  dicrotic.  The  mind  is  clear.  There  is  nothing 
peculiar  about  the  countenance  of  the  patient,  but  it  presents  the  ordinary 
appearance  noticed  in  an  active  febrile  excitement.  Sleeplessness  is  often 
present  on  account  of  the  severe  pains  in  the  limbs.  As  the  disease  pro- 
gresses the  patient  becomes  more  and  more  prostrated  ;  by  the  second  day 
he  may  be  unable  to  turn  in  bed.  The  arthritic  pains  increase  in  severity 
and  often  become  the  most  distressing,  symptoms  of  the  fever. 

As  early  as  the  second  day,  patients  begin  to  complain  of  a  feeling  of 
weight  and  uneasiness  in  the  upper  part  of  the  abdomen,  more  severe  in 
the  left  than  in  the  right  hypochondrium.  Profuse  sweats  are  common 
about  the  second  day,  but  they  afford  no  relief  to  the  urgent  symptoms. 
Usually,  there  is  considerable  enlargement  and  tenderness  of  the  liver.  The 
spleen,  also,  becomes  rapidly  enlarged,  and  its  enlargement  is  attended  with 
quite  severe  pain  and  tenderness.  Moderate  meteorismus  is  not  uncommon. 
The  muscles  of  the  body  are,  however,  the  seat  of  the  most  severe  pain, 
which  is  increased  by  movement  and  by  pressure ;  the  pain  is  piercing  and 
lancinating  in  character.  On  account  of  this  pain,  the  patient  usually  lies 
perfectly  quiet ;  he  is  not  restless  but  sleepless.  Delirium  is  not  an  infre- 
quent symptom,  and  is  sometimes  very  active  ;  yet  in  the  majority  of  mod- 
erately severe  cases  the  mind  remains  undisturbed.  There  may  also  be 
present  irregularities  of  the  pupils,  photophobia,  and  other  symptoms 
which  might  lead  one  to  the  diagnosis  of  meningitis  were  it  not  for  the 
character  of  the  pulse.  The  muscles  of  the  eyes  are  often  stiff  and  im- 
movable ;  the  conjunctivae  are  reddened  and  the  eyelids  are  swollen. 

As  the  disease  progresses,  in  a  certain  proportion  of  cases,  jaundice  is  de- 
veloped ;  this  is  usually  accomcanied  by  vomiting  and  severe  diarrhoea; 
and  these  symptoms  seem  to  ally  the  disease  to  some  forms  of  malarial 
fever  (''bilious  typhoid");  not  infrequently,  especially  in  children,  there 
is  epistaxis.  The  skin  may  be  covered  with  herpes  or  sudamina.  The 
great  prostration  and  rapid  rise  in  temperature  ally  it  to  typhus  fever,  but 
the  rise  is  more  rapid  and  reaches  a  higher  point  within  the  first  twenty- 

1  This  headache  persists  till  the  remission  ;  it  is  unvarying'-  and  intense  ;  the  vertigo  is  so  severe  that 
the  patient  has  to  take  to  his  bed  as  much  from  giddiness  as  pain. 


742 


ACUTE    GENEKAL   DISEASES. 


four  hours  than  it  does  in  typhus  fever.  There  is  sometimes  a  slight  rose- 
colored  eruption  resembling  roseola,  but  having  none  of  the  characteristics 
of  typhus  erujjtion.  The  patient  goes  on  from  day  to  day  gradually  getting 
worse;  the  fever  becomes  more  and  more  intense;  loss  of  strength  and 
emaciation  are  progressive,  and  the  muscular  pains  are  more  severe.  In 
some  cases  the  patient  rejects  everything  taken  into  the  stomach.  The 
pulse  reaches  160  per  minute,  the  tongue  is  brown  and  dry,  extreme  nausea 
and  bilious  vomiting  are  present,  and  the  severity  of  the  symptoms  indi- 
cates that  death  may  speedily  occur ;  when,  on  the  seventh  or  eighth  day 
of  the  fever,  a  remission  suddenly  occurs,  attended  by  a  profuse  perspiration, 
by  a  critical  diarrhoea,  or,  rarely,  by  bleedings  from  mucous  surfaces. 

With  the  occurrence  of  the  profuse  sweating  the  temperature  falls;  in  a 
few  hours  it  may  fall  five,  six,  or  even  seven  degrees ;  the  pulse  becomes 
less  frequent ;  the  respirations,  which  have  been  hurried  and  diflBcult,  be- 
come regular ;  the  pains  in  the  head  and  limbs  pass  away,  the  thirst  disap- 
pears, the  tongue  becomes  moist ;  the  engorgement  of  the  liver  and  spleen 
rapidly  diminishes,  as  is  shown  by  the  rapid  diminution  in  the  size  of  these 
organs  as  determined  by  percussion.  The  bowels  are  constipated.  Within 
twelve  hours  from  the  commencement  of  the  remission,  the  temperature 
may  fall  to  less  than  100°  F.,  perhaps  below  the  normal  standard,  and  the 
pulse  may  fall  to  80  or  90  beats  per  minute. 

As  soon  as  the  remission  occurs  the  patient  feels  perfectly  well,  except  a 
sense  of  weakness.  He  gets  out  of  bed,  and,  if  he  is  in  a  hospital,  per- 
haps insists  upon  his  discharge  ;  his  appetite  begins  to  return,  and  he  ap- 
pears to  be  rapidly  convalescing,  but  in  many  the  pulse  at  this  period  is  as 
slow  as  40  to  60  per  minute,  and  the  first  sound  of  the  heart  is  very  faint, 
the  second  being  intensified. 

His  apparent  convalescence  is  of  short  duration  ;  sometimes  in  three  or 
four  days,  usually  at  the  end  of  a  week,  certainly  by  the  twelfth  or  four- 
teenth day  of  the  disease,  all  the  phenomena  of  the  primary  fever  are 

suddenly  developed,  or  what  is 
termed  the  relapse  occurs.'  Some- 
times the  relapse  occurs  in  the 
morning,  sometimes  in  the  after- 
noon, but  more  frequently  it 
comes  on  at  night.  The  re- 
lapse may  be  ushered  in  by  a 
chill,  or  it  may  occur  without 
a,  chill.  The  pulse  may  begin 
to  increase  in  rapidity,  and  in 
twelve  hours  reach  140  per  min- 
ute. With  the  rapid  pulse,  the 
temperature  rapidly  rises  to  306° 
F.  Usually  the  fever  which  at- 
tends the  relapse  is  more  intense 
than  the  primary  fever,  the  liver 


Fig.  160. 

Temperature  Record  in  a  case  of  Eelapsing  Fever. 

Recovery. 


I  It  is  very  rare  for  the  disease  to  end  in  one  single  paroxysm. 


EELAPSING   FEVER.  743 

and  spleen  becoming  as  enlarged  as  during  the  primary  feyer.  The  relapse 
usually  lasts  three  or  four  days.  In  a  few  cases  I  have  seen  it  last  six  or 
seven  days,  and  in  some  it  does  not  continue  more  than  forty-eight  hours. 
After  it  has  continued  a  certain  period,  a  second  remission  is  developed ; 
this,  like  the  first  remission,  comes  on  suddenly,  is  accompanied  by  a  pro- 
fuse perspiration,  and  in  twenty- four  hours  from  its  commencement  the 
pulse  and  temperature  have  reached  their  normal  standard.  From  this 
period,  the  patient  usually  goes  on  to  complete  recovery. 

As  many  as  three  or  four  relapses  may  occur,  but  ordinarily  the  conva- 
lescence becomes  complete  after  the  second  remission.  Convalescence  from 
relapsing  fever  is  usually  slow,  the  patient  for  a  long  time  remains  in  a 
weak  condition,  suffering  more  or  less  from  arthritic  and  muscular  pains. 
The  appetite  returns  slowly.  An  anaemic  murmur,  which  is  often  very  dis- 
tinct during  the  active  period  of  the  fever,  is  heard  for  two  or  three  weeks 
after  the  commencement  of  convalescence.  CEdema  of  the  feet,  due  to  gen- 
eral anasmia,  is  often  quite  marked  during  convalescence.  The  period  of 
convalescence  is  usually  as  long  as  both  the  period  of  fever  and  remission  ; 
not  infrequently  six  or  eight  weeks  elapse  before  relapsing  fever  patients  are 
able  to  resume  their  accustomed  avocations.  At  the  commencement  of  con- 
valescence, the  decrease  in  the  size  of  the  spleen  is  rapid,  but  frequently  it 
is  a  long  time  before  the  organ  reaches  its  normal  size. 

Complications. — Few  complications  have  been  noticed  during  the  course 
of  relapsing  fever.  In  some  epidemics  pneumonia  has  occurred  quite  fre- 
quently ;  at  other  times  it  has  been  exceedingly  rare.  When  it  does  occur, 
it  is  often  double,  and  terminates  in  gangrene  in  a  number  of  cases. 

Sudden  collapse  may  occur  as  a  complication  of  relapsing  fever>  either 
during  the  primary  fever  or  during  the  relapse.  The  pulse  suddenly  be- 
comes small,  irregular,  or  intermittent,  sometimes  imperceptible.  The 
cardiac  impulse  is  feeble,  the  heart  sounds  are  lost,  and  the  patient  rapidly 
passes  into  a  condition  of  collapse  and  dies.  The  collapse  may  come  on 
suddenly  in  cases  previously  mild ;  with  fatty  heart,  death  in  relapsing  fever 
is  nearly  always  from  this  cause. 

Post-feirile  ophthalmia  is  another  very  remarkable  complication  or 
sequela  of  this  fever.  It  has  been  observed  in  most  epidemics.  It  presents 
two  distinct  stages,  the  amaurotic  and  the  inflammatory.  During  the  first 
stage  the  patient  complains  of  impaired  vision,  with  motes  and  luminous 
circles  floating  before  the  eyes.  The  inflammatory  stage  is  characterized 
by  intense  circumorbital  pains  and  lachrymation,  without  injected  conjunc- 
tivae or  marked  constitutional  disturbance.  Eecovery  is  tedious,  and,  unless 
the  case  is  carefully  treated,  may  end  in  complete  loss  of  sight.  Both  eyes 
are  rarely  attacked  ;  the  right  eye  is  most  frequently  affected.  Iritis, 
choroiditis,  and  retinitis  are  not  uncommon. 

Diarrhoea  and  dysentery  are  common  complications,  and  in  some  epi- 
demics they  are  the  chief  cause  of  death.  They  are  most  likely  to  come  on 
during  the  relapse.  In  our  epidemics  the  most  frequent  complication  is 
hemorrhage  from  the  mucous  surfaces,  especially  from  the  stomach  and 
intestines.     In  two  cases  that  came  iinder  my  observation  hemorrhagic 


744:  ACUTE    GENEEAL   DISEASES. 

pachymeningitis  was  the  cause  of  death.  In  very  rare  instances,  abscess  of 
the  spleen,  accompanied  by  pygemic  symptoms,  has  occurred  during  the 
relapse  and  convalescence.  Pregnant  females,  no  matter  at  what  stage  of 
pregnancy,  asually  abort  during  an  attack  of  relapsing  fever. 

Differential  Diagnosis. — The  diagnosis  of  relapsing  fever  is  not  difficult  if 
one  has  the  entire  history  of  the  case  ;  but  at  the  commencement  of  an 
epidemic,  during  the  primary  fever  the  diagnosis  will  necessarily  be  doubt- 
ful. The  diseases  with  which  it  is  possible  to  confound  relapsing  fever 
are  typhus,  typhoid,  remittent,  yellow  and  dengue  fever,  small-pox  (before 
the  eruption),  and  measles.  It  differs  from  all  but  typhus  in  the  sudden- 
ness of  its  invasion,  in  the  short  duration  of  the  primary  fever,  in  its  termi- 
nation in  a  crisis,  and  in  the  almost  uniform  occurrence  of  a  relapse  be- 
tween the  third  and  fifth  days.  Then  the  muscular  and  arthritic  pains, 
which  are  such  constant  attendants  of  relapsing  fever,  distinguish  it  from 
the  other  forms  of  fever. 

In  typhus,  the  dusky  face,  contracted  pupils,  absence  of  all  abdominal 
pain,  peculiar  smell,  stupor,  apathy  of  mind,  and  pathognomonic  eruption 
on  the  fifth  or  seventh  day  will  be  sufficient  to  distinguish  it  from  relaps- 
ing. 

In  typhoid,  the  slow  invasion,  the  ''step-ladder"  rise  in  temperature, 
the  eruption,  the  characteristic  diarrhoea,  and  the  continuance  without  re- 
mission or  intermission,  will  enable  a  diagnosis  to  be  reached. 

A  severe  form  of  relapsing  fever,  attended  by  Jaundice,  resembles  very 
closely,  in  its  general  appearance,  yellow  fever.  In  yellow  fever  the  pulse 
is  rarely  over  110,  the  spleen  is  normal ;  but  the  high  temperature  and  rapid 
pulse  which  attend  the  development  of  the  former  readily  distinguish  it 
from  the  latter  ;  besides,  when  the  intermission  comes  on,  there  can  no 
longer  be  any  question  as  regards  diagnosis,  for  yellow  fever  is  a  disease 
in  which  only  a  remission  occurs,  not  an  intermission. 

Small-pox  simulates  relapsing  fever  only  during  the  period  of  invasion. 
One  need  make  no  doubtful  diagnosis  after  the  third  day,  when  the  red 
epots  appear  along  the  edges  of  the  hair. ' 

In  measles  the  eruption  following  the  symptoms  of  a  common  cold  and  a 
bronchitis  will  suffice  for  a  diagnosis. 

Prognosis. — The  prognosis  in  relapsing  fever  is  always  good.  During  our 
epidemic  about  three  per  cent,  of  all  the  cases  treated  in  hospitals  termi- 
nated fatally.  This  is  a  lower  rate  of  mortality  than  we  have  with  measles. 
Usually  deaths  from  relapsing  fever  occur,  not  from  the  disease,  but  from 
some  complication.  During  the  epidemic  in  this  city,  syncope  during  re- 
lapse was  the  most  frequent  cause  of  death.  Eelapsing  fever  patients  may 
die  of  hemorrhage  from  some  of  the  mucous  surfaces.  A  fatal  termination 
may  occur  from  bronchitis,  pneumonia,  or  other  pulmonary  complications. 
Diarrhoea  and  dysentery  occurring  during  convalescence  sometimes  cause  a 
fatal  termination  ;  purpura  also.     Sudden  suppression  of  urine,  dependent 


>  In  dengue  fever  the  pains  in  the  joints  are  severe  ;  there  are  glandular  swellings  not  found  in  relaps- 
ing, the  paroxysm  is  shorter  (three  days)  than  in  relapsing  (seven  days)  ;  and  there  is  an  eruption  (like 
scarlatina's)  on  the  palms  and  neck. 


SMALL-POX.  745 

upon  renal  congestion,  may  give  rise  to  acute  uraemia,  and  thus  cause  death. 
My  own  experience  leads  me  to  the  belief  that  the  greatest  danger  in  this 
disease  arises  from  sudden  syncope.  I  remember  one  very  marked  case, 
that  of  a  young  physician  who  seemed  to  be  doing  well  in  his  second  re- 
lapse, when  suddenly  he  passed  into  a  state  of  syncope  and  died.  At  the 
post-mortem  examination  no  condition  of  the  internal  organs  was  found 
which  would  account  for  his  death. 

Treatment. — Dr.  Eutty  stated  more  than  a  century  ago  that  all  those 
cases  of  relapsing  fever  which  were  abandoned  to  whey  and  the  good  provi- 
dence of  God  recovered.  The  experience  of  a  century  has  furnished  no  ac- 
cepted plan  of  treatment.  The  profession  are  still  unsettled  as  to  the  best 
course  to  be  adopted  in  the  management  of  this  disease.  When  this  fever 
appeared  in  our  midst,  we  thought  we  could  control  it  by  large  doses  of 
quinine,  but  we  soon  found  that  quinine  was  of  no  service  in  its  treatment. 
Then  arsenic,  aconite  and  veratrum  were  employed  in  full  doses  as  anti- 
pyretics, but  after  a  time  these  were  abandoned  as  useless.  Cold  baths  were 
resorted  to,  as  also  was  sponging  of  the  surface  in  order  to  reduce  the  tem- 
perature, but  in  their  use  we  were  disappointed.  The  temperature  was  re- 
duced while  the  cold  was  being  applied,  but  rose  again  very  soon  after  the 
patients  were  removed  from  the  baths,  and  there  was  no  evidence  that  it 
diminished  the  severity  or  shortened  the  duration  of  the  primary  fever,  or 
prevented  the  occurrence  of  the  relapse.  Opium  in  full  doses  was  then 
tried,  but  with  equally  unsatisfactory  results,  although  its  free  use  was 
found  to  give  more  comfort  to  the  patients  than  did  any  other  plan.  In 
some  cases  stimulants  were  administered  quite  freely,  but  without  any  ap- 
parent beneficial  results. 

The  conclusion  arrived  at  was,  that  relapsing  fever  patients  were  as  well 
without  as  with  medication.  I  would  insist  that  relapsing  fever  patients 
shoiild  be  kept  quiet  in  bed  during  the  primary  fever,  and  should  not  be 
allowed  to  leave  their  rooms  until  the  period  of  relapse,  shall  have  passed 
and  that  the  greatest  care  should  be  exercised  to  guard  against  the  occur- 
rence of  syncope.  If  there  is  any  evidence  of  heart-failure,  digitalis  and 
stimulants  should  be  administered  according  to  indications.  Beyond  this 
I  have  nothing  to  suggest.  My  experience  leads  me  to  place  relapsing 
fever  patients  under  the  best  hygienic  management,  with  free  ventilation 
and  a  milk  diet,  and  then  carefully  watch  lest  some  complication  should 
occur. 

SMALL-POX. 

{Yariola.) 

There  are  three  recognized  types  of  variola,  viz., — "variola  discreta," 
"  variola  confluens,"  and  ''  variola  hemorrhagica."  ' 

Morbid  Anatomy. — Besides  those  anatomical  lesions  which  occur  upon 
the  mucous  membranes  and  skin,  there  is  more  or  less  intense  congestion 

'  Small-pox  is  a  very  ancient  disease.  Before  the  Christian  era  a  Goddess  had  been  worshiped  in  India 
as  a  protectress  agninst  it.  The  Arabians  gave  the  first  detailed  account  of  variola.  During  the  thirteenth, 
fourteenth  and  fifteenth  centuries  it  prevailed  in  Europe,  and  two  centuries  later  it  appeared  on  the 
American  coutinent.  During  the  eighteenth  century  one-sixth  to  one-twelfth  of  the  total  mortality  in 
Europe  was  caused  by  small-pox. 


746  ACUTE   GENERAL   DISEASES. 

of  the  lungs,  brain,  liver,  spleen  and  kidneys.'  In  the  hemorrhagic  form 
of  small-pox  small  hemorrhages  occur  in  nearly  all  the  viscera,  with  ecchy- 
moses  in  the  serous  membranes  and  blood-stained  fluid  in  the  serous  cavi- 
ties. The  mucous  membrane  of  the  stomach  and  rectum  is  oftenest  the 
seat  of  these  extravasations. 

The  characteristic  anatomical  lesion  of  small-pox  is  to  be  found  upon  the 
mucous  membranes  and  upon  the  skin.  This  lesion  is  usually  spoken  of 
as  the  eruption.  It  does  not  differ  essentially  in  the  different  varieties  ; 
the  modifications  which  are  met  with  are  due  rather  to  its  duration  and 
the  order  of  its  development.  These  surface  lesions  pass  through  regular 
stages  of  development  and  decline. 

The  first  step  in  the  formation  of  a  small-pox  pustule  is  congestion  of 
the  skin  in  discrete  spots  ;  the  vessels  of  the  corium  are  dilated  and  tortu- 
ous, and  the  connective-tissue  of  the  papillae,  in  the  centre  of  the  congested 
zone,  shows  more  or  less  cedema.  The  non-elevated  red  spot  (looking  at 
first  like  a  flea-bite)  is  a  macule.  Next,  the  skin  is  elevated  at  these  (macu- 
lar) points  and  o.  papule  forms,  from  changes  in  the  cells  of  the  rete  Mal- 
pighii.  Soon  the  papule  becomes  a  vesicle  ;  in  its  centre  the  epidermis 
becomes  distended  with  serum  and  cells.  As  the  effusion  increases  the 
cells  change  ;  the  horny  layer  above  is  raised,  and  the  summit  of  the  papule 
becomes  the  centre  of  the  vesicle.  The  changed  cell  elements  are  pressed, 
separated,  and  massed  into  groups  from  pressure  of  the  effusion,  and  a 
stringy  mesh-work  is  formed  in  the  vesicle.  Meanwhile  proliferation  of 
the  adjoining  cells  forms  a  peripheral  wall  for  the  vesicle,  the  contents  of 
which  soon  become  turbid. 

Umhilication  of  the  vesicles  now  occurs.  Trabeculse  slowly  spread  from 
roof  to  floor  of  the  vesicle,  and  hold  down  its  centre,  while  marginal  cell 
proliferation  and  the  accumulation  of  serum  bulge  out  its  periphery.'^ 
After  the  vesicles  are  fully  formed,  pus-cells  appear  in  them,  and  as  a  re- 
sult the  vesicles  change  in  color,  and  become  pustules.  At  the  same  time 
an  inflammatory  process,  more  or  less  extensive,  is  going  on  in  the  walls  of 
the  pustule,  and  in  the  surrounding  cellular  tissue,  which  terminates  in  a 
destruction  of  tissue  at  the  point  where  the  papillary  congestion  first  oc- 
curred. If  only  the  superficial  layer  of  the  skin  is  involved,  the  infiltra- 
tion of  pus-cells  into  the  vesicle  and  the  formation  of  the  pustule  may  take 
place  without  extension  of  the  inflammation  into  the  cellular  tissue  beneath, 
and  necrosis  or  death  of  the  part  will  not  follow  ;  but  if  the  inflammation 
extends  into  the  deeper  tissues,  a  slough  will  be  produced  which  necessarily 
will  be  followed  by  a  cicatrix  and  pitting.     After  the  pustule  is  formed 

1  Enlargement  of  the  spleen  is  rather  an  infrequent  event  in  small-pox.  Weigert  states  that  the  blood- 
vessels of  the  lymphatic  glands  and  abdominal  viscera  are  often  filled  vrith  micrococci,  that  necrosis  of  the 
cells  about  these  colonies  induces  pus  accumulation,  the  direct  result  of  "coagulation  necrosis"  (see 
Inflammation)  :  but  that  abscesses  rarely  form  ;  some  find  an  analogy  between  these  and  the  skin  dis- 
eases. 

2  Some  explain  it  by  saying  that  each  papule  and  subsequent  vesicle  holds  imprisoned  at  its  centre 
either  a  hair-follicle  or  the  duct  of  a  sweat-gland,  and  that  when  this  epidermidal  layer  of  the  papule  is 
elevated  by  the  serous  exudation  or  infiltration,  the  portion  immediately  about  the  hair-follicle  or  the 
sweat-duct  is  held  down,  and  a  depression  is  produced  by  the  exact  point  where  the  hair-follicle  or  duct  of 
the  gland  may  be  situated  ;  but  since  umhilication  is  present  when  neither  structure  is  found,  this  view 
cannot  be  accepted. 


SMALL-POX.  747 

the  inflammatory  products  begin  to  dry  down,  and  a  crust  is  formed  which 
contracts  in  tlie  central  portion,  and  the  same  umbilicated  appearance  is 
presented  that  is  seen  in  the  umbilicated  vesicle.  The  incrustation  begins 
at  the  centre.  The  crusts  are  made  up  of  dried  pus-cells  and  detritus. 
After  a  time  these  crusts  are  separated  by  the  ordinary  changes  which 
occur  in  the  subsidence  of  an  inflammatory  process,  and  recovery  is  com- 
plete, except  that  there  is  left  behind  a  cicatrix  which  undergoes  the  same 
changes  as  does  a  cicatrix  formed  under  any  other  circumstances.  These 
pustules  may  be  formed  upon  any  mucous  membrane.  They  occur  often- 
est  in  the  nose,  mouth,  trachea,  bronchial  tubes  and  larynx. 

There  is  nothing  specific  or  essentially  different  in  the  development  of 
the  pustules,  in  liemorrhagic  small-pox,  except  that  they  contain  blood  in- 
stead of  serum  or  pus.  In  the  hemorrhagic  variety,  larger  or  smaller 
hemorrhages  take  place  into  the  ceHular  tissues  and  into  the  cutis  ;  in 
the  milder  forms  they  take  place  only  in  the  layer  beneath  the  papillae  ; 
while  in  the  severer  forms  they  take  place  beneath  all  the  cutaneous 
layers  ;  even  the  subcutaneous  fat  may  be  infiltrated  with  blood.  No 
changes  in  the  walls  of  the  vessels  have  as  yet  been  discovered  which  will 
account  for  these  hemorrhages.  These  extravasations  more  frequently  oc- 
cur in  those  cases  in  which  death  takes  place  before  the  period  of  pustula- 
tion  is  reached-  In  hemorrhagic  variola  blood  eitravasations  occur  into 
the  substance  of  all  the  organs,  the  marrow  of  the  bones,  and  on  mucous 
and  serous  surfaces,  and  infarctions  in  the  lungs  are  the  rule.  Hyper- 
semia  and  cedema  of  the  brain  sometimes  occur. 

Etiology. — The  disease  is  propagated  only  by  contagion  ;  it  is  a  disease 
which  can  only  be  produced  by  its  own  specific  poison,  and  is  communica- 
ble only  to  persons  who  are  not  protected  from  its  influence.  There  has  been 
considerable  question  as  to  loliere  the  virus  of  small-pox  Is  located.  Some 
claim  that  it  is  exclusively  in  the  pustule,  and  that  it  is  not  possible  for  a 
person  suffering  from  small-pox  to  give  the  disease  to  an  unprotected  in- 
dividual unless  some  of  the  virus  from  the  pustule  is  brought  in  con- 
tact with  a  cutaneous  or  mucous  surface.  This  is  a  mistake.  That  small-pox 
can  be  conveyed  by  means  of  virus  taken  from  a  pustule  there  can  be  no 
question, — "contagion  by  inoculation," — but  the  cutaneous  surface  of  an 
unprotected  person  may  be  rubbed  with  pus  taken  from  a  small-pox  pus- 
tule, and  unless  there  is  an  abrasion  of  the  surface  the  person  will  not  be- 
come inoculated  with  the  disease ;  but  if  the  virus  is  brought  in  contact 
with  a  mucous  surface  of  an  unprotected  person  he  will  almost  certainly 
contract  the  disease.  It  is  equally  certain  that  the  disease  can  be  com- 
municated from  one  person  to  another  by  means  of  the  breath  and  exhala- 
tions from  the  skin. 

There  is  no  evidence  that  the  disease  can  be  conveyed  by  the  discharges 
from  the  bowels.  Perhaps  if  a  pustule  should  be  developed  somewhere 
along  the  line  of  the  intestine  the  discharges  might  become  so  contamina- 
ted as  to  have  the  power  of  communicating  the  disease.  Small-pox  can 
also  be  conveyed  from  one  individual  to  another  through  the  atmosphere. 
In  the  open  air  the  distance  of  contagion  is  about  two  and  one-half  feet. 


748  ACUTE   GENEEAL   DISEASES. 

In  a  small  room  the  atmosphere  may  be  so  contaminated  that  an  unpro- 
tected person  will  contract  the  disease  upon  a  single  entrance  into  the 
room.  The  disease  can  be  conveyed  in  clothing,  and  the  poison  will  re- 
main for  a  long  time  in  clothing  unless  it  has  been  exposed  for  a  consider- 
able time  to  the  air.  In  other  words,  there  is  no  doubt  but  that  it  is  a 
portable  disease.  In  order  that  the  disease  may  be  transferred  by  means 
of  the  clothing  or  mercliandise,  it  is  necessary  that  the  clothing  or  mer- 
chandise contain  the  pus  or  crusts  from  the  small-pox  pustules  ;  how  long 
a  time  may  elapse  before  the  virus  loses  its  vitality  is  not  known.  There 
are  well-authenticated  cases  in  which  it  has  retained  its  virulence  for 
more  than  a  year. 

No  period  of  life  is  exempt  from  the  contagion  of  small-pox  ;  even  intra- 
uterine life  is  in  danger  from  infection.  Rarely  does  an  individual  have  a 
second  attack,  I  remember  one  exception,  that  occurred  in  the  person  of 
a  young  Swedish  woman,  who,  under  my  observation,  passed  through  three 
well-developed  attacks  of  the  disease  ;  the  last  attack  was  the  most  severe. 
Concerning  the  exact  nature  of  the  small-pox  virus  nothing  definite  is 
known.'  Some  claim  that  the  earliest  period  at  which  one  suffering  from 
this  disease  can  infect  the  unprotected,  is  the  period  of  suppuration  ;  others, 
that  the  infecting  period  is  during  the  stage  of  desiccation.  There  are  well- 
authenticated  cases,  however,  which  prove  that  infection  may  take  place 
during  any  stage  of  the  disease,  even  during  the  period  of  incubation. 
There  is  little  doubt  but  that  the  suppurative  stage  is  the  most  infectious 
period. 

There  are  many  views  as  to  the  manner  in  which  the  small-pox  poison 
gains  entrance  into  the  system ;  the  most  probable  of  these  views  is,  that 
it  is  principally  absorbed  by  the  mucous  membrane  of  the  respiratory  tract 
during  respiration,  and  it  is  also  probable  that  exceedingly  fine  particles 
detach  from  the  pustules  and  crusts,  which  are  suspended  in  great  nurab3rs 
in  the  air  surrounding  small-pox  patients,  and  that  these  convey  the  con- 
tagion. There  are  no  facts  to  sustain  the  views  as  to  the  parasitic  nature 
of  this  contagion. 

The  length  of  time  which  elapses  after  exposure  to,  and  reception  of, 
the  variola  contagion  before  the  disease  is  developed  varies  from  five  to 
thirty  days,  giving  the  extremes.  This  is  called  the  period  of  incubation, 
during  which  the  recipient  of  the  poison  usually  presents  no  abnormal 
symptoms.  If  the  poison  is  introduced  into  the  system  through  inocula- 
tion, only  forty-eight  hours  elapse  before  the  characteristic  phenomena  of 
the  variola  are  manifested.  It  is  not  known  what  change  takes  place  in 
the  body  of  the  infected  person  during  this  period  of  incubation.  Usually, 
twelve  to  fourteen  days  after  exposure,  one  who  has  contracted  small-pox 
begins  to  feel  chilly  ;  this  feeling  of  chilliness  increases  until  he  has  a  dis- 
tinct chill.  This  has  been  termed  the  initial  stage,  or  the  stage  of  initiatory 
fever.  Measles  and  small-pox  poisons  may  be  latent  at  the  same  time  in 
the  same  individual ;  also  scarlet  fever  and  small-pox. 

Symptoms.— The  transition  from  the  stage  of  incubation  to  that  of  the 

1  Cohnheim  and  Weigert  state  that  the  micrococci  in  the  vesicles  are  the  contagious,  specific  elements. 


SMALL-POX 


749 


initiatory  fever  is  sometimes  abrupt  and  sometimes  gradual  ;  usually  it 
occupies  two  days,  and  is  followed  by  the  eruption.  lu  this  stage  there  is 
greater  variation  in  the  intensity  than  in  the  duration  of  the  symj^toms. 
The  intensity  of  the  symptoms  bears  no  relation  to  the  severity  of  the 
attack.  Not  infrequently,  the  most  violent  symptoms  in  the  initial  stage 
are  followed  by  a  mild  attack  of  variola;  while  mild  symptoms  lu  the 
initial  stage  may  be  followed  by  the  gravest  form  of  small-pox.  The  head- 
ache, which  usually  precedes  the  fever,  grows  more  intense,  only  subsiding 
as  the  eruption  appears.  With  the  chill,  which  may  be  more  or  less  severe, 
there  is  pain  in  the  head  and  back,  especially  in  the  middle  of  the  back 
and  loins,'  with  this  pain  there  will  be  rapid  rise  in  temperature.  The 
chill  is  more  severe  than  in  any  other  exanthem.  During  the  first  day  the 
temperature  may  rise  to 
104"  F.,  during  the  sec- 
ond day  to  105°  F.,  and 
by  the  third  day  it  may 
reach  106°  F.  or  107°  F. ; 
in  some  cases  it  has  been 
said  to  have  reached 
109°  F.  Sweating  be- 
gins with  the  first  rise  in 
temperature,  and  con- 
tinues till  the  period  of 
eruption.  With  this  rise 
in  temperature  there  will 
be  an  acceleration  of 
pulse  ;  it  may  reach  100 
or  120  beats  per  minute.  fiq.  lei. 

In  the  stronff  and  robust  Temperature  Record  in  a  case  of  Discrete  Small-pox. 

person,  the  pulse  will  be  full  and  not  easily  compressed.  In  females,  and 
in  the  weak  and  feeble,  the  pulse  has  less  volume  and  usually  is  more  fre- 
quent ;  it  may  reach  140  beats  per  minute.     In  children,  160. 

At  the  onset,  there  is  usually  more  or  less  nausea  and  vomiting,  and 
soreness  of  the  throat.  This  soreness  of  the  throat  may  have  preceded  the 
chill  by  twenty-four  hours,  but  now  in  many  cases  it  will  be  quite  severe, 
and  the  patient  will  complain  of  more  or  less  dysphagia,  and  pain  in  the 
pharynx.  The  extent  of  the  throat  symptoms  will  depend  upon  the  sever- 
ity of  the  attack.  In  the  severer  forms  of  the  disease,  by  the  third  or  even 
before  the  end  of  the  second  day,  there  may  be  delirium.  In  all  cases, 
the  face  will  be  flushed,  the  conjunctivse  congested,  and  there  will  be  throb- 
bing of  the  carotids.  With  these  symptoms,  there  will  be  great  restlessness, 
and  an  anxious  expression  of  countenance,  with  somnolence.  The  respira- 
tions will  be  short,  frequent,  and  labored,  many  complaining  of  dyspnoea 
in  whom  there  are  no  lung  complications.  Many  suffer  from  extreme 
vertigo,  and  in  children  convulsions  are  not  infrequent.  By  the  evening  of 
the  second  or  morning  of  the  third  day  swelling  and  diffuse  redness  of  the 

1  Incomplete  paraplegia  haa  occurred,  disappearing,  however,  with  the  appearance  of  the  eruption. 


750  ACUTE   GENERAL  DISEASES. 

tonsils  and  soft  palate  are  present ;  not  infrequently  the  swelling  and  red- 
ness of  the  mucous  membranes  extend  into  the  larynx,  causing  hoarseness 
and  huskiness  of  the  voice  and  a  stridulous  cough. 

During  the  fever  of  invasion  patients  are  languid  and  weak  in  propor- 
tion to  the  severity  of  the  fever. "  Frequently  within  twenty-four  hours 
after  the  ushering-in  chill,  the  strongest  and  most  vigorous  will  be  unable 
to  get  out  of  bed.  Paralysis  of  the  bladder  may  occur  in  this  stage.  The 
tongue  is  coated.  There  is  epigastric  pain  and  tenderness.  If  vomiting 
occurs  it  is  present  at  the  very  beginning,  and  continues  with  great  ob- 
stinacy throughout  its  entire  course.  In  the  hemorrhagic  variety  the 
matters  vomited  may  contain  blood.  There  is  constipation,  but  diarrhoea 
is  not  infrequent  in  children. 

Stage  of  Eruption. — By  the  third  day  of  the  disease,  at  least  after  the 
initial  fever  has  continued  three  full  days,  an  eruption  will  make  its  ap- 
pearance upon  the  face,  especially  along  the  edges  of  the  hair.^ 

The  eruption,  as  it  develops  in  a  moderately  severe  case  of  discrete 
variola,  first  appears  in  the  form  of  slightly  elevated  maculae.  These  are 
of  a  pale  red  color,  varying  in  size  from  a  millet-seed  to  a  pin's  head,  or 
even  larger.  These  little  red  spots  look  very  much  like  flea-bites.  In  most 
cases  the  forehead,  nose,  and  upper  lip  are  first  covered  ;  they  gradually  in- 
crease in  size,  the  increase  being  attended  by  a  sensation  of  itching  and  burn- 
ing of  the  surface.  Usually,  about  twelve  hours  after  their  appearance 
upon  the  face,  similar  small  red  points  appear  upon  the  neck  and  wrists, 
then  on  the  chest,  arms,  and  legs.  In  children  they  may  first  appear  on  the 
loins,  nates,  genitals,  or  about  an  excoriated  or  a  blistered  surface.  They 
are  always  less  abundant  on  the  body  and  extremities  than  on  the  face. 

On  the  second  day  of  the  eruption,  these  spots  assume  a  darker  red  color, 
become  elevated,  and  have  a  distinctly  papular  feel,  like  shot  under  the  skin. 
In  a  majority  of  instances,  as  they  enlarge  a  depression  is  formed,  which 
gives  them  an  umbilicated  appearance.  The  appearance  of  the  eruption 
is  attended  by  a  subsidence  of  the  febrile  symptoms,  the  patient  no  longer 
complains  of  pains  in  the  head  and  back,  the  temperature  falls  two  or  three 
degrees,  and  the  pulse  diminishes  fifteen  or  twenty  beats  in  frequency,  some- 
times to  normal.  Vesicles  are  also  seen  in  the  mouth,  pharnyx,  upper  part 
of  the  larynx,  etc.,  etc. 

Stage  of  Suppuration. — About  the  sixth  day  of  the  eruption  the  contents 
of  the  vesicle,  from  the  admixture  of  pus-corpuscles,  gradually  become 
turbid,  and  by  the  eighth  day  the  pustules .  become  fully  formed,  and  the 
disease  enters  on  the  stage  of  suppuration.  The  integument  ia  the  im- 
mediate vicinity  of  the  pustule  now  becomes  red,  cedematous,  and  tumefied, 
each  pustule  being  surrounded  by  a  broad  red  base,  the  "  halo,"  and  where 
they  are  thickly  set  they  become  confluent.     The  face  swells  to  a  shapeless 

1  Trousseau  and  many  others  state  that  the  longer  the  skin  manifestations  are  delayed,  the  more  harm- 
less the  disease,  and  the  more  rapidly  the  eruption  comes  on  the  more  dangerous  is  it. 

^  Prior  to  the  eruption  a  diffuse  scarlatina-like  redness  sometimes  covers  all  the  body,  and  a  few  suda- 
mina  may  appear  in  the  erythema.  At  this  point  haste  may  lead  to  a  diagnosis  of  scarlet  fever  or  measles. 
Petechise  and  ecchymoses  are  less  frequently  seen  ;  they  are  not  necessarily  followed  by  variola  hemor- 
ihagica. 


SMALL-POX.  751 

mass,  and  the  patient  becomes  frightfully  deformed.  The  eyes  are  closed, 
and  the  hands  and  feet  look  like  round  balls.  The  itching  now  becomes 
almost  unbearable  and  causes  the  patient  to  scratch  himself,  thus  causing 
ultimate  disfigurement.  During  this  period  a  characteristic  sickish  odor 
is  emitted.  The  eruption  passes  through  its  stages  two  or  three  days  later 
on  the  extremities  than  it  does  on  the  face  ;  consequently,  sujDpuration  may 
be  complete  on  the  face  while  it  is  incipient  on  the  extremities,  and  the 
eruption  may  be  perfectly  discrete  on  the  trunk  while  it  is  confluent  on  the 
face.  About  the  eighth  or  ninth  day  of  the  eruption  the  pustule  is  fully 
formed ;  the  stage  of  suppuration  is  complete.  Then  commence  the  retro- 
grade changes.  The  pustule  either  ruptures,  discharges  its  contents,  dries 
up  and  forms  a  yellowish  crust,  or  it  shrivels  and  dries  up  without  ruptur- 
ing ;  this  is  the  period  of  desiccation. 

Stage  of  Desiccation. — Desiccation  commences  in  those  parts  in  which  the 
eruption  first  appeared,  and  commonly  on  the  twelfth  day  of  the  disease. 
As  the  drying  down  of  the  pustules  takes  place,  the  redness,  tenderness  and 
oedema  of  the  skin  lessen,  and  the  countenance  begins  to  assume  a  more 
natural  appearance.  At  first  the  crust  adheres  quite  firmly  to  the  surface, 
but  about  the  fourteenth  day  of  the  eruption  it  becomes  separated  and 
falls,  leaving  a  stain  of  reddish-brown  color,  with  elevated  edges  and  de- 
pressed centre,  which  remains  visible  for  five  or  six  weeks.  These  spots 
gradually  become  lighter  in  color,  until  finally,  if  there  has  been  destruc- 
tion of  the  cutis,  and  if  excoriation,  ulceration  and  renewal  of  the  scab 
have  occurred,  a  pit  will  be  formed  of  greater  or  less  depth,  of  a  white 
color,  giving  to  the  face  a  "  pock-marked  "  appearance,  which  will  remain 
during  the  life  of  the  individual.  The  febrile  symptoms  gradually  increase 
m  severity  until  the  third  day  of  the  disease,  when  the  eruption  appears 
and  the  fever  subsides.  Then  the  vesicles  form,  the  formation  of  which 
is  attended  by  only  moderate  fever. 

On  the  eighth  day  the  pustules  are  fully  formed,  and  the  "  suppurative,''^ 
or  secondary  fever  comes  on.  This  secondary  fever  often  commences  with 
a  distinct  chill.  The  fever  is  highest  in  the  evening  ;  it  is  of  a  distinctly 
remittent  type,  the  pulse  becomes  frequent,  the  temperature  rapidly  rises, 
perhaps  reaches  a  higher  elevation  than  it  did  during  the  initial  fever, 
sometimes  rising  as  high  as  108°  or  109°  F.  ;  it  reaches  its  maximum  when 
suppuration  is  at  its  height.  As  desiccation  commences,  the  temperature 
begins  to  fall,  and  by  the  time  the  crusts  are  fully  formed  the  temperature 
reaches  very  nearly  a  normal  standard.  If  the  temperature  rises  again,  its 
rise  is  due  to  some  complications  such  as  erysipelas  or  some  phlegmonous 
process.  With  the  fall  of  the  crusts,  the  patient's  appetite  returns,  and  he 
is  able  to  sleep;  convalescence  is  now  fully  established.'  The  dividing 
lines  between  the  different  varieties  of  small-pox  are  not  sharply  defined  ; 
one  variety  gradually  passes  into  another.  It  is  unnecessary  to  consider  all 
the  forms  into  which  this  disease  has  been  divided  by  some  writers ;  fre- 
quently the  basis   of  the  division   is   merely  arbitrary.      Our  attention 

'  Thi;  meiiBes  appear  in  the  initial  stage  in  the  large  majoritj'  of  women  with  small-pox,  even  though  it 
be  not  the  proper  time.    (Q,uinclce,  Leo,  Knecht,  Curshmann,  Bucli:,  Obermeier,  and  others.') 


753  ACUTE   GENERAL  DISEASES. 

will  therefore  be  confined  to  the  more  common  and  well-recognized 
varieties. 

Confluent  Small-pox,  or  Variola  Confluens. — This  is  a  much  more  severe 
form  of  the  disease  than  variola  discreta.  It  develops  far  more  rapidly  and 
is  much  more  fatal  in  its  results.  The  fever  of  invasion  is  usually  much 
more  severe,  and  of  shorter  duration,  frequently  not  lasting  more  than  forty- 
eight  hours.'  The  eruption  spreads  rapidly  over  the  entire  body,  often 
appearing  simultaneously  on  the  face  and  the  other  portions  of  the  body. 
The  red  dots  which  mark  the  first  appearance  of  the  eruption  are  very 
numerous,  especially  on  the  face  and  hands  ;  on  the  first  day  of  their  ap- 
pearance they  are  almost  confluent.  The  conjunctivae  are  early  involved 
and  suppurative  keratitis  is  not  uncommon  in  this  variety  ; — the  whole  eye 
may  be  converted  into  an  abscess.  On  the  second  day  the  skin  is  intensely 
red  and  swollen,  and  so  thickly  studded  with  large  flat  vesicles  that  they 
rapidly  unite,  suppuration  speedily  follows,  and  flattened,  yellowish-colored 
confluent  patches  are  formed  upon  a  dark,  reddened,  swollen  skin.  Gradu- 
ally these  patches  run  together  over  a  still  larger  surface,  and  the  epidermis 
is  elevated  in  the  form  of  large,  flat  bullse,  which  are  filled  with  a  sero- 
purulent  fluid  and  are  tense  and  elastic.  In  this  way  the  entire  skin  of  the 
face  is  covered  by  an  immense  bulla,  and  the  patient  is  as  unrecognizable 
as  though  he  wore  a  mask.  While  the  eruption  may  be  completely  con- 
fluent on  the  face  and  hands,  on  other  parts  of  the  body  it  remains  discrete, 
and  never  becomes  confluent  except  over  limited  spaces. 

The  period  of  desiccation  is  slowly  reached.  Large  concentric  crusts  are 
formed  over  the  confluent  patches  ;  these  adhere  firmly  to  the  skin,  while 
beneath  them  suppuration  of  the  papillary  layer  continues.  The  true  skin 
is  more  or  less  extensively  destroyed,  and  when  the  crusts  have  fallen, 
there  is  left  extensive  loss  of  substance  in  the  cutis,  giving  rise  to  pits  and 
ugly  scars,  which  have  a  tendency  to  contract,  often  producing  permanent 
and  unsightly  disfigurements.  In  this  variety  of  small-pox,  the  eruption 
is  often  confluent  upon  the  mucous  membrane  of  the  mouth  and  throat  ; 
it  may  involve  the  mucous  membrane  of  the  posterior  nares  and  extend 
into  the  larynx.  In  some  cases  the  attending  pharyngitis  is  so  severe  as  to 
render  deglutition  impossible.  The  pharyngeal  inflammation  is  submu- 
cous, and  is  frequently  accompanied  by  more  or  less  enlargement  of  the  pa- 
rotid and  sublingual  glands.  When  this  condition  exists  there  is  danger 
of  the  sudden  development  of  oedema  glottidis,  for  the  occurrence  of  which 
one  should  be  on  the  watch. ^ 

In  confluent  small-pox  hemorrhage  may  occur  in  the  pustules  ;  this  is 
not  variola  hemorrhagica,  but  a  hemorrhagic  pustular  confluent  small-pox. 
In  confluent  variola  the  skin  may  exhibit  erysipelas,  phlegmon,  gangrene 
or  multiple  abscesses.  In  confluent  small-pox  the  severity  of  the  consti- 
tutional symptoms  corresponds  to  the  severity  of  the  local  manifestations. 

1  The  thermometer  not  infrequently  shows  a  fever  of  106°  to  110°  F.  for  a  short  time,  which  sinks  to 
103°  to  104°  till  suppuration,  then  rising  even  higher  than  before. 

2  During  the  year  thar,  I  had  charge  of  the  Small-pox  Hospital,  there  were  three  cases  in  the  hospital  of 
oedema  glottidis  :  one  case  terminated  fatally  before  I  reached  the  patient  ;  life  was  saved  in  the  other 
two  cases  by  the  performance  of  laryngotomy. 


SMALL-POX. 


753 


The  temperature  during  the  initial  fever  often  reaches  106°  V.  or  107°  F., 
and  in  very  severe  types  of  the  disease  it  may  rise  as  high  as  110°  F.     The 


Pig.  16-2. 
Temperature  Record  in  a  case  of  Confluent  Small-pox. 

pulse  is  correspondingly  frequent  and  feeble.  After  the  appearance  of 
the  eruption  the  temperature  falls  slowly  to  103°  F.  or  104°  F.,  where  it 
remains  until  the  stage  of  suppuration  is  reached ;  then  it  again  rises,  in 
some  cases  even  higher  than  during  the  period  of  invasion.  Violent  delirium 
is  very  frequently  present  during  the  fever  of  invasion,  as  well  as  during  the 
period  of  secondary  fever,  and  not  infrequently  patients  pass  quite  sud- 
denly into  a  state  of  coma.  Uncontrollable  vomiting  and  obstinate  diar- 
rhoea are  not  infrequent,  coming  on  during  the  fever  of  invasion  and  con- 
tinuing throughout  the  course  of  the  disease. 

In  all  severe  cases  typhoid  symptoms  manifest  themselves  soon  after 
the  appearance  of  the  eruption,  and  patients  often  lie  for  days  in  a  semi- 
conscious state,  with  dry,  brown  tongue,  subsultus,  a  low  muttering  deli- 
rium, and  all  the  attendant  phenomena  of  intense  nervous  depression.  In 
such  cases  albumen  appears  temporarily  in  the  urine.  Complications  oc- 
cur much  more  frequently  in  confluent  than  in  discrete  small-pox.  Inflam- 
mations of  the  serous  membranes,  especially  pleurisy  and  pericarditis,  are 
the  most  common.  Croupous  and  catarrhal  pneumonia  and  acute  laryn- 
gitis frequently  complicate  the  severe  bronchial  inflammation  from  which 
so  few  patients  with  confluent  small-pox  escape.  Permanent  alopecia  often 
follows  confluent  small-pox. 

Variola  hemorrhagica '  is  a  form  of  small-pox  which  can  hardly  be 
regarded  as  a  distinct  variety,  but  rather  as  a  modification  of  other  vari- 
eties, called  the  black  or  malignant  small-pox.  It  differs  from  the  varie- 
ties already  described,  not  in  the  manner  of  its  development  as  far  as  the 
initial  fever  is  concerned,  but  in  the  appearance  of  the  eruption.  This  hem- 
orrhagic tendency  is  often  manifested  as  early  as  the  first  appearance  of  the 
eruption,  by  the  dark  color  which  the  eruption  assumes.     Sometimes  the 

>  Zulzer  found  that  in  eighty-five  to  ninety  per  cent,  of  hijn  cases  of  hemorrhagica,  the  period  of  incuba- 
tion was  only  hIx  to  eight  days,  i.  e.,  half  as  long  as  in  simple  small-pox. 
48 


754  ACUTE    GENEEAL   DISEASES. 

papules  become  hemorrhagic  from  the  very  moment  of  their  development) 
at  other  times  they  first  become  vesicles,  and  then  become  hemorrhagic. 
Again,  at  other  times,  the  hemorrhage  first  shows  itself  after  the  vesicles  be- 
come pustules.  In  some  cases  the  eruption  over  the  whole  body  becomes 
hemorrhagic  ;  in  other  cases,  it  is  hemorrhagic  in  spots.  In  the  majority  of 
cases,  the  eruption  becomes  hemorrhagic  as  soon  as  the  papules  have  at- 
tained the  size  of  a  lentil,  and  the  hemorrhagic  change  comes  on  slowly, 
generally  commencing  on  the  lower  extremities.  Petechise  and  ecchymoses 
often  appear  between  the  points  of  eruption. 

In  connection  with  the  hemorrhagic  eruptions,  hemorrhages  from  the 
various  mucous  membranes  of  the  body  will  simultaneously  occur — from 
the  mucous  membrane  of  the  nose,  perhaps  from  the  bronchial  mucous 
membrane,  and  sometimes  large  ecchymotic  spots  may  be  seen  upon  the 
mucous  surfaces  of  the  mouth  and  throat.  Haematuria,  conjunctival 
hemorrhages,  melsena,  hsematemesis,  haemoptysis,  bleedings  from  the  gums, 
and  particularly  epistaxis  are  met  with.  It  is  rare  for  this  form  of 
small-pox  to  reach  the  stage  of  suppuration,  for  before  this  sta.ge  is  reached 
patients  die.  During  the  initial  stage  of  this  variety  of  small-pox,  the 
constitutional  symptoms  do  not  differ  from  those  which  attend  the  de- 
velopment of  the  other  forms  of  this  disease.  It  is  impossible,  from  their 
character  and  intensity,  to  predict,  with  any  degree  of  certainty,  the  subse- 
quent development  of  hemorrhagic  variola.  It  has  been  said  that  the  pains 
in  the  back  and  limbs  are  more  severe  ;  but  these  are  not  characteristic. 
Frequently  the  fever  of  invasion  is  exceedingly  violent,  while  during  the 
eruptive  period,  and  during  the  entire  subsequent  course  of  the  disease,  the 
temperature  is  comparatively  low.  In  cases  in  which  extensive  hemorrhages 
have  occurred,  the  temperature  often  falls  below  the  normal,  while  the 
pulse  ranges  from  140  to  160,  and  is  exceedingly  feeble  in  character.  Only 
when  comparatively  few  of  the  vesicles  become  hemorrhagic  does  the  case 
terminate  in  recovery. 

Differential  Diagnosis. — The  first  question  that  arises  is  :  how  early  can 
>small-pox  be  recognized  ?  One  who  has  seen  very  many  cases  of  the  disease 
may  be  able  to  reach  a  diagnosis  on  the  third  day,  that  is,  the  first  day  of 
:the  eruption,  although  at  that  time  there  is  nothing  characteristic  about 
the  eruption  or  the  ushering-in  symptoms.  It  is,  however,  better  and  safer 
to  wait  until  the  second  or  third  day  of  the  erujDtion  before  making  a  posi- 
tive diagnosis,  for  there  is  little  to  be  feared  from  infection  until  the  vesi- 
cles are  fully  formed. 

The  eruption  of  measles,  in  its  early  stages,  is  liable  to  be  taken  for 
small-pox.  If  one  defers  making  the  diagnosis  until  the  vesicles  are  fully 
developed,  no  such  mistake  will  be  made.  In  measles  there  is  coryza,  a 
cough,  sneezing,  redness  and  suffusion  of  the  eyes.  These  symptoms  are 
not  present  in  small-pox.  In  small-pox,  when  the  stage  of  eruption  is 
reached,  the  temperature  falls ;  while  in  measles,  when  the  eruption  ap- 
pears, the  temperature  continues  to  rise.  The  range  of  temperature  is  two 
to  three  degrees  higher  in  small-pox  than  in  measles.  In  these  respects  the 
two  diseases  differ  sufficiently  to  enable  a  differential  diagnosis  to  be  made. 


SMALL-POX.  755 

Again,  if  one  waits  until  the  vesicles  become  umbilicated,  it  will  be  impos- 
sible that  a  mistake  in  diagnosis  should  be  made. 

During  the  period  of  initial  fever  it  is  possible  to  mistake  small-pox  for 
typhus  fever.  In  both  diseases  there  may  be  delirium,  pain  in  the  head, 
vertigo,  high  temperature,  and  evidence  of  great  disturbance  of  the  nervous 
system.  There  is  no  system  which  will  enable  a  positive  diagnosis  to  be 
made  during  the  very  early  period  of  the  disease.  Of  course,  if  typhus  fe- 
ver is  prevailing,  or  if  small-pox  is  prevailing,  and  the  patient  has  been  ex- 
posed to  either  one  of  these  contagions,  one  will  be  able  to  make  a  diag- 
nosis without  difficulty.  Usually  there  is  greater  loss  of  muscular  power 
in  typhus  fever  than  in  small-pox,  but  this  symptom  is  not  always  well 
marked.  By  the  third  day,  the  appearance  of  the  eruption  upon  the  face, 
where  it  is  first  seen,  settles  the  question  of  diagnosis.  The  eruption  of  ty- 
phus fever  is  first  seen  upon  the  abdomen,  and  may  extend  over  the  whole 
body  without  appearing  on  the  face.  It  rarely  appears  before  the  fifth  day 
of  the  fever.  Therefore,  the  differential  diagnosis  between  small-pox  and 
typhus  fever  can  be  readily  made  as  soon  as  an  eruption  appears.  The 
temperature  falls  as  soon  as  the  eruption  occurs  in  small-pox,  and  does  not 
in  typhus. 

Meningitis  is  another  disease  which  small-pox,  in  its  initial  stage,  resem- 
bles. There  is  always  considerable  cerebral  disturbance  and  a  full,  hard, 
bounding  pulse  in  the  initial  stage  of  small-pox.  Photophobia,  intense 
pain  in  the  head,  nausea  and  vomiting  may  be  present  in  both  diseases. 
Unless  it  may  be  the  expression  of  the  face,  there  is  often  no  distinguish- 
ing mark  between  the  two  diseases  in  their  early  stages.  In  meningitis, 
there  is  usually  a  pale,  anxious  expression  of  countenance,  whereas  early  in 
small-pox  the  face  is  flushed,  and  day  by  day  the  flush  deepens  until  the 
eruption  appears.  The  fever  in  meningitis  is  lower  than  in  small-pox  by  2°  to 
3°  F.,  the  pulse  is  smaller,  less  compressible,  and  not  as  rapid  as  in  variola ; 
and  the  vomiting  is  projectile  in  meningitis,  while  it  is  retching  in  char- 
acter in  variola.  On  the  appearance  of  the  eruption,  the  differential  diag- 
nosis between  these  two  diseases  is  readily  made. 

Prognosis. — The  prognosis  in  any  case  of  small-pox  depends  upon  the 
amount  of  the  eruption  ;  the  more  abundant  the  eruption,  the  greater  the 
danger  to  life.  The  prognosis  also  depends  upon  the  type  of  the  disease.  Un- 
less some  complication  arises,  most  cases  of  discrete  small-pox  recover ;  while 
of  confluent  small-pox  nearly  one-half  the  cases  prove  fatal. '  The  best  record 
obtained  in  the  small-pox  hospital  on  Blackwell's  Island  was  one  death  in 
every  five  cases.  Only  a  very  few  cases  of  the  hemorrhagic  variety  recov- 
ered, and  when  recovery  did  take  place  it  was  only  reached  after  the  patient 

1  In  twenty  years  the  "Loudon  Small-pox  Hospital "  gives  the  following  definite  statistics  : 

No.       Mortality. 
Patients  admitted  with  small-pox 4,8~9 

A.  With  1  vaccine  scar 2,001    7  7-10  per  cent. 

B.  "      2       *'        scars 1,446    4  7-10    "    " 

C.  "      .3        "  "       518    19-10    "    " 

D.  "      4  or  more  scars 544         1-3    "    " 

E.  Said  to  have  been  vaccinated,  but  no  scar  visible 370    2.3  1-2    "    " 

In  the  "  London  Small-pox  Hospital "  the  mortality  is:  4  per  cent,  of  discrete,  simple  variola;  8per  cent, 
of  semi-confluent  variola  ;  and  50  per  cent,  of  confluent  variola. 


756  ACUTE   GENERAL   DISEASES. 

had  passed  through  an  apparently  fatal  condition  of  coma.  The  ratio  of 
mortality  is  always  lower  at  the  end  than  at  the  beginning  of  an  epidemic. 
The  disease  is  more  fatal  in  the  summer  than  in  the  winter. 

The  age  of  the  patient  greatly  influences  the  prognosis.  In  infancy  and 
old  age  the  ratio  of  mortality  reaches  its  maximum.  Among  adults  the 
prognosis  is  worse  in  females  than  in  males.  In  the  intemperate  the  prog- 
nosis is  always  bad,  for  with  this  class  of  persons  the  disease  is  liable  to 
assume  a  hemorrhagic  type.  The  intemperate  die  in  discrete  small-pox 
when  the  temperate  would  almost  certainly  recover.  In  the  overworked 
and  badly-nourished  the  prognosis  is  bad.  The  robust  and  healthy  pass 
through  a  severe  type  of  the  disease  much  more  safely  than  those  enfeebled 
by  chronic  disease.  The  severity  of  the  fever  of  invasion  is  not  a  safe  guide 
in  prognosis.  Sometimes  a  severe  initial  stage  precedes  a  mild  form  of  the 
disesse  ;  sometimes  patients  with  this  disease  pass  into  a  state  of  complete 
unconsciousness,  remain  in  that  condition  for  some  time;  then  the  erup- 
tion begins  to  change  in  color,  and  finally  recovery  takes  place.  Such 
cases,  however,  are  exceptional.  However  well-developed  the  eruption 
may  be,  or  however  well-filled  the  vesicles,  it  is  to  be  remembered  that  the 
eighth  day  is  the  commencement  of  the  suppurative  fever,  which  is  the 
period  of  the  greatest  danger.  Upon  this  day  the  patient  may  pass  into  a 
state  of  collapse,  the  result  of  the  depressing  influence  upon  the  nervous 
system  produced  by  the  large  extent  of  surface  involved  in  the  suppurative 
process.  In  most  cases  in  which  patients  do  not  die  until  the  second  week 
of  the  disease,  the  fatal  result  is  due  to  exhaustion,  although  death  may 
occur  from  complications.  Usually  they  pass  into  a  typhoid  condition,  the 
result  of  the  excessive  drain  upon  the  system  by  the  suppurative  process. 

Pregnancy  is  a  bad  complicating  condition  ;  in  the  confluent,  the  ab- 
sorption that  is  so  liable  to  occur  is  likely  to  be  attended  by  fatal  hleecUng. 
The  most  frequent  complications  which  cause  death  are  those  which  occur 
in  the  throat  and  air-passages.  In  some  instances  swelling  of  the  glands 
of  the  neck  and  mucous  membrane  of  the  throat  takes  place  to  such  an 
extent  as  to  seriously  interfere  with  deglutition  and  respiration.  When 
this  occurs  it  becomes  an  element  of  great  danger,  and  materially  affects 
the  prognosis.  The  tongue  may  become  swollen  to  such  an  extent  that  the 
patient  will  be  unable  to  protrude  it,  or,  being  able  to  protrude  it,  will  not 
be  able  to  retract  it.  Under  such  circumstances  deglutition  is  almost  im- 
possible. There  may  be  laryngeal  ulcers,  and  ulcers  occurring  in  the 
trachea  and  in  the  bronchial  tubes.'  Whenever,  in  the  course  of  the 
disease,  the  urine  becomes  scanty  and  high-colored,  but  especially  when  it 
becomes  so  at  the  commencement  of  the  secondary  fever,  it  is  certain  that 
kidney  complication  exists.     Under  these  circumstances  the  patient  may 

I  Keratitis,  choroiditis,  iritis,  conjunctivitis,  inflammation  of  tlie  middle  ear,  ulcers  in  the  nose,  acute 
arthritis  (of  the  large  joints),  pericarditis,  ulcerative  endocarditis,  pycemia,  and  erysipelas— these  are  all 
occasional  complications.  Diphtheria  is  a  common  complication  of  hemorrhagic  variola.  Cerebral  hemor- 
rhagei&not  an  infrequent  complication  of  small-pox;  aphasia  may  also  occur,  and  thrombosis  of  the 
basiliar  artery  may  induce  a  "dementia-like"  condition.  (Collie.)  Boils,  abscesses,  and  phlegmons  of 
the  skin  are  frequent  sequelae  of  small-pox.  Blindness  and  deafness  also  not  infrequently  follow,  as  also 
paralysis  of  the  bladder  and  paraplegia,  due  (according  to  Westphal)  to  acute  disseminated  myelitis  that 
has  complicated  the  fever. 


SMALL-POX.  757 

pass  into  a  condition  in  which  convulsions  will  be  developed,  and  coma 
and  death  ensue. 

Treatment. — The  first  question  that  arises  is  : — have  we  any  means  by 
which  we  can  arrest  small-pox  after  the  initial  fever  has  been  established  ? 
In  vaccination,  properly  performed,  we  undoubtedly  possess  a  means  by 
which  we  may  prevent  one  from  contracting  the  disease  when  exposed  to 
its  infection.  But  the  question  arises  :  have  we  any  power  to  arrest  the 
development  or  mitigate  the  severity  of  the  disease  after  the  initial  fever  is 
established  ?  No  reliable  affirmative  answer  has  been  given  to  this  ques- 
tion. It  has  been  proposed  to  accomplish  this  by  blood-letting,  emetics, 
diaphoretics,  purgatives,  cold  baths,  and  more  recently  by  the  subcutane- 
ous injection  of  the  vaccine  virus.  All  of  these  means  have  been  tested, 
and  have  failed  to  accomplish  the  desired  result.  The  assertion  that  large 
doses  of  quinine,  given  during  the  stage  of  invasion,  will  shorten  the  dura- 
tion and  modify  the  course  of  the  disease  is  verified  only  by  the  experience 
of  its  author  (Stiemer).  Quite  recently,  it  has  been  claimed  that  carbolic 
and  salicylic  acids  destroy  the  septic  poison  of  the  variola,  and  thus  shorten 
and  modify  the  course.  My  own  experience  as  regards  their  use  has  not 
been  sufficient  to  decide  the  question,  and  I  am  unable  to  find  any  statistics 
which  sustain  such  an  assertion.' 

During  the  fever  of  invasion  all  that  can  be  done  is  to  treat  special  symp- 
toms. Place  the  patient  in  bed  in  a  large  well- ventilated  apartment ;  if 
possible,  keep  the  temperature  of  the  room  below  60°  F.  I  remember  that, 
in  the  Small-pox  Hospital,  those  patients  did  best  who  were  placed  in  bar- 
racks, which  were  so  open,  that  frequently,  during  the  winter  months, 
when  I  made  my  morning  visit,  I  would  find  little  snow-drifts  on  the  floor 
between  the  beds.  When  the  body  temperature  ranges  as  high  as  107°  F. 
or  108°  F.,  it  is  recommended  to  employ  cold  to  the  surface,  and  to  give 
antipyretic  doses  of  quinine  to  rediice  the  temperature.  If  the  headache 
is  severe  and  the  face  flushed,  iced  compresses  and  ice-bags  to  the  head  will 
usually  afford  relief.  If  the  vomiting  is  severe  and  constant,  iced  carbonic 
acid  water  may  be  given,  and  if  the  vomiting  is  attended  by  great  restless- 
ness, hypodermic  injections  of  morphine  are  indicated.  Administer  such 
food  as  can  be  readily  assimilated.  I  have  found  nothing  better  than  iced 
milk  and  seltzer  water.  If  the  bowels  are  constipated,  it  is  well  to  relieve 
them  by  enemata  of  cold  water.  In  those  cases  in  which  the  eruption  is 
tardy  in  making  its  appearance,  and  the  temperature  is  higher,  sometimes, 
if  the  patient  is  kept  in  a  warm  bath  for  fifteen  or  twenty  minutes,  the  de- 
velopment of  the  eruption  is  hastened. 

When  the  eruption  has  appeared,  the  measures  to  be  employed  will  vary 
with  the  character  of  the  eruption.  The  milder  forms  of  discrete  variola 
require  no  interference.  In  the  severer  forms  the  attendant  symptoms 
will  decide  the  means  to  be  employed.  Sooner  or  later,  sometimes  very 
early  in  the  severer  forms  of  the  disease,  the  patient  will  be  found  sinking 
from  the  depressing  effects  either  of  the  small-pox  poison  or  of  the  sup- 

1  Zulzf.T  Cone  of  the  authors  in  Ziemsfen)  states  that  xylol  given  internally  coagulates  the  contents  of 
the  pustules  and  cuts  short  their  development. 


758  ACUTE   GEN"BRAL  DISEASES. 

purafcive  process  which  is  taking  place  upon  the  surface  of  the  body. 
Under  such  circumstances  stimulants  are  indicated.  There  is  no  question 
but  that  the  free  use  of  stimulants  for  a  few  days,  just  at  the  period  of 
suppuration,  in  very  many  cases  does  much  to  save  life.  At  this  time  the 
patient  has  a  dry  tongue,  a  frequent,  feeble  pulse,  blue  lips  and  finger  ends, 
giving  evidence  that  he  is  rapidly  passing  into  a  state  resembling  that  met 
with  in  the  later  stages  of  typhoid  fever.  Active  delirium  is  frequently 
present ;  the  patient  insists  upon  getting  out  of  bed.  Under  these  circum- 
stances, life  will  often  be  saved  by  the  judicious  use  of  stimulants.  If  the 
delirium  is  excessive,  hypodermics  of  morphine  may  be  combined  with 
the  administration  of  stimulants. 

During  the  stage  of  desiccation,  warm  baths  employed  every  day  or  every 
other  day  give  great  comfort,  and  assist  in  the  removal  of  the  crust.  After 
the  baths  the  surface  should  be  freely  oiled.  Complications  will  be  treated 
according  to  the  general  rules  which  govern  their  treatment.  If  abscesses  oc- 
cur in  the  subcutaneous  tissue,  they  should  be  freely  opened  at  once.  We  are 
powerless  when  we  come  to  deal  with  the  hemorrhagic  form  of  small-pox. 
Although  tonics  and  stimulants  have  been  highly  recommended,  they  do 
little  good.  Transfusion  has  been  proposed  and  practised  with  no  definite 
results.  If  the  mouth  and  pharynx  are  very  much  involved,  and  there  is 
difficulty  in  deglutition,  ice-cold  carbonated  water  with  a  weak  solution  of 
the  muriated  tincture  of  iron  used  as  a  gargle  will  often  give  great  relief. 
Sometimes  the  stronger  antiseptic  gargles,  such  as  carbolic  acid  and  the 
permanganate  of  potash,  will  be  of  service. 

There  is  still  one  point  in  the  treatment  of  small-pox  which  is  deserving 
of  attention,  and  that  is,  what  means  may  be  employed  to  prevent  the 
pitting,  especially  upon  the  face,  which  is  so  frequent  a  result.  The  erup- 
tion first  makes  its  appearance  upon  the  face ;  there  it  is  usually  most 
abundant,  and  is  most  liable  to  be  followed  by  pitting,  and  there  it  passes 
more  quickly  through  all  its  stages  than  upon  any  other  part  of  the  body. 
In  order  to  prevent  pitting  it  has  been  proposed  by  some  to  exclude 
light  and  air  from  the  surface  covered  by  the  eruption.  For  this  purpose 
a  great  many  substances  have  been  employed,  such  as  collodion,  gutta- 
percha, certain  forms  of.  plaster,  liquid  paper,  etc.,  etc.  All  these  sub- 
stances are  to  be  so  applied  as  to  form  a  mask  for  the  face,  which  completely 
excludes  light  and  air  from  the  surface. '  The  pitting  is  due  to  the  forma- 
tion of  a  slough,  and  the  slough  is  seated  in  the  areolar  tissue  ;  if  by  any 
means  you  can  so  interfere  with  the  inflammatory  process  as  to  prevent  the 
formation  of  a  slough,  you  will  prevent  the  pitting.  It  was  claimed  by 
those  who  advanced  the  theory  that  excluding  light  and  air  prevented  the 
pitting,  and  that  it  did  this  by  preventing  the  occurrence  of  sloughing. ° 

1  Gold  leaf,  mild  mercurial  ointments,  bismuth,  chalk  and  sweet-oil,  linseed  meal  poultices,  collo- 
dion, carbolic  acid  and  white  lead  paint  have  all  been  extensively  used. 

»  When  I  had  charge  of  so  many  small-pox  patients,  I  took  pains  to  test  all  those  applications  which 
at  that  time  had  been  and  are  still  recommended  for  the  purpose,  and  I  satisfied  myself  that  about 
the  same  results  were  obtained  in  the  use  of  every  remedy,  and  in  no  case  was  pitting  prevented.  Certain 
patients  were  much  more  scarred  than  others,  but  that  was  the  natural  result  of  the  disease.  Some  have 
■nroposed  to  coagulate  the  serum  in  each  vesicle  by  nitrate  of  silver,  and  to  paint  each  papule  with  iodine, 
and   so  arrest  the  inflammatory  process   and  prevent  pitting.    But  the  use  of  tkese  means  has  been 


INOCULATION    AND   VACCINATION.  i'59 


ESrOCULATIOTiT    AISTD    VACCESTATION. 

There  are  two  recognized  methods  of  protection  against  the  infection  of 
small-pox  :  inoculation  and  vaccination.  Inoculation  was  first  introduced 
into  England  by  Lady  Montague,  who  first  practised  it  upon  her  own  child.' 
Subsequently  it  was  quite  generally  practised  throughout  Great  Britain. 
Pus  from  a  small-pox  pustule  was  introduced  beneath  the  epidermis  of  one 
who  had  been  prepared  by  diet  and  general  hygienic  measures  for  the  safe 
development  of  the  disease.  It  was  claimed  that  the  disease  resulting  from 
inoculation  was  a  modified  small-pox,  differing  from  the  original  disease  in 
that  it  ran  its  course  more  rapidly,  was  attended  by  few  pustules,  perhaps 
no  more  than  twenty  or  thirty,  and  was  said  to  rarely  terminate  fatally,  the 
ratio  of  mortality  being  about  one  in  one  hundred.  Those  who  were  inocu- 
lated were  as  fully  protected  from  small-pox  as  those  who  had  the  disease 
in  the  ordinary  manner.  The  disease  developed  by  inoculation  passed 
through  the  regular  stages  of  small-pox. 

Early  in  1776  Edward  Jenner  observed  that  in  some  of  the  northern  coun- 
ties of  England  persons  employed  in  dairies,  who  suffered  from  a  certain 
form  of  ulcer  upon  their  hands,  did  not  contract  small-pox  when  exposed 
to  it.'  He  also  found  that  these  ulcers  upon  the  hands  resembled  pustules 
found  upon  the  udder  of  the  cow,  and  seemed  to  have  been  caused  by  con- 
tact with  them.  Jenner  made  a  thorough  investigation  of  the  subject,  and 
arrived  at  conclusions  sufficiently  satisfactory  to  himself  to  warrant  the  ex- 
periment of  taking  matter  from  one  of  these  pustules  found  upon  the  udder 
of  the  cow  and  introducing  it  into  the  arm  of  the  individual  who  was  sup- 
posed to  be  unprotected  from  the  contagion  of  small-pox.  After  the  sore 
upon  the  arm  had  run  its  course,  he  exposed  the  individual  to  the  infec- 
tion of  small-pox,  and  in  this  way  he  established  its  protecting  power.  In 
1796  he  made  his  first  vaccination  on  man.  In  1798  he  published  his  first 
paper  on  the  subject.^  Vaccination  was  introduced  into  this  country  in 
the  year  1799,  by  Waterhouse  of  Boston,  and  very  soon  became  the  practice 
of  the  profession.     In  1800  it  was  first  practised  in  France.     At  the  pres- 

attended  by  the  same  unsatisfactory  results.  The  only  means  which  I  found  of  certain  value  was  a  simple 
cold-water  dressing  applied  over  the  face,  after  having  ruptured  each  vesicle  before  it  became  a  pustule. 
In  this  way,  I  was  able  to  diminish  the  intensity  and  extent  of  the  inflammation.  This  plan  of  treatment 
I  adopted  in  twenty  cases  of  confluent  small-pos,  and  it  not  only  gave  the  patients  very  great  comfort,  re- 
lieving them  to  a  certain  extent  from  the  intense  itching,  thus  avoiding  rupture  of  the  vesicles  by  scratch- 
ing, but  not  in  a  single  case  that  recovered  was  there  bad  pitting.  In  the  treatment  of  smnll-pox,  the  pre- 
vention of  pitting  is  of  greatest  importance  to  certain  patients,  especially  young  unmarried  females. 

1  In  1717  Lady  Montague,  writing  from  Adrianople,  in  Turkey,  where  the  practice  of  inoculation  was  in 
vogue,  says  :  "  They  take  the  small-pox  here  for  diversion  ;  I  have  tried  it  on  my  dear  little  son  ;  I  am 
going  to  bring  this  useful  invention  into  fashion  in  England."    In  1718  it  did  become  the  fashion. 

^  In  1771  a  Holstein  schoolmaster  vaccinated  three  pupils,  and  in  1774  an  English  farmer  vaccinated  his 
wife  because  of  his  belief  in  the  power  of  bovine  virus  as  seen  in  his  dairymaids. 

3  During  six  years  no  member  of  tlie  profession  ever  received  more  anathemas  or  more  scurrilous  abuse 
than  Jenner.  He  was  attacked  by  the  leading  physicians  and  surgeons  of  Great  Britain,  and  persecution 
and  ridicule  so  followed  him  that  placards  with  caricatures  of  Jenner  were  posted  throughout  the  streets 
of  London  and  the  principal  towns  of  Great  Britain  ;  Jenner  kept  steadily  at  work  and  repeated  his  ex- 
periments, until  he  became  fully  convinced  that  by  vaccination  perfect  protection  could  be  obtained 
against  small-pox.  Within  the  short  space  of  six  years  Jenner  compelled  the  profession  to  admit  his  state- 
ments and  adopt  his  practice,  and  within  the  five  or  six  years  following  its  first  recognition,  the  pracUCCOS 
vaccination  became  generally  recognized  and  practised. 


760  ACUTE   GENERAL  DISEASES. 

ent  time  there  is  no  question  among  the  intelligent  portion  of  the  pro- 
fession but  that  vaccination,  properly  performed,  is  a  perfect  protection 
against  the  infection  of  small-pox  ;  if  persons  contract  small-pox  after  they 
have  been  vaccinated,  then  it  has  not  been  properly  performed. 

There  are  two  methods  of  performing  vaccination.  One  method  is  to 
take  the  virus  directly  from  the  cow  ;  this  is  called  hovine  virus  ;  the  other 
method  is  to  take  the  virus  from  a  vesicle  developed  upon  the  human  body, — 
perhaps  a  vesicle  removed  from  the  original  by  several  vaccinations, — this 
is  called  humanized  virus.  To-day  good  humanized  virus  is  warmly  advo- 
cated ;  first,  because  it  is  more  successful  (98  per  cent.)  than  bovine  virus 
(only  70  per  cent. )  ;  and  secondly,  because  it  is  a  surer  safeguard.  Jenner 
found  that  there  were  several  pustules  developed  on  the  udder  of  the  cow 
which  closely  resembled  each  other,  but  that  only  one  contained  the  virus 
which  afforded  protection  from  small-pox.  In  obtaining  bovine  virus  it  is 
of  the  greatest  importance  that  the  genuine  vesicle  be  selected.  In  order 
to  make  the  selection,  it  is  necessary  one  should  be  familiar  with  the  pe- 
culiarities of  each  variety.  If  humanized  virus  is  used,  there  is  danger  of 
introducing  into  the  system  the  infection  of  other  diseases.  I  have  in  my 
possession  facts  which  prove  beyond  the  possibility  of  a  doubt  that  syphilis 
can  be  conveyed  from  one  person  to  another  by  vaccination.  Cutaneous 
eruptions  may  also  be  conveyed  by  humanized  vaccine  virus,  which  cause 
the  development  of  very  extensive  and  serious  cutaneous  diseases.  Again, 
if  any  chronic  or  acute  skin  disease  exist  at  the  time  the  vaccine  vesicle  is 
running  its  course  the  protective  power  of  the  vaccination  will  be  altogether 
destroyed  or  very  greatly  modified.'  The  vaccine  virus  is  usually  intro- 
duced by  scarifying  the  surface  so  as  to  redden  it,  scarcely  drawing  blood  ; 
then  the  surface  of  the  quill  containing  the  virus  is  applied  to  the  scarified 
part,  or  the  lymph  is  conveyed  from  one  to  the  other  by  direct  transmis- 
sion. 

Any  irregularity  in  the  development  of  the  vesicle  destroys  in  a  greater 
or  less  degree  its  protecting  power.  When  an  individual  has  been  once 
vaccinated,  a  second  vaccination  is  liable  to  run  an  irregular  course. 

A  primary  vaccination,  such  as  the  first  vaccination  of  a  child,  sTiould 
pass  through  the  following  regular  stages,  and  if  it  does  not  it  fails  to  give 
protection :  upon  the  third  day  after  the  introduction  of  the  virus  there 
will  be  noticed  at  the  point  where  it  was  introduced  a  little  red  spot, — a 
papular  elevation.  By  the  fourth  day  this  little  red  spot  will  be  occupied 
by  a  bluish- white  vesicle,  and  at  the  commencement  of  the  fifth  day  there 

1  In  obtaining  vaccine  virus  for  use,  both  the  bovine  and  the  humanized  virus  should  be  taken  from  the 
vesicle  on  the  eighth  day.  The  lymph  should  be  taken  from  the  vesicle  before  the  inflammatory  process 
has  commenced  which  is  to  change  it  into  a  pustule.  Jenner's  "  Golden  Rule  "  was,  any  vesicle  which 
manifests  an  areola  must  be  discarded  in  the  matter  of  withdrawing  lymph.  A  few  years  ago  it  was  the  com- 
mon practice  in  this  city  to  use  the  vaccine  crusts,  but  this  practice  has  fallen  almost  entirely  into  disuse 
because  of  the  great  danger  of  thereby  transmitting  other  diseases.  I  prefer  bovine  virus  when  It  is  possible 
to  obtain  it.  If  compelled  to  use  the  humanized  virus,  use  the  lymt)h.  The  vesicles  must  be  punctured  in 
such  a  manner  that  the  Ij'mph  cannot  be  contaminated  by  the  blood  ;  this  is  best  done  by  introducing  the 
instrument  parallel  with  the  arm.  The  vesicle  must  be  tapped  in  several  places.  The  lymph  which  spon- 
taneously flows  from  such  a  puncture  can  be  preserved  upon  the  convex  surface  of  a  piece  of  quill,  and 
conveyed  from  one  individual  to  another.  Vaccine  virus  secured  from  the  human  arm  in  this  maimer  is 
less  liable  than  any  other  form  of  humanized  virus  to  do  permanent  harm  to  the  vaccinated  individual. 


INOCULATION    AND    VACCINATION.  761 

will  appear  around  the  vesicle  a  little  yellow  margin.  This  vesicle  goes 
on  increasing  in  size  up  to  the  eighth  day,  when  it  will  become  umbilicated 
and  there  will  appear  around  it  a  distinct  areola  ;  about  the  seventh  day 
there  has  been  a  trifling  areola  present ;  on  the  eighth  or  ninth  day  it  be- 
comes very  distinct,  Now  a  change  is  to  take  place  in  the  vesicle,  and  by 
the  next  day  it  will  be  noticed  that  the  areola  has  extended,  perhaps  so  as 
to  measure  an  inch  in  diameter  ;  this  areola  goes  on  extending  itself 
through  the  ninth,  tenth  and  eleventh  days,  when  it  will  have  reached  its 
maximum  extent,  which  may  be  one  or  two  inches  from  the  vesicle  in  all 
directions.  It  is  now  a  deep  red  color.  The  part  over  which  the  areola 
has  spread  is  more  or  less  elevated,  the  arm  is  considerably  swollen  and 
painful,  and  the  adjacent  glands  more  or  less  enlarged  and  tender  to  the 
touch.  The  extent  of  the  enlargement  of  the  gland  adjacent  to  the  vac- 
cine vesicle, — the  axillary  gland,  if  the  vesicle  is  upon  the  arm,  the  inguinal, 
if  it  is  upon  the  thigh, — varies  considerably  in  different  persons.'  In  some 
it  is  very  great,  in  others  it  is  scarcely  noticeable.  The  maximum  degree  of 
inflammation  in  the  vesicle  has  now  been  attained,  and  there  is  a  distinct 
infiltration  of  the  tissues  about  it. 

On  the  twelfth  or  thirteenth  day  the  pustule  ruptures,  and  the  contents 
escape.  The  rupture  belongs  to  the  natural  course  of  the  vaccine  vesicles, 
and  is  independent  of  mechanical  violence.  From  this  time  the  inflamed 
areola  becomes  less  and  less  distinct,  and  by  the  fourteenth  or  fifteenth  day 
the  crust  has  assumed  a  dark,  brownish  appearance,  which  goes  on  deep- 
ening until  on  the  seventeenth  day  a  deep-brown  crust  is  formed  having  a 
central  depression  and  no  areola  of  inflammation.  It  may  be  attached 
to  the  surface  only  in  one  or  two  places,  and  can  be  readily  removed.  If 
permitted  to  remain,  it  usually  falls  off  on  the  eighteenth  to  the  twenty- 
first  day.  This  is  the  course  pursued  by  a  perfect  vaccine  vesicle.  The 
shape  and  size  of  the  crust  will  correspond  to  the  shape  and  size  of  the 
vesicle.  If  the  eighth  day  a  pustule  is  formed  instead  of  a  vesicle,  it  is 
evident  that  the  regular  development  of  the  vesicle  has  been  disturbed,  and 
that  it  will  not  afford  complete  protection. 

The  inflammatory  process  around  the  vesicle  is  usually  more  active  when 
the  bovine  virus  is  used,  than  when  the  humanized  virus  is  introduced,  and 
there  is  more  constitutional  disturbance.  Ordinarily,  during  the  develop- 
ment of  the  vaccine  vesicle  and  pustule,  there  is  but  little  constitutional 
disturbance ;  this  is  usually  self -limiting,  and  not  sufficiently  severe  to 
require  treatment.  In  children,  eruptions,  transitory  in  character,  are 
liable  to  occur  about  the  eighth  or  tenth  day.  About  the  eighth  or  ninth 
day  the  person  vaccinated  may  feel  a  little  chilly,  and  have  severe  headache  ; 
in  most  cases  there  is  a  slight  rise  in  temperature. 

The  regular  course  of  the  vaccine  vesicle  may  be  interfered  with  by  the 
occurrence  of  an  erysipelatous  inflammation,  and  if  such  an  inflammation 
does  occur  during  the  course  of  its  development,  it  entirely  destroys  the 
protecting  power  of  the  vaccination.  Again,  if  a  large  quantity  of  pus  has 
been  discharged,  and  healing  of  the  ulcei-  does  not  take  place  for  two  or 

'  Tiie  axillary  swelling  is  sometimes  so  intense  that  abscess  results.— §Mam's  Diet 


763 


ACUTE   GENEKAL  DISEASES. 


three  months,  it  is  probable  that  something  besides  genuine  vaccine  virus 
has  been  introduced  into  the  arm,  and  that  the  vaccination  is  not  pro- 
tective. As  I  have  already  stated,  the  presence  of  a  vesicular  eruption  upon 
the  surface  at  the  time  vaccination  is  performed  will  interfere  with  its  de- 
velopment, therefore  I  would  advise  never  to  vaccinate  one  who  has  an  ec- 
zematous  eruption  upon  any  part  of  the  body,  unless  he  has  been  exposed 
to  the  contagion  of  small-pox,  for  it  is  very  probable  that  the  vaccination 
will  not  be  a  protective  one.  It  is  better  never  to  vaccinate  a  person  having 
any  form  of  skin  disease,  especially  if  the  eruption  is  vesicular  in  character. 
The  best  time  for  the  first  performance  of  vaccination  is  in  infancy,  between 
the  third  and  fifth  months. 

Eevaccination  should  be  performed  after  puberty,  and  always  after  or 
preceding  a  new  exposure  to  the  contagion  of  small-pox,  for  the  period  dur- 
ing which  revaccination  will  afford  complete  protection  is  not  the  same  in 
every  individual.  In  some  cases  a  single  vaccination  will  afford  complete 
protection  for  a  lifetime.  In  other  cases  it  is  necessary  to  frequently  repeat 
the  vaccination,  perhaps  every  two  years,  in  order  to  secure  the  desired 
protection.^ 

VAEIOLOID. 


During  every  epidemic  of  small-pox  there  is  a  certain  number  of  cS,ses 
concerning  which  there  will  be  doubt  as  to  whether  they  are  cases  of  variola 
or  varioloid.  Certain  persons  who  have  never  been  vaccinated  may,  through 
a  naturally  slight  susceptibility  to  the  infection  of  small-pox,  have  so  mild  a 
form  of  variola  that  it  is  difficult  to  distinguish  it  from  varioloid. 

Varioloid  differs  from  small-pox  in  the  rapid  development  and  decline  of 
the  symptoms,  in  the  small  number  of  the  pustules,  and  in  the  short  time 
required  for  the  formation  and  separation  of  the  crusts.     The  entire  period 

of  the  eruptive  stage  often  does  not 
last  more  than  a  week.  Earely  are 
cicatrices  or  pits  left  after  the  erup- 
tion. In  varioloid  the  period  of  in- 
cubation is  about  one-half  as  long  as 
in  variola,  hence  the  onset  of  the 
graver  disease  may  be  anticipated  by 
vaccinating  one  who  is  known  to 
have  been  exposed,  and  who,  other- 
wise, would  go  on  and  have  the  un- 
modified disease. 

In  varioloid  and  variola  the  pus- 
tules pass  through  similar  stages.  We 
first  have  the  small  red  spot,  then 
vesicles  form,  often  within  twelve 
hours  after  the  appearance  of  the  erup- 
iton.  These  vesicles  rapidly  increase 
sometimes  they  are  umbilicated  ;  by  the  end  of  the  third  day  their 


PiG.163. 
Temperature  Record  in  a  case  of  Varioloid. 


m  size 


The  best  plan  is  to  vaccinate  at  intervals  until  the  individual  has  four  good  scars. 


CHICKEN-POX.  763 

contents  sometimes  become  purulent,  without  any  tumefaction  of  the  sur- 
rounding skin.  Many  vesicles  abort ;  they  do  not  become  pustules.  On 
the  fifth  day  desiccation  commences,  which  is  often  complete  by  the  seventh 
day.  The  majority  of  the  pustules  simply  dry  up,  without  previously 
bursting,  and  form  brown  crusts  which  are  thinner  and  smaller  than  those 
of  variola.  In  varioloid  there  is  no  regular  period  of  development  as  in 
variola.  In  variola  there  is  the  period  of  eruption,  during  which  the  vesi- 
cle is  perfected  ;  this  is  succeeded  by  the  period  of  suppuration,  then  by 
desiccation,  about  fourteen  days  being  required  to  complete  the  process  ; 
while  in  varioloid  the  course  of  the  eruption  is  irregular,  and  is  usually 
completed  within  one  week.  Secondary  fever  is  slight  or  absent.  Again, 
in  varioloid  there  is  but  little  constitutional  disturbance  after  the  appear- 
ance of  the  eruption.  By  the  end  of  the  first  or  commencement  of  the  sec 
ond  day  the  temperature  is  usually  normal.  It  resembles  variola  in  the 
severity  of  the  symptoms  during  the  period  of  invasion,  but  as  soon  as  the 
eruption  appears  there  is  an  entire  cessation  of  all  the  active  febrile  symp- 
toms. During  the  period  of  invasion  varioloid  may  be  said  very  closely  to 
resemble  variola.  When  an  unprotected  individual  is  exposed  to  varioloid, 
the  most  severe  confluent  small-pox  may  be  the  result.  This  fact  proves 
that  varioloid  is  a  modified  form  of  small-pox.  Varioloid  is  small-pox  hav- 
ing a  shorter  duration  and  a  milder  course  than  usual.' 

Prognosis. — Usually  the  prognosis  is  good.  The  rapidity  with  which  the 
vesicles  are  developed,  their  shorter  duration,  the  subsidence  of  the  fever, 
and  the  appearance  of  the  eruption,  together  with  the  usual  duration  of  an 
attack,  are  sufficient  to  distinguish  it  from  variola. 

Treatment. — The  treatment  for  varioloid  is  the  same  as  for  a  mild  or  mod- 
ified form  of  small-pox.  The  patient  should  be  placed  in  a  large,  well- 
ventilated  room,  and  quarantined  the  same  as  though  suffering  from  vari- 
ola. If  the  form  of  invasion  is  severe,  saline  cathartics  may  be  adminis- 
tered. When  delirium  is  present,  and  the  pain  in  the  back  is  very  severe, 
the  moderate  use  of  opium  is  admissible.  As  soon  as  the  eruptive  period 
of  varioloid  is  reached,  no  further  treatment  is  required  ;  the  patient  passes 
on  to  a  rapid  and  complete  convalescence. 

CHICKE]Sr-POX. 

(Varicella.) 

Varicella  is  an  acute  contagious  febrile  disease  accompanied  by  a  vesicu- 
lar eruption,  which  chiefly  affects  children.  It  has  been  called  "  spurious 
variola,"  swine-pox,  etc.,  etc. 

Morbid  Anatomy. — The  only  lesion  of  this  disease  is  the  eruption,  which 
consists  of  small  slightly  elevated  rose-spots,  varying  in  number  from  twenty- 
five  to  two  hundred,  which  in  from  ten  to  twenty-four  hours  become  small 

>  It  may  be  said  that  we  modifj'  small-pox  by  inoculation.  We  do  not :  we  only  modify  its  intensity. 
There  is  the  same  regular  development  of  the  disease  after  inoculation  that  we  have  in  the  ordinary  form 
of  small-pox  ;  while  by  vaccination  we  not  only  lessen  the  severity  of  the  disease  but  we  are  able  to  so 
modify  the  stages  of  its  development  as  to  shorten  its  duration. 


7G4  ACUTE   GENERAL  DISEASES, 

vesicles  with,  clear  contents.  They  vary  in  size  from  a  pin's  head  to  a  pea. 
They  are  usually  discrete,  but  may  run  together  and  form  bullae  three- 
fourths  to  two  inches  in  diameter.  They  rest  on  a  hypersemic  zone  of  skin. 
In  many  cases  the  areola  is  absent.  As  the  vesicles  enlarge,  they  become 
globular  or  ovoid  in  shape  and  their  contents  are  translucent,  glistening 
and  opalescent,  never  acid  as  in  sudamina.  Sometimes  the  vesicles  are  di- 
vided into  compartments.  On  the  third  day  pustulation  of  a  few  vesicles 
may  occur.  On  the  fourth  day  the  vesicles  commence  to  dry  up  ;  on  the 
sixth  crusts  are  formed.  One  crop  occupies  rarely  more  than  six  days,  and 
as  a  second  crop  appears  or  starts  also  on  the  second  and  third  day  of  the 
firsi  crop,  the  whole  number  of  days  of  the  eruption  is  from  seven  to  nine. 

According  to  the  shape  of  the  vesicles,  varicella  is  called  lenticular,  glob- 
ular, conoidal,^  etc.  Pitting  rarely  occurs  ;  should  cicatrices  remain,  they 
disappear  in  two  years. 

Etiology. — Opinions  are  still  divided  as  to  the  identity  of  variola  and  vari- 
cella. Hebra  claims  that  there  is  one  poison  for  the  two  diseases.  Senator, 
Thomas,  and  others  regard  it  as  a  specific  disease.  It  occurs  sporadically 
and  epidemically.  Inoculation  has  given  negative  results.  The  period  of 
incubation  varies  from  eight  to  seventeen  days. 

Symptoms. — Twenty-four  hours  preceding  the  eruption  there  is  usually 
lassitude  and  a  feeling  of  malaise.  The  eruption  appears  first  on  the  back 
or  cheek,  and  then  on  the  face  or  scalp.  It  spreads  irregularly  to  the  abdo- 
men and  extremities.  About  the  second  day  vesicles  may  appear  upon  the 
tongue,  lips,  cheeks,  palate,  and  on  the  mucous  membrane  of  the  genitals. 
On  the  second  day  after  the  first  crop  of  the  eruption  a  new  crop  appears, 
and  in  many  cases  there  is  a  third  crop  on  the  following  day.  The  tem- 
perature rarely  rises  over  100°  or  101°  F. 

Diiferential  Diagnosis. — The  points  of  differential  diagnosis  between 
varicella  and  variola  are  as  follows  : — varicella  runs  rapidly  through  its 
stages  ;  small-pox  has  three  distinct  periods — the  papular,  the  vesicular, 
and  the  pustular.  The  eruption  of  varicella  is  complete  by  the  third,  while 
the  eruption  of  variola  is  never  complete  until  the  ninth  day.  In  both 
natural  and  modified  small-pox  prodromata  occur  before  the  eruption  ap- 
pears, and  then  the  temperature  falls  ;  in  varicella  there  are  no  prodromata, 
and  a  rise  in  temperature  folloios  the  eruption.  Varicella  spreads  irregu- 
larly. Small-pox  vesicles  are  umbilicated  and  multilocular ;  those  of 
chicken-pox  are  globular  or  pointed,  unicellular,  and  collapse  on  pressure. 
Small-pox  is  inoculable,  varicella  is  not.^  The  stage  of  incubation  is  much 
longer  in  chicken-pox  than  in  small-pox,  and  vaccination  does  not  protect 
against  it ;  and  during  its  progress  a  child  can  be  successfully  vaccinated. 
It  is  very  doubtful  whether  varicella  ever  attacks  the  same  individual  twice. 

Prognosis. — The  prognosis  is  always  good. 

Treatment. — The  treatment  is  rest  in  bed,  cleanliness,  a  non-stimulating 
diet,  and  cooling  drinks. 

1  Conoidal  is  also  called  swine-pox. 

2  Small-pox  and  vaccinia  are  often  early  followed  in  tlie  same  individual,  say  within  two  or  three 
years,  by  chicken-pox,  or  vice  versa.  Chicken-pox,  vaccinia,  and  small-pox  have  been  known  to  follow 
in  immediate  succession  in  the  same  individual. 


SCARLET   FEVER.  765 


SCARLET    FEVER. 

Scarlet  fever  or  scarlatina  is  an  inflammation  of  the  tegumentary  invest- 
ment of  the  entire  body,  both  cutaneous  and  mucous,  accompanied  by  a 
fever  of  an  infectious  or  contagious  character.  This  name  has  been  given 
on  account  of  the  bright  red  appearance  of  its  eruptions.  It  is  a  disease  of 
childhood,  but  may  occur  at  any  age. 

Its  development  and  course  are  divided  into  three  periods  :  first,  the 
period  of  invasion,  which  lasts  from  twenty-four  to  forty-eight  hours  ; 
second,  the  period  of  eruption,  which  lasts  from  five  to  seven  days  ;  third, 
W\Q,  period  of  desquamation,  during  which  the  entire  epithelial  surface  is 
removed.  Some  classify  the  disease  according  to  its  severity  ;  others  ac- 
cording to  the  prominent  organs  of  the  body  which  are  involved  ;  others 
according  to  the  prominent  phenomena  which  attend  its  development. 
The  more  common  classification,  and  certainly  the  simplest,  is  that  which 
divides  it  into  scarlatina  simplex,  scarlatina  anginosa,  and  scarlatina 
maligna.     I  shall  adopt  this  classification. 

Morbid  Anatomy. — It  has  no  characteristic  anatomical  lesions,  except 
those  which  occur  in  the  skin  and  mucous  membranes.  The  eruption  is 
its  distinguishing  lesion  ;  it  makes  its  appearance  on  the  second  or  third 
day  after  the  commencement  of  the  febrile  symptoms.  At  that  time  it  con- 
sists of  very  numerous  and  closely  aggregated  points  about  the  size  of  a 
pin's  head  ;  between  these  the  skin  is  of  its  natural  color.  In  typical  cases, 
these  points  are  equally  distributed  over  the  entire  body,  except  the  face. 
These  red  spots  are  usually  circular  in  shape,  slightly  elevated,  ahove  the 
surrounding  skin,  and  so  close  to  each  other  that  they  give  a  confluent  red- 
ness to  the  entire  surface.  In  mild  cases  the  red  points  remain  isolated, 
and  do  not  become  confluent ;  as  the  eruption  develops,  these  red  points 
unite.  In  severe  cases  the  skin  becomes  turgid  and  swollen,  and  presents 
a  uniformly  red  and  glistening  appearance.  In  malignant  cases  the  hyper- 
aemia  of  the  skin  is  often  accompanied  by  more  or  less  extensive  hemor- 
rhages, causing  petechise  and  extensive  ecchymosis.  The  redness  of  the 
eruption  gradually  increases  up  to  a  certain  point,  which  is  not  the  same 
in  all  cases,  then  remains  unchanged  for  twelve  or  twenty-four  hours,  after 
which  time  the  redness  slowly  joasses  away.  During  the  course  of  the  dis- 
ease, the  color  often  changes  with  the  exacerbations  and  remissions  of  the 
fever.  As  a  rule,  the  degree  of  redness  depends  upon  the  intensity  of  the 
fever,  and  may  vary  from  a  pale  red  to  a  deep  scarlet.  If  the  respiration 
becomes  impeded,  the  eruption  assumes  a  bluish-red  hue.  During  the  first 
forty-eight  hours  after  the  appearance  of  the  eruption,  when  the  respiration 
is  unimpeded,  the  redness  completely  disappears  under  firm  pressure,  and 
reappears  as  soon  as  the  pressure  is  removed.  After  this  period,  the  pressed 
point  does  not  entirely  lose  its  red  color.  In  a  certain  proportion  of  cases, 
the  eruption  only  appears  in  spots  on  the  surface  of  the  body,  on  the  trunk, 
or  face,  or  about  the  flexor  surfaces  of  the  joints.  When  it  only  appears  on 
the  face,  the  diagnosis  is  difficult. 


766  ACUTE    GENEEAL    DISEASES. 

In  addition  to  the  cutaneous  hypersemia  which  gives  the  redness  to  the 
surface,  there  is  more  or  less  serous  and  lymphoid,  exudation  into  the  "  rete 
Malpighii,"  which  is  followed,  on  the  decline  of  the  redness  of  the  surface, 
by  an  abundant  epidermic  exfoliation.  Blood  extravasations  into  the  sweat- 
glands  often  occur.  The  exfoliation  marks  the  period  of  desquamation, 
which  may  immediately  follow  the  decline  of  the  redness  or  may  be  delayed 
a  few  days.  This  is  due  to  an  excessive  production  of  newly-formed  epi- 
dermis, and  the  process  may  last  only  a  few  days,  or  if  the  eruption  is  abun- 
dant it  may  continue  for  several  weeks,  and  may  recur  a  second  time  on  the 
same  surface.  After  the  desquamation  has  ceased,  it  does  not  reappear,  ex- 
cept in  cases  of  relapse  ;  these  are  followed  by  renewed  and  sometimes  by  a 
very  complete  desquamation.  Desquamation  has  not  infrequently  occurred 
on  skin  that  has  7iever  been  the  seat  of  the  eruption. 

In  connection  with  these  cutaneous  changes  the  scarlatina  poison  causes 
changes  in  the  mucous  membrane  of  the  mouth  and  throat,  the  most  fre- 
quent of  which  is  catarrhal  pharyngitis,  which  at  first  gives  to  the  mucous 
surface  of  the  tonsils  and  pharynx  a  red,  swollen,  and  dry  appearance.  After 
a  little  time,  these  mucous  surfaces  become  covered  with  a  tenacious  mucus. 
Upon  the  reddened  mucous  membrane  small  elevations  arise,  like  the  smaller 
follicles  in  an  ordinary  catarrh.  In  mild  cases,  all  these  changes  disappear 
in  a  few  days ;  in  the  severer  cases,  the  mucous  surface  assumes  a  dark, 
livid  color,  the  parts  become  more  or  less  cedematous,  and  are  covered  by 
an  abundant  secretion.  Follicular  ulcers  also  form.  The  oedema  may  be 
so  extensive  as  to  render  deglutition  difficult  ;  the  tonsils  are  often  so 
swollen  that  they  touch  each  other. 

Besides  the  redness  and  oedema  of  the  mucous  membrane  of  the  mouth 
and  throat,  there  is  often  inflammation  of  the  parotid  and  sublingual 
glands  as  well  as  of  the  connective-tissue  of  the  neck.  This  glandular  in- 
flammation may  end  in  resolution,  but  often  it  terminates  in  suppurative 
or  diffused  necrosis.  It  may  give  rise  to  extensive  gangrene  of  the  tonsils 
and  adjacent  soft  parts ;  sometimes  it  is  followed  by  extensive  abscesses 
and  destruction  of  the  cellular  tissue  about  the  neck  ;  the  skin  in  the  region 
may  slough,  and  not  infrequently  fatal  hemorrhage  results  from  the  de- 
struction of  small  vessels  ;  or  the  whole  region  may  lie  open  as  if  dissected 
out. 

Diphtheria  is  so  often  a  complication  of  scarlatina  anginosa,  that  it  has 
been  assumed  that  there  is  some  necessary  relation  between  the  two  dis- 
eases.' Yet  diphtheria  is  as  frequently  met  with  in  the  mild  as  in  the 
severe  types  of  scarlatina,  and  occurs  in  every  stage  of  the  disease  ;  it  is 
often  present  during  the  period  of  incubation,  so  that  the  symptoms  of  the 
two  diseases  appear  simultaneously.  Again,  it  is  met  with  during  the 
period  of  convalescence.  In  some  instances,  scarlatina  seems  to  complicate 
diphtheria. 

In  a  mild  form  of  scarlet  fever,  when  the  disease  runs  a  regular  course, 
the  nasal  mucous  membrane  is  usually  pale,  and  its  secretion  is  not  in- 

1  Hubner  states  that  the  pseudo  membranes  are  much  thinner  in  scarlatinal  than  in  ordinary  diphtheria, 
and  that  in  the  former,  fibrin  is  found  between  the  epithelia  and  in  the  mucous  and  submucous  connective- 
tissue. 


SCARLET   FEVER.  767 

creased.  "When  the  disease  is  severe,  the  nasal  mucous  membrane  becomes 
secondarily,  never  primarily,  involved.  This  is  the  result  of  a  catarrhal 
affection  of  the  throat.  It  is  a  purulent  catarrh  of  the  posterior  nares, 
which  gradually  extends  to  the  anterior  nares,  and  gives  rise  to  a  very 
troublesome  form  of  coryza.  During  the  eruptive  period  of  scarlatina, 
affections  of  the  ear  frequently  occur  in  connection  with  those  of  the  throat. 
Usually  these  have  their  seat  in  the  middle  ear,  pus  being  the  product. 
They  are  always  tedious  and  may  become  chronic.  The  eye  maybe  involved; 
keratitis  and  ulcers  are  not  uncommon. 

Next  to  the  skin  and  mucous  surfaces,  the  kidneys  are  the  organs  most 
frequently  affected  in  this  disease.  There  is  no  question  but  that,  in  a  cer- 
tain proportion  of  cases,  recovery  takes  place  without  any  kidney  lesions  ; 
but  these  are  the  exceptions  and  not  the  rule.  In  some  ej^idemics  the 
scarlatina  poison  induces  a  so-called  "  croupous"  inflammation  of  the  urin- 
iferous  tubules.  The  tubules  of  the  cortical  substance  of  the  kidneys  are 
most  extensively  affected  ;  the  morbid  processes  commencing  at  the  Mal- 
pighian  tufts  '  follow  the  course  of  the  convoluted  tubules.  If  the  tubules 
are  only  slightly  affected  there  will  be  no  symptoms  except  a  slight  albu- 
minuria. The  kidney  changes  are  rarely  well  marked  before  the  second  or 
third  week  of  the  disease,  and  usually  terminate  in  complete  recovery.  The 
character  and  extent  of  these  kidney  changes  vary  in  different  epidemics. 
During  some  epidemics,  the  kidney  changes  are  slight  ;  during  other 
epidemics  almost  every  case,  whether  mild  or  severe,  will  be  attended  by 
extensive  kidney  lesions. 

At  the  post-mortem  examination  of  one  who  has  died  of  scarlet  fever, 
there  will  be  found  more  or  less  extensive  congestion  of  the  internal  organs, 
the  brain,  liver,  spleen,  etc.,  but  these  congestions  do  not  differ  from  those 
met  with  in  other  acute  infectious  diseases.  The  changes  in  the  con- 
stituents of  the  blood  ^  are  such  as  to  diminish  its  coagulating  power. 
The  Peyerian  patches  will  often  be  found  presenting  the  '^shaven-beard 
appearance."  There  may  be  parenchymatous  degeneration  of  the  gastric 
tubules. 

Etiology. — The  cause  of  scarlet  fever  is  a  contagion,  which  is  transferable 
from  the  sick  to  the  healthy.  It  has  been  claimed  that  sporadic  cases  do 
occasionally  occur  ;  but  there  is  little  doubt  that  if  the  history  of  every 
case  of  supposed  spontaneous  scarlet  fever  could  be  carefully  taken,  it  would 
be  found  that  at  no  place  and  at  no  time  had  the  disease  ever  been  of  spon- 
taneous origin.  It  may  be  conveyed  directly  from  the  affected  to  the 
healthy  by  contact,  through  the  atmosphere  and  by  clothing  which  has  been 
thoroughly  saturated  with  the  scarlet  fever  poison ;  therefore  it  may  be 
considered  a  portable  disease.  Animals  that  have  been  around  those  sick 
with  scarlet  fever  may  convey  it.  I  recall  an  instance  in  which  the  scar- 
let fever  poison  was  conveyed  in  this  way  : — For  a  number  of  days  a  little 
dog  had  been  around  children  sick  with  scarlet  fever,  and  by  a  single  visit 

1  There  is  proliferation  of  epithelial    nuclei  in  the    glomeruli,  distending  them  to  twice  their  size, 
and  thus  comprc«sing  the  vascular  tuft.     There  is  hyaline  degeneration  of  the  capillaries  (Klein). 
'^  Micrococci  are  found  in  the  blood. 


768  ACUTE    GENERAL   DISEASES. 

of  the  dog  to  the  children  of  another  family  the  disease  was  conveyed. 
There  has  been  considerable  discussion  as  to  whether  the  disease  Can  or 
cannot  be  conveyed  in  milk.     This  is  possible.' 

The  infection  of  scarlatina  is  not  so  certain  as  that  of  measles  or  small- 
pox. When  one  member  of  a  family  is  sick  with  measles,  usually  every 
other  member  of  that  family  who  has  not  had  measles  will  contract  the  dis- 
ease ;  whereas  one  member  of  a  family  may  be  sick  with  scarlet  fever  and 
every  other  member  may  escape.  Some  seem  to  have  a  certain  idiosyn- 
crasy, so  that  when  they  are  brought  in  contact  with  the  poison  of  scarlet 
fever  they  do  not  contract  the  disease.  The  poison  which  they  receive  into 
the  system  has  power  to  produce  some  of  the  symptoms  but  has  not  power 
to  fully  develop  the  disease. 

Scarlet  fever  can  be  communicated  from  one  individual  to  another  by  in- 
oculation. If  some  of  the  watery  material  or  serum  that  can  be  obtained 
from  the  minute  vesicles  occasionally  seen  upon  the  surface  of  the  body  in 
connection  with  the  scarlet  fever  eruption,  be  taken  and  introduced  into 
the  body  of  an  individual  who  has  not  had  scarlet  fever,  it  will  develop  the 
disease.  It  has  been  proposed  to  inoculate  those  who  have  not  had  scarlet 
fever  in  the  same  manner  as  one  would  inoculate  those  who  have  not  had 
small-pox,  and,  by  so  doing,  produce  a  modification  of  the  disease.  But  it 
has  been  found  by  experiment  that  those  who  have  been  inoculated  for 
scarlet  fever  have  suffered  more  severely  than  those  who  contracted  the  dis- 
ease by  any  of  the  common  methods  of  contagion.  There  is  no  question 
but  that  the  scarlet  fever  poison  can  also  be  introduced  into  the  system 
through  the  respired  air,  but  whether  it  can  be  taken  into  the  system 
through  the  medium  of  food  or  fluids  is  still  an  unsettled  question. 

A  question  of  great  practical  importance  is  :  if  the  disease  can  be  con- 
veyed by  clothing,  is  it  safe  for  a  physician  to  visit  patients  sick  with  scar- 
let fever,  and  go  from  them  directly  to  those  who  have  not  had  the  disease  ? 
Unquestionably  it  is  possible  to  so  convey  the  disease,  but  in  my  own  ex- 
perience I  know  of  no  case  where  it  has  been  so  conveyed.  The  clothing 
in  order  to  be  sufficiently  impregnated  with  the  poison  to  render  it  a  means 
of  contagion  must  be  longer  exposed  than  is  the  case  when  a  physician 
makes  a  visit  of  ordinary  length.  Unquestionably,  nurses  who  have  been 
with  a  scarlet  fever  patient  for  a  number  of  days,  and  whose  clothing  has 
become  filled  with  the  poison,  may  carry  the  disease.  These  should  change 
their  clothing  before  they  go  from  the  sick  to  the  healthy.  The  real  nature 
of  the  scarlatina  poison  is  undetermined.  The  period  at  which  this  disease 
is  most  infectious  is  probably  the  desquamative  period,  although  some  main- 
tain that  it  is  most  infectious  during  the  eruptive  period. 

An  individual  is  almost  certain  never  to  have  a  second  attack. 

The  period  of  incubation  varies  from  two  to  ten  days,  the  average  dura- 
tion being  from  three  to  five.  It  may  be  only  three  hours.  Age  has  a 
great  influence  on  individual  predisposition.  The  greatest  susceptibility 
to  the  influence  of  the  poison  exists  between  the  second  and  seventh  years  ; 

'  Quain  says  :  "Milk  is  a  great  medium  for  carrying  scarlet  fever,  and  cream,  even  more  than  mUk, 
often  carries  it  from  sick  to  well." 


SCARLET   FEVER.  769 

it  rapidly  diminishes  after  the  ninth  year,  so  that  adults,  and  especially  the 
aged,  have  only  a  slight  predisposition  to  the  infection.  Those  who  have  just 
undergone  surgical  operations  seem  to  be  especially  prone  to  contract  the 
disease.  Scarlet  fever  may  be  endemic  or  epidemic.  No  reason  can  be  as- 
signed for  its  variations  in  type  or  severity.  For  years  the  type  of  fever 
•vfhich  appears  in  a  given  locality  will  be  exceedingly  mild  in  character, 
when  suddenly,  without  any  assignable  cause,  a  most  malignant  epidemic 
will  prevail.  Usually  epidemics  of  scarlatina  prevail  in  the  autumn  and 
spring.' 

Symptoms. — The  symptoms  of  scarlet  fever  vary  with  the  type  and  with 
the  severity  of  the  fever.  In  moderately  severe  eases,  before  the  appear- 
ance of  the  eruption,  the  patient  will  have  a  more  or  less  severe  headache, 
pain  in  the  back  and  limbs,  and  at  first  coldness  of  the  surface.  Epistaxis 
is  not  rare.  In  some  cases  I'igors  will  occur,  and  perhaps  distinct  chills. 
In  children  convulsions  and  coma  often  occur.  These  ushering-in  symp- 
toms are  immediately  followed  by  a  sensation  of  intense  heat,  with  great 
acceleration  of  the  joulse,  which  at  this  time  often  beats  120  or  130  per 
minute.  There  will  also  be  nausea  and  vomiting,  frequently  most  jaer- 
sistent  and  distressing.  Besides,  there  will  be  a  rapid  rise  in  temperature. 
It  may  reach  103°  F.  or  l04°  F.,  within  a  few  hours. 

Within  a  period  lasting  from  twelve  to  forty-eight  hours,  the  average 
being  thirty-six  hours,  the  eruption  makes  its  apj^earance,  and  the  fever 
increases.  The  elevation  in  temperature  is  accompanied  by  restlessness,  a 
burning  sensation,  perhaps  delirium ;  the  nausea  and  vomiting  become 
more  urgent,  and  now  the  papillge  of  the  tongue  become  swollen,  and  the 
organ  presents  the  appearance  of  a  strawberry  : — (the  "  strawberry  tongue" 
of  scarlet  fever) .  This  appearance  is  not  commonly  seen  in  the  milder  cases, 
but,  as  a  rule,  is  present  in  all  the  severer  cases.  With  the  appearance 
of  the  eruption,  all  the  symjDtoms,  perhaps  exce23ting  the  pain  in  the  head, 
increase  in  severity.  The  urine,  if  it  has  been  scanty,  will  now  become 
more  so,  and  may  be  nearly  suppressed ;  if  it  has  been  sufficiently  abun- 
dant, not  infrequently,  as  the  eruption  makes  its  appearance,  it  becomes 
scanty  and  high-colored.  In  some  cases  the  disease  is  so  mild  that  there 
is  but  little  disturbance,  except  that  caused  by  the  eruption,  the  tempera- 
ture being  not  over  102°  F.  In  other  cases  the  disease  is  ushered  m  by 
violent  nervous  symptoms,  such  as  delirium  and  coma,  accompanied  by 
extreme  exhaustion,  and  the  patient  dies  before  the  eruption  makes  its  ap- 
pearance. In  other  words,  the  patient  dies  during  the  period  of  invasion, 
from  the  overwhelming  of  the  nervous  system  with  the  scarlet  fever  poison. 

During  the  earlier  stages  of  the  disease  the  throat  symptoms  are  quite 
characteristic.  Adults  and  older  children  complain  of  a  pricking  sensation 
in  the  throat,  and  difficulty  in  deglutition  ;  the  tonsils,  uvula,  and  posterior 
Avail  of  the  pharynx  are  red  and  CBdematous,  and  from  their  aj)pearance, 
with  the  attendant  symptoms,  in  most  instances,  one  is  able  to  very  early 

'  Trojanowsky  and  Thomas  describe  a  variety  called  "  recurrent,"  where  two  series  of  eruptions  over- 
lap, as  it  were,  and  finally  merge  into  one  attack.    But  the  latter's  cases  all  occurring  in  marshy  districts, 
hf;  inclines  to  the  view  that  the  poisons  of  malaria  and  scarlatina  were  combined  and  perhaps  modified  by 
each  an  unicii. 
49 


770  ACUTE   GENERAL  DISEASES. 

decide  that  the  ease  is  one  of  commencing  scarlatina.  There  are  cases 
in  which  the  throat  symptoms  are  altogether  absent  at  first,  and  do  not 
come  on  until  later  in  the  disease.  The  symptoms  which  mark  the  de- 
velopment of  this  disease  remain  to  be  studied  in  detail. 

As  already  stated,  the  whole  course  of  scarlet  fever  may  conveniently  be 
divided  into  three  stages.  First,  the  stage  of  invasion,  or  the  febrile 
stage.     Second,  the  stage  of  eruption.     Third,  the  stage  of  desquamation. 

The  duration  of  the  stage  of  invasion  varies  with  the  type  of  the  dis- 
ease. In  most  cases,  it  is  from  twelve  to  twenty-four  hours ;  it  may  be 
four  or  five  days.  Usually  the  onset  is  marked  by  chilliness  and  slight 
rigors,  followed  by  a  rapid  rise  in  temperature.  The  skin  becomes  dry,  the 
face  flushed,  and  the  pulse  accelerated.  At  the  same  time  there  is  slight 
soreness  of  the  throat,  the  face  appears  red  and  dry,  the  neck  is  stiff,  the 
eyes  suffused,  and  there  is  some  tenderness  about  the  joints.  Vomiting 
and  thirst  are  prominent  symptoms.  The  tongue  is  red  at  its  tip  and 
edges,  the  papillae  are  enlarged,  and  it  presents  the  so-called  strawberry 
appearance.  Lassitude,  pain  in  the  head,  aching  of  the  limbs,  and  rest- 
lessness are  generally  present.  There  may  be  some  delirium  at  night. 
Twenty-four  hours  after  commencement  of  the  fever  of  invasion,  the 
eruption  may  make  its  appearance.  The  period  which  elapses  between  the 
exposure  and  the  appearance  of  the  eruption  varies.  In  some  cases  the 
eruption  is  said  to  have  appeared  as  early  as  twenty-four  hours  after  ex- 
posure, while  in  others  one  or  two  weeks  have  elapsed  after  the  exposure 
before  the  disease  was  developed.  No  definite  statement  in  regard  to  the 
duration  of  the  period  between  the  exposure  and  the  appearance  of  the 
eruption  can  be  made.  The  eruption  first  makes  its  appearance  upon  the 
neck  and  upper  portion  of  the  chest,  and  is  first  seen  as  little  red  dots, 
varying  in  size  from  a  line  to  a  line  and  a  half  in  diameter.  These  gradu- 
ally coalesce  and  the  eruption  extends  over  the  entire  surface  of  the  body, 
perhaps  on  the  face,  and  lastly  it  appears  on  the  lower  extremities.  It 
presents  its  brightest  appearance  upon  the  evening  of  the  fourth  day. 
After  the  second  day  of  the  eruption,  if  not  before,  the  entire  surface 
will  present  a  uniform  redness,  the  color  varying  with  the  severity  of  the 
disease. 

In  the  milder  cases  one  will  have  a  bright  rose-red  eruption  or  rash,  while 
in  the  severer  types  the  eruption  will  assume  an  appearance  resembling  the 
deep-red  color  of  the  boiled  lobster.  The  darker  the  eruption,  the  more  se- 
vere the  form  of  the  disease  and  the  greater  the  danger.  When  the  erup- 
tion is  fully  developed,  it  will  be  noticed  that  the  surface  is  somewhat  ele- 
vated, the  parts  present  a  swollen  appearance,  the  vessels  of  the  skin  seem 
to  be  congested,  and  there  will  be  soreness  of  the  throat  more  marked  thar 
in  the  febrile  stage.  Miliaria  appear  when  the  rash  is  most  intense,  anQ 
sudamina  are  common. 

Usually,  vomiting  is  present  at  the  commencement  of  the  disease,  but 
becomes  more  severe  and  a  more  marked  symptom  as  the  stage  of  eruption 
is  ushered  in  ;  if  not  present  at  the  commencement,  it  is  certain  to  make 
its  appearance  with  the  appearance  of  the  eruption.     The  vomiting  is  pe- 


SCAELET  FEVEE. 


771 


culiar,  not  on  account  of  the  matters  ejected,  but  the  ad  of  vomiting  is 
projectile  in  character. 

In  scarlatina  the  condition  of  the  throat  depends  upon  the  severity  of  the 
disease.  In  some  cases  there  is  simply  a  blush  of  redness  over  the  posterior 
portion  of  the  pharynx  and  uvula  and  anterior  pillars  of  the  soft  palate.  In 
other  cases  a  general  tumefaction  and  oedema  of  all  the  soft  parts  of  the 
throat  will  be  seen,  and  the  tonsils  will  be  the  seat  of  a  more  or  less  intense 
parenchymatous  inflammation,  which  gives  rise  to  a  swelling  that  encroaches 
more  or  less  upon  the  pharynx.  Again,  ulcerative  pharyngitis  will  occur, 
or  upon  the  surface  of  the  enlarged  tonsils  and  swollen  mucous  membrane 
of  the  pharynx  there  may  be  an  exudation,  which  will  be  more  fully  de- 
scribed hereafter. 

In  this,  the  ordinary  form  of  scarlatina,  when  it  runs  its  ordinary  course, 
there  will  not  be  much  swelling  of  the  glands  about  the  neck,  nor  very  much 
tumefaction  of  the  soft  tissues  in  the  pharynx.  On  the  morning  of  th,e  fourth 
day,  if  the  finger-end  is  drawn  across  the  surface,  a  clear,  well-defined  line 
will  be  made,  which  will  remain  for  some  time.  This  distinct  white  line 
is  a  point  of  some  importance  in  distinguishing  scarlatina  from  roseola. 
Usually  the  eruption  begins  to  fade  upon  the  fourth  day,  and  by  the  sixth 
day  it  has  entirely  disappeared,  and  desquamation  has  commenced.  During 
the  time  the  eruption  is  developing,  the  temperature  continues  to  rise  until 
perhaps  it  has  reached  106°  F.  or  107°  P.  In  the  meantime  the  pulse  may 
increase  to  120  or  even  140,  or  perhaps  150  beats  per  minute,  and  not  in- 
frequently there  is  some  delirium  during  this  stage  ;  there  may  be  also  more 
or  less  stupor.  There  is  an  intense  itching  and  burning  upon  the  surface, 
and  a  great  restlessness. 

Between  the  fifth  and  eighth  days  of  the  eruption,  the  temperature  be- 
gins to  decline,  and  at  the  same  time 
the  eruption  fades.  This  fading  of 
the  eruption  goes  on  rapidly,  so  that 
by  the  end  of  the  eighth,  certainly 
early  on  the  ninth  day,  sometimes  as 
early  as  the  sixth  day,  it  is  no  longer 
visible.  With  the  disappearance  of 
the  rash,  desquamation  commences, 
and  with  this  there  will  be  a  still 
more  marked  fall  in  temperature,  and 
diminished  frequency  of  the  pulse. 
All  the  febrile  symptoms  disappear,  all 
the  throat  symptoms  subside,  there  is 
no  longer  any  difficulty  in  deglutition, 
there  is  no  more  pain  in  the  throat, 
no  more  swelling  of  the  external 
glands,  if  previously  it  had  existed. 

The  period   of  desquamation  lasts  Fro.  i64. 

about  two  weeks,  during  which    time         Temperature  Kecord  in  a  case  of  Scarlatina. 

there  is  the  greatest  danger  of  communicating  the  disease.     At  the  end 


Da 


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772  ACUTE    GENERAL   DISEASES. 

Of  that  period,  if  no  complication  occur,  the  patient  is  well.  The  fine 
scales  which  are  so  abundantly  thrown  off  contain  the  specific  poison,  and 
they  are  so  delicate  that  they  are  blown  about  with  every  breath,  and  car- 
ried in  every  current  of  air,  and  are  in  the  most  favorable  condition  to  be 
taken  into  the  system  in  the  respired  air.  Some  have  maintained  that  the 
contagious  period  in  this  disease  does  not  occur  until  the  period  of  des- 
quamation. This  statement  is  not  sustained  by  clinical  facts.  The 
amount  of  the  desquamation  depends  upon  the  intensity  of  the  eruption. 
The  skin  has  a  dry  feel  before  desquamation  commences.  Where  the  skin 
is  thin  the  epidermis  comes  off  in  thin  scales,  '' branny"  desquamation. 
Where  the  skin  is  thick,  as  on  the  palms  of  the  hands  and  the  soles  of  the 
feet,  it  peels  off  in  extensive  patches,  "  scaly  "  desquamation.  With  the 
desquamation,  the  fever  subsides  more  or  less  rapidly.  The  entire  period 
occupied  by  a  case  of  scarlet  fever,  when  it  runs  its  regular  course,  is  from 
two  to  three  weeks. 

Scarlet  fever  is  liable  to  irregularities  which  it  is  important  to  consider. 
It  is  claimed  by  some  that  these  irregularities  depend  upon  the  organ  or 
set  of  organs  primarily  affected  by  the  scarlet  fever  poison.  They  are 
rather  due  to  some  peculiarity  in  the  type  of  the  disease,  to  the  degree  of 
poisoning,  and  in  some  instances  to  the  particular  set  of  organs  that  are 
involved  in  the  different  epidemics.  In  some  epidemics  even  milder  forms 
of  the  disease  than  have  been  described  are  seen.  The  attack  may  be  so  mild, 
and  there  may  be  so  little  fever  that  if  the  eruption  was  not  present  one 
would  not  be  able  to  recognize  the  scarlet  fever  ;  and  even  that  may  be  so 
light  that  the  stage  of  eruption  and  the  stage  of  desquamation  may  pass 
unnoticed,  and  one  may  be  scarcely  able  to  decide  whether  the  patient  has 
or  has  not  had  an  attack  of  scarlet  fever. 

The  most  frequent  irregularity  in  the  manifestation  of  the  disease  is 
noticed  in  that  class  of  cases  where  we  have  complications  resulting  from 
the  overwhelming  of  the  cerebro-spinal  system  with  the  scarlatina  poison. 
This  is  due  to  some  peculiarity  of  the  poison,  and  is  characteristic  of  cer- 
tain epidemics.  In  a  large  number  of  cases  in  the  febrile  stage,  especially 
in  young  children,  convulsions  may  occur,  but  they  do  not  depend  upon 
the  peculiarity  referred  to.  In  the  class  of  cases  to  which  reference  has. 
been  made,  where  complications  arise  from  the  overwhelming  of  the  cerebro- 
spinal system  with  the  scarlatina  poison,  from  the  very  onset  of  the  disease 
there  seems  to  be  a  tendency  to  stupor  and  delirium,  a  peculiar  restlessness, 
an  apparent  wandering,  a  picking  at  the  bed-clothes,  accompanied  by  a 
peculiarity  in  the  appearance  of  the  eruption,  which  may  caujse  it  to  assume 
the  boiled-lobster  appearance,  or  even  a  darker  hue.  The  eruption  is  slow 
in  its  development,  and  there  is  not  that  uniform  redness  over  the  entire 
body  that  is  seen  in  ordinary  cases ;  it  appears  in  patches,  and  with  it  there 
is  exhibited  a  tendency  to  blueness  of  the  finger-ends,  indicating  that  there 
is  acting  upon  the  nervous  system  a  poison  which  possesses  the  power  of 
very  greatly  lowering  the  vitality  of  the  patient.  These  symptoms  pre- 
dominate in  some  epidemics. 

There  is  a  class  of   cases  in  which  there  is  not  much  swelling  of  the 


SCAELET   FEVER.  773 

throat,  nor  is  the  pulse  more  frequent  than  130  or  140  per  minute,  but 
during  the  second  day  of  the  eruption  the  temperature  ranges  very  high, 
reaching  107*^  or  108°  F.,  and  then  the  pulse  becomes  intermittent.  Under 
such  circumstances  the  disturbance  of  the  nervous  system  is  due  to  the 
high  temperature  which  may  have  been  present  for  two  or  three  days  ; 
these  disturbances  may  be  j)revented  if  the  temperature  is  not  allowed  to 
rise  above  103°  or  104°  F. 

Again,  in  cases  where  there  is  marked  swelling  of  the  throat,  and  a 
general  infiltration  of  the  tissues  and  glands  of  the  neck,  the  develojjment 
of  the  nervous  phenomena  is  due  to  an  interference  with  the  return  circu- 
lation. The  condition  which  gives  rise  to  the  cerebral  symptoms  is  one  of 
mechanical  cerebral  congestion. 

There  is  still  another  class  of  cases  in  which  the  marked  nervous  j)he- 
nomena  appear  still  later  in  the  course  of  the  disease.  Under  such  cir- 
cumstances they  often  indicate  a  typhoid  condition.  This  typhoid  condi- 
tion is  not  induced,  nor  are  the  nervous  phenomena  developed,  on  account 
of  the  peculiar  effect  produced  upon  the  nerve  centres  by  the  scarlet  fever 
poison,  nor  are  they  due  to  the  effects  produced  by  a  high  temperature, 
nor  by  an  interference  with  the  return  circulation,  but  they  are  due  to 
septic  poisoning,  a  poisoning  entirely  different  from  scarlet  fever  poisoning. 
The  nervous  phenomena  develop  after  the  eruption.  During  the  develop- 
ing period,  there  may  be  noticed  a  peculiar  ichorous  discharge  from  the 
nostrils,  and  frequently  it  is  said  that  the  patient  has  become  repoisoned 
by  scarlet  fever  poison — but  this  is  not  the  case  ;  he  has  become  repoisoned 
by  the  septic  element  of  these  discharges.  During  the  period  of  desqua- 
mation the  nervous  system  may  be  involved  in  consequence  of  the  presence 
of  urgemic  poisoning. 

The  mere  terms,  scarlatina  simplex,  scarlatina  anginosa,  and  scarlatina 
maligna,  do  not  indicate  all  that  may  be  embraced  under  each  of  the  divi- 
sions. 

Scarlatina  maligna  is  that  form  of  the  disease  in  which  tl>e  cerebro- 
spinal system  becomes  early  involved.  What  the  changes  are  that  produce 
these  nervous  phenomena,  when  high  temperature  is  present,  is  still  an  un- 
settled question. 

Again,  scarlet  fever  may  run  an  irregular  course  in  those  cases  in  which 
there  is  present  an  extensive  infiltration  of  the  tissue  of  the  neck,  with 
inflammatory  products,  swelling  of  the  glands,  and  extensive  suppuration. 
Not  infrequently  these  cases  terminate  fatally  ;  doubtless  in  some  cases  the 
extensive  suppuration  in  the  areolar  tissue  about  the  neck  produces  this 
result,  and  in  other  cases  it  is  produced  by  the  interference  with  respira- 
tion caused  by  enlargement  of  the  glands  and  swelling  of  the  tissues  of  the 
neck.  Exhaustion  from  sloughing  is  a  cause  of  death.  In  these  cases 
there  is  danger  from  oedema  glottidis,  the  consequence  of  extension  of  the 
inflammation  from  the  adjacent  tissues. 

There  are  cases  in  which  the  eruption  is  not  very  well  marked  ;  the  pa- 
tient passes  safely  through  the  stage  of  eruption,  and  the  stage  of  desqua- 
mation is  fully  established  ;  but,  instead  of  making  a  good  recovery  from 


774  ACUTE    GENERAL   DISEASES. 

this  point,  immense  abscesses  are  rapidly  developed  in  the  cervical  region, 
blood-changes  begin  to  manifest  themselves — changes  that  favor  hemor- 
rhages. Hemorrhages  are  then  petechial  in  character  and  occur  on  the 
mucous  surfaces,  and  the  patient  passes  into  a  typhoid  condition,  with  hem- 
orrhages occurring  from  the  nose,  mouth,  intestines,  etc.,  and  death  en- 
sues. Such  a  result  is  produced  by  the  peculiar  action  of  the  septic  poison 
developed  during  the  suppurative  process,  and  perhaps  from  outside  influ- 
ences (as  bad  hygiene). 

I  regard  scarlatinal  coryza,  in  which  the  discharge  contains  elements 
capable  of  producing  septic  poisoning,  as  an  unfavorable  symptom.  The 
clear  serum  which  runs  over  the  lip  never  causes  death  ;  but  the  fact  that 
it  sometimes  produces  excoriation  and  ulceration  of  the  tissues  with  which 
it  comes  in  contact,  indicates  that  there  are  nasal  and  pharyngeal  changes 
which  may  destroy  life  ;  especially  is  this  the  case  in  young  children. 
Sloughing  ulcers  sometimes  develop  in  the  mouth  and  throat ;  and  when 
they  do  occur,  the  patient  is  said  to  have  ulcerative  stomatitis  ;  but  these 
ulcerations  are  really  due  to  a  peculiarity  of  the  scarlatina  poison.  Under 
such  circumstances  the  patient  may  go  on  through  the  period  of  eruption, 
enter  the  stage  of  desquamation,  and  then  rapidly  sink  and  die,  with  symp- 
toms similar  to  those  which  attend  diphtheria.  Although  the  odor  of  the 
breath  may  very  closely  resemble  that  noticed  in  some  cases  of  diphtheria, 
there  is  no  diphtheritic  exudation  present. 

Scarlatina  may  also,  run  an  irregular  course  by  the  development  of  in- 
flammation of  the  internal  ear.  This  inflammation  extends  from  the 
throat  up  the  Eustachian  tube,  involves  the  middle  ear,  and  gives  rise  to  a 
train  of  symptoms,  such  as  intense  pain,  delirium,  and  rolling  of  the  head, 
all  of  which  suggest  the  presence  of  acute  meningitis.  I  recall  several  in- 
stances in  which  the  diagnosis  of  acute  meningitis  was  made,  where  from 
the  after-history  of  the  case  there  was  no  question  but  that  the  symptoms 
were  due  to  such  an  inflammation  of  the  middle  and  internal  ear. 

Complications  and  Sequelce. — The  most  common  sequela  is  anasarca. 
The  anasarca  of  scarlatina  usually  appears  at  the  time  the  patient  is  conva- 
lescing, during  the  period  of  desquamation,  or  just  as  desquamation  is  being 
completed.  It  has  been  thought  that  anasarca  is  due  to  some  exposure  to 
the  influence  of  cold  during  this  period.  It  is  possible  that  the  changes  in 
the  kidney  which  give  rise  to  the  anasarca  may  sometimes  be  produced  by 
the  influence  of  cold,  and  undoubtedly  anasarca  is  occasionally  developed  in 
this  manner;  but  in  the  majority  of  cases  it  is  due  to  some  peculiarity  in 
the  scarlet  fever  poison,  or  to  some  peculiar  atmospherical  condition.  Dur- 
ing some  years  anasarca  is  a  very  common  sequela  of  scarlet  fever  ;  while 
during  other  years  in  equally  severe  cases,  scarcely  a  case  of  anasarca  occurs. 
While  we  recognize  the  fact  that  it  is  possible  for  kidney  lesions  to  be  de- 
veloped which  shall  give  rise  to  anasarca  in  consequence  of  exposure  to 
cold,  it  is  also  of  importance  that  we  recognize  the  fact  that  the  lesions  and 
the  anasarca  may  be  developed  independent  of  such  exposure.  The  ana- 
sarca first  shows  itself  on  the  face,  and  from  the  face  it  extends  over  the 
entire  body,  and  if  it  becomes  general  more  or  less  ascites  is  developed. 


SCARLET   FEVER.  775 

In  most  cases,  at  the  time  of,  or  previous  to,  the  occurrence  of  the  anasarca, 
certain  premonitory  symptoms  occur,  and  it  is  of  great  importance  to  be 
familiar  with  these  symptoms,  and  be  on  the  watcli  for  their  appearance. 
For  two  or  three  days  previous  to  their  development  a  certain  restlessness 
will  he  noticed,  with  nausea  and  vomiting.  Tliese  symptoms  are  almost 
universally  present.  The  nausea  and  vomiting  so  commonly  present  dur- 
ing the  early  periods  of  the  disease  have  subsided,  and  now,  during  the 
period  of  desquamation,  or  perhaps  after  it  has  been  completed,  the  vomit- 
ing returns.  The  patient  has  some  pain  in  the  head,  has  loss  of  appetite, 
is  annoyed  by  the  light,  does  not  sleep  well,  and  the  temperature  is  raised 
perhaps  two  or  three  degrees.  But  the  pulse  now  grows  remarkably  slow  : — 
50  to  60  in  children.  When  a  patient  complains  in'this  manner  during  the 
desquamative  stage  of  scarlet  fever,  our  suspicions  should  be  aroused,  and 
if  the  urine  has  not  yet  been  examined,  an  examination  should  be  made 
at  once. 

The  urine  may  be  entirely  suppressed  for  a  day,  and  then  it  will  usually 
be  found  scanty  and  high-colored,  will  contain  albumen  and  casts.  Haema- 
turia  and  hsemoglobinuria  both  occur  quite  frequently.  If  previous  exam- 
inations of  the  urine  have  been  made  before  the  development  of  these  symp- 
toms, a  cloudiness  will  have  been  noticed  (non-albuminous)  due  to  epi- 
thelia  and  hyaline  material,  but  now  there  are  present  casts  which  indicate 
the  existence  of  scarlatinal  nephritis.  After  the  anasarca  has  been  present 
two  or  three  days,  and  the  abdomen  has  become  tense,  swollen  and  painful, 
if  the  case  is  to  have  a  favorable  termination  it  will  begin  to  decline,  will 
be  less  and  less  marked  about  the  face  and  feet,  the  tendency  to  stupor 
which  has  accompanied  it  will  begin  to  disappear  ;  and  as  the  dropsy  sub- 
sides, and  the  patient  is  not  so  lethargic,  the  appetite  begins  to  return,  the 
urine  increases  in  quantity,  the  albumen  diminishes,  the  casts  disappear, 
and  convalescence  is  fully  established.  Anasarca  may  have  been  developed, 
all  the  symptoms  have  disappeared,  and  the  patient  have  recovered  within 
two  weeks  from  the  commencement  of  the  attack.  If,  however,  after  the 
anasarca  is  developed,  the  case  is  to  go  on  to  an  unfavorable  termination, 
the  anasarca  instead  of  diminishing  will  increase ;  the  face  will  become 
more  and  more  pufFy,  the  legs  more  and  more  cedematous,  the  abdomen 
more  and  more  distended,  the  pulse  more  and  more  frequent  and  feeble, 
the  temperature  more  and  more  elevated,  until  a  condition  of  coma  is 
finally  reached,  which  condition  is  sometimes  preceded  by  convulsions,  and 
followed  by  death. 

Another  sequela  of  scarlatina  is  inflammation  of  the  serous  memhranes. 
The  serous  membrane  most  liable  to  be  involved  is  the  endocardium,  and 
this  inflammation  may  pass  unrecognized  unless  its  occurrence  is  closely 
watched,  and  there  may  be  no  rational  symptoms  present.  Endocarditis, 
when  it  does  occur,  is  liable  to  be  ulcerative  in  character.  Inflammation 
of  the  pericardium  may  occur  as  a  complication  of  scarlet  fever,  but  it  does 
so  much  less  frequently  than  inflammation  of  the  endocardium.  Inflam- 
mation of  the  pleura,  and  occasionally  inflammation  of  the  peritoneum,  is 
met  with  as  a  sequela  of  this  disease.     If  peritonitis  does  occur  it  is  usually 


776  ACUTE    GENEEAL   DISEASES. 

subacute  in  character.  It  is  possible  to  have  peritonitis  developed  as  a 
sequela  to  scarlet  fever  and  to  be  entirely  recovered  from.  Rheumatism 
may  be  developed  during  the  desquamative  period  of  scarlet  fever.  Under 
such  circumstances  it  assumes  the  ordinary  appearances  of  inflammatory 
rheumatism.  It  is  not  a  serious  sequela,  and  a  complete  recovery  usually 
occurs  within  ten  or  fourteen  days  from  the  commencement  of  the  attack. 
Suppurative  inflammation  of  the  joints  is  sometimes  a  sequela  of  scarlet 
fever. 

Another  serious  complication  of  scarlet  fever  is  diphtheria.  It  may 
occur  at  any  period  of  the  fever  ;  usually  it  occurs  during  the  period  of 
desquamation.  There  is  developed  the  characteristic  exudation  of  the  dis- 
ease, with  the  attendant  depression  noticed  in  a  case  of  diphtheria  devel- 
oped independently  of  scarlet  fever.  It  differs  in  no  respect  from  primary 
diphtheria,  except  in  the  rapidity  of  its  development  and  in  its  fatality. 
In  scarlet  fever  there  is  no  more  serious  complication.  Usually  it  appears 
quite  suddenly,  and  perhaps  does  not  occur  more  frequently  in  those  who 
have  a  severe  form  of  the  disease  than  in  those  who  have  a  mild  scarlet 
fever.  The  lympliatic  glands  may  be  enlarged  and  swollen,  i.  e.,  a  lym- 
phadenitis may  be  a  sequel  of  scarlatina.  Keratitis,  retinitis,  and  total 
blindness  are  rare  sequelae  of  scarlet  fever.  Anaemia,  paralysis  of  single 
nerves,  spinal  disease,  chronic  Bright's,  deafness,  chorea,  epilepsy  (melan- 
cholia and  mania  in  adults),  valvular  diseases,  stone  in  the  bladder,  etc., 
etc.,  are  also  named  as  sequelae. 

Differential  Diagnosis, — The  diagnosis  of  scarlet  fever  is  usually  not  diflB- 
cult  after  the  eruption  has  made  its  appearance,  for,  in  well-marked  cases, 
that  alone  will  readily  distinguish  it  from  the  other  eruptive  fevers.  At 
the  very  onset  of  the  eruption,  and  sometimes  in  irregular  cases,  the  differ- 
ential diagnosis  is  difficult.  The  eruptive  diseases  which  are  most  liable  to 
be  mistaken  for  scarlet  fever  are  measles,  small-pox,  roseola,  and  an  erythema 
which  sometimes  appears  in  surgical  cases.  In  all  doubtful  cases  a  careful 
study  of  the  history  of  the  patient  is  necessary  before  making  a  diag- 
nosis. 

In  measles  the  appearance  of  the  eruption  is  preceded  by  a  cough  and 
coryza.  These  symptoms  are  never  present  in  the  ushering-in  stage  of 
scarlatina,  but  maj  folloiv  the  eruption.  Besides,  the  eruption  of  measles 
first  appears  on  the  face,  whereas  the  eruption  of  scarlet  fever  first  makes 
its  appearance  upon  the  neck  and  chest.  The  fever  in  scarlatina  persists 
after  the  eruption,  while  in  measles  (and  in  small-pox  too)  it  falls  when 
ihe  eruption  appears.  The  incubation  period  is  shorter  in  scarlet  fever  and 
the  early  pyrexia  is  higher  than  in  measles.  After  these  diseases  are  once 
fully  developed,  the  course  of  the  one  so  differs  from  that  of  the  other  that 
there  will  rarely  be  any  chance  for  doubt  after  the  first  week  of  the  disease. 
The  minute  punctate  appearance  of  the  scarlatina  eruption  before  it  be- 
comes confluent  is  an  important  element  in  its  diagnosis. 

Although  the  eruption  of  confluent  variola,  for  the  first  twenty-four  hours, 
may  sometimes  resemble  that  of  scarlatina,  yet  the  development  of  the  first 
Tesicle  settles  the  question. 


8CAELET    FEVER.  777 

The  appearance  of  erythema  bears  a  close  resemblance  to  a  perfectly  de- 
Yeloped  scarlatina  eruption  ;  it  is  not,  however,  present  on  the  extremities, 
neck,  and  portions  of  the  trunk,  and  it  spreads  in  a  very  irregular  manner, 
whereas  in  scarlatina  such  is  not  the  case.  But  if,  on  account  of  the  scanti- 
ness of  the  scarlatina  eruption,  any  doubt  arises  as  to  the  nature  of  tlie  erup- 
tion, the  fact  that  in  scarlatina  the  throat  symptoms  are  rarely  absent,  that 
the  tongue  presents  the  strawberry  appearance,  and  that  at  an  early  period 
there  is  usually  some  swelling  of  the  cervical  glands,  will  decide  the  case. 
In  those  cases  in  which,  during  the  early  part  of  the  disease,  it  is  impossible 
to  make  a  diiierential  diagnosis,  the  diagnosis  will  be  readily  made  when  the 
period  of  desquamation  is  reached. 

The  differential  diagnosis  between  roseola  and  a  very  mild  form  of  scar- 
latina is  sometimes  attended  with  great  difficulty.  If  scarlatina  is  prevail- 
ing, and  a  child  has  an  eruption  which  lasts  for  two  or  three  days,  then 
disappears,  and  is  not  followed  by  desquamation,  it  may  be  thought  that  the 
case  is  one  of  scarlatina ;  and  yet  the  sequel  proves  that  the  case  was  one  of 
roseola.  Such  a  form  of  roseola  sometimes  prevails  epidemically,  and 
attacks  children  in  a  certain  locality,  whether  they  have  or  have  not  had 
scarlatina.  Under  such  circumstances,  adults  and  children  are  said  to  have 
had  a  second  attack  of  scarlet  fever.  In  making  a  differential  diagnosis 
between  this  form  of  roseola  and  scarlatina,  the  duration  of  the  eruption 
and  the  character  of  the  throat  symptoms  must  decide.  In  scarlatina  the 
posterior  part  of  the  pharynx  is  affected,  while  in  roseola  the  redness  is  con- 
fined to  the  anterior  portion  ;  besides,  the  throat  affection  in  roseola  is 
much  milder  than  in  scarlatina.  In  roseola  the  white  line  that  the  finger 
leaves  disappears  immediately  ;  while  in  scarlatina  it  remains — indeed,  a 
letter  may  be  traced  on  the  skin  in  well-marked  cases. 

One  can  hardly  mistake  erysipelas  for  scarlatina,  for  erysipelas  com- 
mences at  one  point  and  gradually  extends  from  it ;  there  is  also  marked 
oedema  of  the  connective-tissue,  and  there  is  a  very  marked  difference  in 
the  constitutional  symptoms  of  the  two  diseases. 

Malignant  cases  of  scarlet  fever,  in  which  no  eruption  appears,  prove 
rapidly  fatal.  In  such  cases,  the  fact  that  an  epidemic  of  scarlet  fever  is 
prevailing  (which  is  usually  the  case),  the  rapid  development  of  the  disease, 
the  very  high  range  of  temperature,  and  the  very  grave  nervous  phenomena, 
will  aid  in  the  diagnosis,  and  these  can  only  be  accounted  for  on  the  ground 
that  the  patient  is  overwhelmed  by  some  very  active  blood-poison.  In  this 
class  of  cases  the  entire  surface  of  the  body  should  frequently  be  examined, 
for  the  eruption  is  sometimes  very  transient,  perhaps  appearing  only  for  a 
few  hours  on  the  neck  or  extremities. 

It  is  sometimes  difficult  to  draw  the  line  of  distinction  between  scarlatina 
without  an  eruption,  but  with  swelling  of  the  cervical  glands  and  ulcera- 
tion of  the  throat,  and  diplitheria.  If  a  patient  has  swelling  of  the 
cervical  glands  and  well-marked  febrile  symptoms,  which  have  come  on 
gradually — ^that  is,  have  been  two  or  three  days  developing — and  yet  no 
scarlatina  eruption  has  appeared,  but  a  gangrenous  ulceration  has  developed, 
involving  the  tonsils,  the  posterior  wall  of  the  pharynx,  and  the  anterior 


778  "  ACUTE    GEN"EEAL   DISEASES. 

pillar  of  the  soft  palate,  and  if  scarlet  fever  is  prevailing  in  the  locality, it  is 
very  difficult  to  decide  between  it  and  diphtheria.  There  can  be  no  doubt 
but  that  scarlatina  poison  may  excite  a  tubular  nephritis  without  an  erup- 
tion appearing  on  the  surface  of  the  body,  or  without  any  of  the  other 
ordinary  symptoms  of  scarlatina. 

Prognosis. — The  prognosis  in  scarlet  fever  is  always  uncertain.  It  will 
be  influenced  more  by  the  character  of  the  prevailing  epidemic  than  by  any 
other  circumstance.  According  to  statistics,  the  rate  of  mortality  ranges 
from  one  death  in  five  to  one  in  twenty.  Some  epidemics  are  very  mild. 
During  one  epidemic,  in  one  month,  I  treated  fifty  cases  of  scarlet  fever, 
with  only  two  deaths.  During  the  same  month  of  the  following  year, 
I  treated  twenty  cases,  with  seven  deaths.  In  giving  a  prognosis  one  must 
always  take  into  account  the  type  of  the  prevailing  disease.  Even  when 
the  disease  is  mild  in  character,  and  is  running  a  perfectly  regular  course, 
dangerous  symptoms  may  suddenly  arise  without  any  assignable  cause. 

The  conditions  of  a  favorable  prognosis  are  as  follows  :  when  the  erup- 
tion appears  within  forty-eight  hours  from  the  commencement  of  the 
attack,  and  rapidly  completes  its  course,  reaching  its  maximum  on  the 
second  day  ;  when  the  throat  symptoms  are  mild,  little  difficulty  being  ex- 
perienced in  swallowing ;  when  the  cervical  glands  are  but  slightly  enlarged; 
when  the  temperature  does  not  rise  higher  than  104°  F.,  and  the  pulse  beats 
only  120  per  minute  ;  when  the  cerebral  symptoms  are  not  severe,  and  are 
of  short  duration  ;  and  when  the  disappearance  of  the  eruption  is  attended 
by  a  steady  decline  in  temperature.  Even  if  there  is  a  slight  affection  of 
the  Joints  and  a  moderately  severe  nephritis  during  the  period  of  desquama- 
tion, a  favorable  termination  may  be  predicted.  The  nephritic  symptoms 
will  almost  always  entirely  disappear  during  the  third  or  fourth  week. 

The  conditions  for  an  unfavorable  prognosis  are  an  irregular  course ;  a 
temperature  rising  above  105°  F.,'  with  dyspnoea  and  extreme  frequency  of 
the  pulse  ;  symptoms  of  collapse  attended  by  a  cold  surface  and  a  small 
pulse,  an  eruption  of  a  livid  hue,  and  abundant  hemorrhages  in  the  skin  ; 
ulcerative  pharyngitis,  especially  when  it  extends  to  the  nasal  passages,  ac- 
companied by  copious  coryza  and  infiltration  of  the  glands  and  tissues  of 
the  neck  ;  severe  nervous  symptoms,  with  typhoid  symptoms  and  long  con- 
tinued vomiting  with  diarrhoea  coming  on  at  the  commencement  of  the 
attack ;  early  nephritic  symptoms  and  general  dropsy,  excessive  hsema- 
turia,  or  almost  complete  suppression  of  urine,  with  high  temperature. 
The  occurrence  of  any  of  the  more  serious  complications,  such  as  pneu- 
monia, diplitheria,  pericarditis,  oedema  glottidis,  etc.,  always  renders  the 
prognosis  bad. 

Before  making  a  prognosis,  decide  whether  the  scarlet  fever  is  regular  or 
irregular  in  its  course,  and  if  irregular,  what  are  the  causes  of  the  irregu- 
larity. It  is  also  important  to  determine  the  patient's  power  of  resisting 
disease.    Autumn  is  the  most  unfavorable  season.     Favorable  hygienic  sur- 

I  A  temperature  of  110"  has  been  reached  and  yet  followed  by  recovery  ;  it  rose  to  115°  F.  in  a  fatal  case. 
Scarlet  fever  is  an  intensely  febrile  disease  ;  hence  the  temperature  is  not  such  a  very  important  element 
in  the  prognosis. 


SCARLET   FEVER.  779 

roundings,  good  nursing,  and  well-directed  medical  treatment  will  greatly 
lessen  the  death  rate  in  scarlet  fever  epidemics,  and  these  should  he  con- 
sidered elements  of  the  prognosis.  Patients  with  scarlet  fever  do  better 
when  left  to  themselves  than  when  badly  nursed,  even  if  under  the  care  of 
skilful  medical  attendants. 

Age  is  an  important  element  of  prognosis.  The  period  of  greatest  mor- 
tality is  from  infancy  to  five  years  of  age.  Beyond  this  period  until  adult 
life,  the  prognosis  is  decidedly  better.  Five  per  cent,  of  the  whole  mortality 
falls  in  the  first  year,  fifteen  per  cent,  in  the  second,  twenty  per  cent,  in 
each  of  the  next  two  years,  and  then  decreases  progressively.  In  adults, 
the  mortality  is  greatest  in  pregnant  women,  and  those  who  are  suffering 
from  some  organic  disease,  especially  some  disease  of  the  heart  or  kidneys. 

Treatment. — In  connection  with  the  treatment  of  this  affection,  the  first 
question  that  presents  itself  relates  to  prophylaxis  ot  preventmi. 

ThQ  prophylaxis  of  scarlet  fever  is  a  system  of  the  strictest  quarantine. 
The  sick  must  be  removed  from  the  healthy.  All  useless  articles  of  furni- 
ture must  be  removed  from  the  sick-room.  Fresh  air  renders  the  contagion 
of  scarlet  fever  less  powerful ;  therefore,  free  .ventilation  is  of  the  utmost 
importance.  All  the  clothes  and  excretions  of  the  patient  should  be  dis- 
infected in  the  same  manner  as  in  typhoid  fever.  To  prevent  the  dissemina- 
tion of  the  dusty  particles  of  the  desquamating  epidermis,  during  the  period 
of  desquamation  the  surface  of  the  body  should  be  frequently  sponged,  and 
after  each  sponging  the  surface  should  be  rubbed  with  olive  oil.  Those  con- 
valescing from  this  disease  should  not  be  allowed  to  leave  their  apartment 
until  desquamation  is  completed,  which  usually  requires  at  least  three 
weeks  after  the  commencement  of  the  jjeriod  of  desquamation.  The 
sick-room  and  everything  which  has  been  used  about  the  patient  should 
be  thoroughly  disinfected,  and  the  windows  and  doors  of  the  apartment 
should  be  allowed  to  remain  open  for  a  long  time  before  it  is  again 
occupied. 

To  prevent  the  spread  of  the  disease,  nurses  and  attendants  upon  the 
sick  should  not  be  allowed  to  have  any  intercourse  with  the  healthy  until 
the  period  of  desquamation  is  passed,  and  after  that  time  not  until  there 
has  been  thorough  cleaning  and  disinfecting.  The  funeral  of  those  dying 
of  scarlet  fever  should  not  be  public.  There  is  no  known  prophylactic 
treatment,  except  isolation,  and  a  thorough  disinfectioij  of  everything  con- 
taminated by  the  contagion. 

A  theory  has  been  advanced  that  belladonna  has  power  to  prevent  the 
development  of  this  disease  in  those  who  have  been  exposed  to  its  con- 
tagious influence.  This  drug  has  been  very  extensively  administered  in 
order  to  test  its  effects  as  a  preventative  in  scarlet  fever.  After  having 
carefully  examined  the  subject,  both  in  its  literature  and  clinically,  I  am 
convinced  that  belladonna  has  no  power  to  prevent  the  development,  or 
mitigate  the  severity,  of  the  fever  in  those  who  have  been  exposed  to  its 
infection.  Fresh  air  is  the  only  agent  which  can  render  the  contagious  in- 
fluence of  this  fever  less  powerful. 

Medicinal  Treatment. — The  medicinal  treatment  of  scarlet  fever  is  al- 


780  ,  ACUTE    GEI^ERAL   DISEASES. 

most  entirely  expectant.  It  is  a  disease  which  cannot  be  aborted,  and  if 
left  to  its  natural  course  tends  to  recovery  if  the  fever  and  the  local  symp- 
toms remain  within  certain  bounds.  It  has  certain  stages  to  pass  through, 
and  one  cannot  safely  interfere  with  its  regular  course.  To  stand  by  and 
watch,  and,  as  far  as  possible,  to  guard  against  complications  are  the  physi- 
cian's chief  duties.  There  are  certain  details  which  it  is  important  to  attend 
to.  The  bed  and  body  linen  should  be  frequently  changed.  As  soon  as 
the  period  of  desquamation  has  been  reached  the  patient  should  have  a 
warm  bath  once  or  twice  during  the  day,  the  surface  of  the  body  being 
well  washed  with  carbolized  soap.  The  baths  hasten  the  process  of  des- 
quamation and  aid  in  bringing  the  skin  into  a  healthy  condition  as  rapidly 
as  possible  ;  the  kidneys  will  also  be  relieved,  and  serious  lesions  of  these 
organs  may  thus  be  prevented.  Such  general  means  as  are  applicable  in 
the  treatment  of  all  fevers  may  be  employed. 

If  the  temperature  of  the  patient  rises  above  104°,  certainly  if  it  rises 
above  105^  F.,  it  is  important  that  some  measures  be  resorted  to  for  its  re- 
duction. The  temperature  should  never  be  allowed  to  remain  at  105°  F. 
longer  than  twenty-four  hov.rs.  The  means  which  are  to  be  employed  to 
accomplish  this  reduction  are  the  antipyretic  measures  already  referred  to, 
such  as  the  application  of  cold  to  the  surface  by  means  of  sponging  and 
baths,  and  the  administration  of  large  doses  of  quinine.  There  is  a  strong 
prejudice  against  the  application  of  cold  to  the  surface  of  the  body  in 
scarlet  fever.  I  am  by  no  means  certain  that  cold  baths  are  al  ways  safe, 
or  that  in  all  cases  the  application  of  cold  to  the  surface  is  Judicious  treat- 
ment. It  is  said  that  the  kidneys  will  be  most  readily  relieved  of  the  scar- 
let fever  poison  when  cold  is  used  for  the  purpose  of  reducing  the  temper- 
ature. It  is  claimed  that  when  the  temperature  of  a  patient  is  kept  below 
103°  F.,  scarlatinal  nephritis  rarely  occurs.  This  statement  is  not  sustained 
by  facts  ;  it  has  been  found  that  kidney  complications  are  as  extensive  in 
the  cases  where  cold  is  employed  as  in  those  cases  where  the  temperature 
ranges  higher  and  cold  to  the  surface  is  not  employed.  We  should  be  gov- 
erned by  the  same  rules  in  the  application  of  cold  to  the  surface  in  scarlet 
fever  as  govern  us  in  the  treatment  of  typhoid  fever. 

With  regard  to  the  use  of  quinine  as  an  antipyretic,  I  need  add  nothing 
to  what  has  already  been  said  in  connection  with  its  antipyretic  power  in 
the  treatment  of  other  fevers.  Unless  the  temperature  in  a  case  of  scarlet 
fever  ranges  above  105°  F.,  do  not  apply  cold  to  the  surface,  or  give  quin- 
ine in  antipyretic  doses.  With  such  a  temperature  there  will  be  probably  be 
delirium,  but  it  must  be  regarded  as  one  of  the  phenomena  of  the  disease, 
requiring  no  special  treatment.  If  the  temperature  rises  above  105°  F. , 
perhaps  reaching  106°  or  107°  F.,  and  the  patient  manifests  the  nervous 
phenomena  which  have  been  referred  to,  such  as  restlessness,  tossing,  blue- 
ness  of  the  surface,  tendency  to  coma,  etc.,  the  temperature  is  to  be  re- 
duced either  by  the  application  of  cold  to  the  surface  or  by  the  administra- 
tion of  one  or  two  antipyretic  doses  of  quinine. 

In  all  cases  the  patient  is  to  be  sponged  frequently  with  tepid  water,  and 
if  there  is  intense  burning  of  the  surface,  a  saline  is  to  be  added  to  the 


SCARLET  PEVER.  781 

water.  Sponging  in  this  manner  will  give  the  patient  very  great  comfort. 
Some  advise  that  the  surface  be  anointed  with  oil  for  the  relief  of  the 
burning.  My  own  experience  has  led  me  to  rely  upon  simple  tepid  saline 
water.  I  have  found  that  it  gives  patients  greater  relief,  is  more  easily 
applied,  and  is  every  way  more  agreeable  than  any  of  the  substances  which 
have  been  used  for  this  purpose.  I  have  not  found  that  the  application  of 
oil  to  the  surface  has  any  effect  in  controlling  the  temperature,  nor  does  it 
seem  to  have  any  effect  on  the  process  of  desquamation.  As  soon  as 
desquamation  commences  the  process  should  be  assisted  by  frequent  wash- 
ings with  soap  and  water. 

For  the  throat  complications,  which  will  give  more  or  less  trouble  in  all 
severe  cases,  especially  when  there  is  much  enlargement  of  the  glands  at 
the  angle  of  the  jaw,  causing  difficulty  in  swallowing,  leeches  were  for- 
merly employed,  but  their  use  has  now  been  almost  entirely  abandoned. 
Of  all  the  remedies  which  I  have  employed  for  the  relief  of  throat  comj)li- 
cations,  cold  carbonic  acid  water  proved  best.  Whether  it  does  more  than 
afford  relief,  I  am  not  able  to  say,  but  I  am  certain  that  cold  carbonic  acid 
water  or  pieces  of  ice  held  in  the  mouth,  and  brought  as  much  as  possible 
in  contact  with  the  swollen  mucous  membrane  of  the  throat,  if  used  early, 
afford  most  marked  relief. 

In  the  advanced  stages  of  the  disease,  where  there  is  great  infiltration 
of  the  glands  and  tissues  of  the  neck,  cold  applications  do  not  afford  the 
same  relief  as  when  they  are  used  in  the  early  stage ;  then  cloths  wrung  out 
in  tepid  water  and  applied  to  the  surface  seem  to  be  of  service.  During 
this  stage,  hot  applications  are  generally  much  more  agreeable  to  the  pa- 
tient, and  the  hot  cloths  may  be  covered  with  oil -silk.  These  applications 
will  not  hasten  the  suppurative  process,  unless  suppuration  is  already  estab- 
lished. While  using  hot  applications  externally,  warm  water  gargles  and 
steam  inhalations  may  be  used  internally.  Of  these  methods  of  treating 
throat  affections,  the  one  which  seems  to  be  the  most  rational  plan  of  treat- 
ment should  be  chosen.  In  scarlet  fever  I  favor  the  use  of  hot  water  rather 
than  cold  applications.  The  superficial  and  deep  ulcers  which  are  some- 
times seen  in  the  throat  of  scarlet  fever  patients  can  best  be  treated  by 
spraying  them  with  carbolic  acid,  muriated  tincture  of  iron,  chlorate  of 
potash,  tannic  acid,  or  any  of  that  class  of  remedies.  Whatever  remedy 
maybe  chosen,  it  can  be  much  more  successfully  applied  by  means  of  spray 
than  by  a  camel's-hair  brush  or  a  probang.  Such  local  remedies  thus  ap- 
plied afford  great  relief.  The  pain  from  these  ulcerations  is  sometimes 
very  severe,  and  bromide  of  potassium,  ether,  or  other  anodyne  applications 
in  the  form  of  spray  may  be  used  with  satisfactory  results. 

In  a  certain  class  of  cases,  where  there  is  marked  disturbance  of  the 
nervous  system  accompanied  by  great  depression  of  the  vital  forces  and 
feeble  heart  action,  stimulants  will  be  demanded  early.  It  is  not  necessary 
to  wait  until  a  certain  stage  of  the  eruption  or  of  the  disease  is  reached 
before  commencing  their  administration.  It  may  be  necessary  to  resort  to 
their  use  within  twelve  hours,  or  even  within  a  less  time,  from  the  com- 
mencement of  the  attack.     In  some  cases  the  beneficial  effect  that  may  be 


782  ACUTE    GENEEAL   DISEASES. 

produced  by  the  free  and  early  administration  of  stimulants  will  be  the 
physician's  sole  reliance. 

The  approach  of  kidney  implication  in  scarlet  fever  will  be  indicated  by 
the  development  of  those  premonitory  symptoms  which  precede  the  ana- 
sarca ;  and  whenever  such  symptoms  are  developed,  dry  or  wet  cups,  accord- 
ing to  the  condition  of  the  patient,  should  be  applied  over  the  region  of  the 
kidneys,  upon  either  side  of  the  spine  ;  three  or  four  cups  are  to  be  applied 
on  each  side,  and  their  application  followed  with  hot  fomentations  over  the 
kidneys.  At  the  same  time  the  temperature  of  the  sick-room  is  to  be  raised 
to  73°  or  74°  F.,the  body  of  the  patient  covered  with  flannel,  hot-air  or 
warm  baths  are  to  be  administered,  and  the  administration  of  diuretics  is 
to  be  commenced  early.  Of  these,  digitalis  will  act  most  favorably.  If  the 
anasarca  does  not  disappear  under  the  influence  of  the  digitalis  and  the 
other  means  employed,  calomel  may  be  combined  with  the  digitalis  and 
its  use  continued  for  a  few  days.  Pilocarpin  is  recommended  by  some ; 
my  experience  with  it  has  not  been  satisfactory.  The  action  of  diuretics 
is  increased  by  having  a  mercurial  combined  with  them.  In  certain 
cases,  when  the  patient  is  going  from  bad  to  worse,  when  the  anasarca  is  in- 
creasing, the  tendency  to  coma  is  becoming  more  and  more  marked,  indi- 
cating an  unfavorable  termination  to  the  case,  cups  have  been  applied,  and 
hot  baths  and  diuretics  employed  with  no  satisfactory  result — if  then  small 
doses  of  calomel  are  combined  with  the  diuretics,  and  their  use  continued 
for  two  or  three  days,  the  entire  phase  of  the  case  may  be  changed.  When 
toxic  symptoms  are  marked,  some  advise  carbolic  acid,  the  sulpho-carbo- 
lates,  the  hypophosphites,  inhalation  of  ozone,  etc.,  etc.  In  conjunction 
with  the  measures  recommended,  the  patient  may  drink  as  freely  as  possi- 
ble of  water.  If  convulsions  occur,  or  threatening  symptoms  indicating 
the  approach  of  convulsions  are  developed,  opium,  either  hypodermically 
or  by  the  mouth,  may  be  given.  Under  such  circumstances,  the  effect  of 
opium  is  often  most  satisfactory.  It  not  only  arrests  the  convulsive  tenden- 
cies, but  produces  the  most  profuse  diaphoresis  and  aids  in  restoring  the 
renal  functions. 

MEASLES. 

Measles,  or  ruheola,  is  a  disease  from  which  few  persons  escape.  It  is 
essentially  a  disease  of  childhood,  but  it  may  occur  at  any  age  ;  it  is,  how- 
ever, less  liable  to  occur  in  young  infants  than  in  children  after  the  period 
of  dentition.  A  second  attack  is  of  rare  occurrence.  It  is  characterized  bj 
an  eruj)tion  of  red  spots,  accompanied  by  a  catarrh  of  the  mucous  mem- 
brane of  the  air  passages,  and  a  more  or  less  severe  fever.  It  is  infectious 
and  contagious.  It  may  prevail  as  an  epidemic  or  endemic  disease,  and  not 
infrequently  there  are  sporadic  cases  of  measles. 

Morbid  Anatomy. — Its  anatomical  lesions,  with  the  exception  of  the  erup- 
tion, are  similar  to  those  of  small-pox  and  scarlatina.  There  are  similar 
changes  in  the  blood,  and  the  same  tendency  to  congestion  of  the  internal 
organs.  The  spleen  and  liver  are  moderately  enlarged.  The  mucous  mem- 
branes of  the  nose,  pharynx,  larynx  and  larger  bronchi,  and  the  conjunc- 


MEASLES.  783 

tivse,  are  more  or  less  intensely  congested  and  present  all  the  lesions  of  acute 
catarrh.  In  the  majority  of  instances  this  catarrh  is  most  severe  just  be- 
fore and  during  the  early  period  of  the  eruption ;  generally,  it  begins  to 
disappear  when  the  eruption  has  reached  its  height,  and  within  two  or 
three  days  entirely  disappears.  Where  death  has  resulted  from  measles, 
in  the  majority  of  autopsies,  evidence  of  capillary  bronchitis  is  found,  and 
not  infrequently  of  catarrhal  pneumonia  also. 

Strictly  these  are  not  anatomical  lesions  of  measles,  but  complications  ; 
they  are,  however,  such  frequent  attendants  of  this  disease,  that  they  are 
almost  a  part  of  its  history. 

The  eruption  is  papular  ;  the  papules  first  show  themselves  upon  the 
face,  especially  upon  the  chin  ;  gradually  they  extend  to  all  parts  of  the 
body,  and  lastly  appear  upon  the  back  of  the  hands.  When  the  eruption 
is  well  developed  the  spots  are  slightly  elevated,  and  have  a  diameter  vary- 
ing from  two-fifths  to  one-twentieth  of  an  inch  ;  in  form  they  are  crescent- 
shaped,  their  margins  are  sharply  defined,  usually  their  color  is  bright- 
red,  sometimes  shading  off  into  blue,  in  most  cases  the  spots  are  distinct 
and  separated  from  each  other  by  pale  tracts  of  skin  ;  they  may  become 
confluent,  and  thus  give  to  the  surface  a  uniform  redness.  When  this 
occurs  the  surface  presents  an  appearance  similar  to  that  seen  in  scarlatina. 
The  earlier  papule  in  each  spot  usually  occupies  the  place  of  a  hair-follicle  ; 
hence  some  regard  inflammation  of  a  sebaceous  follicle  of  the  skin  as  the 
first  event.  The  spots  disappear  on  pressure,  but  immediately  return  when 
the  pressure  is  removed.  Sometimes  each  spot  contains  several  papules. 
The  diversity  in  form  and  appearance  of  measle-spots  in  different  cases 
depends  upon  variations  in  size,  elevation,  and  grouping  of  the  papules. 
When  the  spots  assume  a  dark-red  color,  and  do  not  disappear  on  pressure, 
capillary  hemorrhages  have  taken  place  into  the  papules,  and  the  eruption 
is  called  hemorrhagic.  When  the  eruption  is  very  abundant,  little  vesicles 
sometimes  appear  upon  the  papules,  especially  upon  the  trunk  when  there 
has  been  profuse  perspiration,  called  by  some  vesicular  or  miliary  measles. 
As  soon  as  the  spots  have  reached  their  maximum  of  development,  their 
color  begins  to  fade  ;  the  fading  is  progressive,  the  centres  of  the  spots 
retain  their  redness  longest  ;  the  elevations  subside  with  loss  of  color.  In 
a  varying  time,  from  one  to  five  days,  the  spots  entirely  disappear,  leaving 
a  yellowish  or  brownish  stain.  This  staining  is  due  to  pigmentation  of  the 
skin,  and  is  sometimes  visible  for  two  weeks. 

Exfoliation  of  the  epidermis  or  desquamation  takes  place  only  upon  the 
sides  of  the  measle-spots  ;  it  is  never  so  extensive  as  in  scarlet  fever.  The 
skin  does  not  desquamate  in  layers,  but  in  fine  brown  scales,  i.  e.,  is  fur- 
furaceous,  not  squamous,  hence  it  is  called  the  hran-like  desquamation.  It 
may  commence  before  the  redness  of  the  eruption  disappears,  but  it  does 
not  usually  occur  until  the  eruption  has  entirely  faded.  In  most  cases  the 
period  of  desquamation  is  short,  rarely  lasting  a  week. 

Etiology. — It  is  essentially  a  contagious  disease.  So  far  as  has  yet  been 
determined,  it  is  only  propagated  by  contagion.  There  are  places,  extensive 
districts,  and  countries  thickly  inhabited,  where  this  disease  has  never  pre- 


784  ACUTE   GENEEAL  DISEASES. 

vailed.  There  is  no  authentic  evidence  that  it  ever  originated  spontane- 
ously. The  poison  of  measles  is  located  either  in  the  mucous  secretion,  or 
in  the  exhalations  from  the  body  of  the  infected  so  contaminating  the  air 
about  fche  sick  that  when  persons  who  have  not  had  the  disease  are  brought 
within  its  influence  measles  will  be  developed.  It  has  been  proved  that  the 
blood,  the  mucous  secretions,  especially  the  nasal,  and  even  the  tears  have 
the  power  of  conveying  the  disease  by  inoculation. '  There  is  little  question 
but  that  the  disease  can  be  conveyed  in  clothing,  or,  in  other  words,  that 
it  is  a  portable  disease.  One  not  protected  when  exj)Osed  to  measles  is 
much  more  certain  to  contract  the  disease  than  is  an  unprotected  person  to 
contract  small-pox  or  scarlet  fever.  It  is  possible  for  the  infection  to  be 
conveyed  from  one  place  to  another  in  clothing  and  in  fluids.  The  exact 
nature  of  this  poison  is  still  unknown. 

The  average  period  of  incubation  is  eight  days.  During  this  period  the 
poison  remains  latent,  giving  its  possessor  no  knowledge  of  its  presence. 
In  most  cases  a  slight  exposure  is  sufficient  to  induce  the  disease  ;  in  some 
cases  it  is  contracted  only  after  prolonged  exposure.  Susceptibility  to  this 
contagion  is  almost  universal.  All  classes  are  equally  subject  to  the  in- 
fection. Second  attacks  are  exceedingly  rare.  The  exact  time  in  the 
course  of  the  disease  when  measles  is  most  infectious  is  not  definitely  deter- 
mined. Statistics  furnish  almost  absolute  proof  that  it  may  infect  through- 
out its  entire  course. 

Symptoms. — Measles,  like  the  other  exanthematous  fevers,  if  uncompli- 
cated, runs  a  definite  course. 

Premonitory  or  precursory  Stage. — At  the  end  of  the  stage  of  incubation 
or  latent  period  of  the  disease,  which  is  without  fever,  and  free  from  local 
symptoms,  or  from  eight  to  ten  days  after  exposure,  the  patient  begins  to 
suffer  from  coryza,  is  languid,  chilly  and  exceedingly  irritable.  Sometimes 
a  subnormal  temperature  precedes  the  first  symptoms.  Occasionally,  in 
young  children,  convulsions  occur.  The  coryza  and  other  catarrhal  symp- 
toms, at  first,  may  or  may  not  be  accompanied  by  fever,  or  the  sudden 
initial  fever  may  be  very  intense.  Very  soon,  in  either  case,  occurs  a 
marked  febrile  movement.  The  eyes  will  be  injected  and  watery,  there 
will  be  a  burning  sensation  and  an  aversion  to  light,  and  the  eyelids  will  be 
red  and  tumefied.  There  is  a  constant,  irritating,  watery  discharge  from 
the  nose,  with  frequent  sneezing  and  pain  over  the  frontal  sinuses.  Sore 
throat  is  complained  of,  and  the  voice  is  a  little  husky.  Bronchial  catarrh 
is  indicated  by  uneasiness  and  constriction  over  the  chest,  with  a  frequent 
dry,  hoarse  cough,  hurried  respiration,  etc.  The  suffused,  red  appearance 
of  the  eyes  is  peculiar,  and  distinguishes  measles  from  scarlet  fever  and 
other  forms  of  eruptive  fever. 

After  the  early  symptoms  have  continued  perhaps  for  twenty-four  hours 
an  initial  fever  will  be  developed  which,  with  the  catarrhal  symptoms,  con- 

1  An  organized  ferment,  bacterium  or  tarnea  (which  develops  to  a  certain  point  in  a  proper  medium  and 
then  suddenly  ceases  its  career),  has  been  found  in  blood  and  breath  and  in  gl}'cerine  on  which  children 
with  measles  have  breathed.  They  have  been  found  in  the  true  skin.  lymph-spaces  and  sweat-glands  ;  in 
shape  they  are  rod,  spindle  and  canoe  shaped,  also  spherical  and  ovoid.  They  are  also  found  in  the  lungs. 


MEASLES.  785 

tmues  from  forty-eight  hours  to  four  days  ;  then  the  eruption  makes  its  ap- 
pearance. 

Eruptive  Stage. — The  eruption  is  first  seen  upon  the  face  (about  the 
chin,  forehead,  mouth,  and  side  of  the  nose),  then  upon  the  neck,  then 
upon  the  chest  and  over  the  body,  afterwards  upon  the  legs  and  arms,  and 
lastly  upon  the  back  of  the  hand.  The  eruption  on  the  face  feels  like 
small  shot  early  in  the  disease.  The  eru23tion  may  appear  first  on  a  part 
of  the  skin  that  has  been  the  seat  of  injury.  Usually  it  is  about  four  days 
from  the  time  of  the  appearance  of  the  eruption  upon  the  face  before  it  has 
passed  over  the  entire  body,  and  it  begins  to  fade  from  one  part  about  thirty- 
six  hours  after  its  appearance  upon  that  part ;  first,  it  begins  to  fade  from 
the  face,  then  the  neck  and  chest,  and  finally  from  the  back  of  the  hands. 
If  closely  examined,  the  eruption  will  be  found  composed  of  little,  fine,  red, 
crescentic  dots,  which,  after  a  little  time,  will  be  seen  crowded  together  in 
patches  of  irregular  shape.  Between  these  patches  the  skin  usually  has  its 
natural  appearance.  The  odor  is  peculiar  during  this  period.  The  erup- 
tion of  measles  presents  more  of  a  papillary  appearance  upon  the  face  than 
upon  any  other  part  of  the  body.  With  the  appearance  of  the  eruption  there 
is  more  or  less  swelling  of  the  surface,  with  itching  and  burning,  and  the 
color  of  the  eruption  will  vary  from  a  bright  rose-red  to  a  dark  mahogany 
hue.  The  difference  in  color  depends  upon  the  condition  of  the  individual 
and  the  peculiarity  of  the  type  of  the  disease,  rather  than  upon  any  change 
in  the  skin  itself.  The  respirations  are  hurried,  and  convulsions  may,  in 
children,  prove  fatal.  Epistaxis  is  common,  and  the  lymphatic  glands 
are  enlarged.  As  the  eruption  disappears  it  loses  its  bright  red  color  and 
becomes  a  yellowish  red,  until  finally  nothing  but  a  staining  of  the  sur- 
face is  left;  then  desquamation  commences.  Increase  in  fever  and  rise 
in  pulse  and  nocturnal  delirium  often  follow  the  first  outburst  of  the 
eruption. 

Desquamative  Stage. — The  desquamation  which  follows  the  eruption  is 
not  like  the  desquamation  of  scarlet  fever — scaly  or  "  peely," — but  it  occurs 
in  very  fine  dust-like  flakes,  which  may  pass  unobserved.  The  eruption 
reaches  its  height  by  the  third  day  from  the  time  of  its  appearance,  and 
generally  has  disappeared  by  the  end  of  the  sixth  day.  As  a  rule,  during 
the  development  of  the  eruption  the  catan-hal  symptoms  and  fever  are  in- 
creased in  intensity ;  the  patient  will  sneeze  and  cough,  and  frequently 
with  such  severity  and  with  such  a  coarse,  grating  tone,  that  it  has  re- 
ceived the  name  of  "iron  cough.''  It  is  not  the  cough  of  croup  (though  a 
true  croupy  cough  is  sometimes  present)  ;  there  is  no  stridulous  breathing 
accompanying  it,  but  it  is  the  result  of  an  ordinary  catarrhal  laryngitis, 
which  causes  the  patient  to  cough  perhaps  for  two  or  three  days  without 
expectoration,  or  any  attempt  at  expectoration.  During  this  period  the 
pulse  will  range  from  100  to  120  beats  per  minute,  and  in  young  chil- 
dren it  may  reach  IGO.  In  the  majority  of  cases  the  temperature  does 
not  rise  above  103°  F.,  but  it  may  rise  as  high  as  106°  or  107°  F.  As 
soon  as,  or  eve^i  lefore  the  eruption  begins  to  decline  the  temperature  often 
falls  two  or  tfiree  degrees.  As  the  decline  in  the  eruption  goes  on,  the 
50 


78G 


ACUTE    GENEEAL   DISEASES. 


Fig.  165. 
Temperature  Record  in  a  Case  of  Measles. 


temperature  gradually  falls,  until  by  the  time  the   eruption  has  entirely 

disappeared    the    patient    will    be 
Y!^  fully  convalescent. 

Measles,  like  scarlet  fever,  is  lia- 
ble to  irregularities  in  its  develop- 
ment. When  it  is  prevailing  in  a 
locality,  cases  occur  in  which  all 
the  catarrhal  symptoms  of  the  dis- 
ease are  present  without  an  erup- 
tion :  again,  there  is  an  eruption 
closely  resembling  that  of  measles, 
with  no  catarrhal  symptoms  ;  from 
the  appearance  of  the  eruption  one 
will  not  be  able  to  say  whether  the 
patient  has  or  has  not  measles  ;  if 
the  subject  has  been  exposed  to  the 
contagion  of  the  disease,  the  case 
will  probably  be  regarded  as  one  of 
measles,  and  yet  if  there  are  no 
catarrhal  symptoms,  but  simply  an 
eruption,  such  a  diagnosis  would  be 
made  with  a  question. 
There  is  a  form  of  roseola  which  very  closely  resembles  measles  in  every 
aspect  of  the  disease,  except  the  catarrhal  symptoms.  There  is  an  irregu- 
lar form  of  measles  which  prevails  epidemically,  which  is  characterized  by 
a  tendency  to  ulceration  of  mucous  surfaces.  This  form  shows  its  peculiar 
tendency  by  the  development  of  ulcers  at  the  angle  of  the  mouth,  within 
the  nose,  around  the  vulva,  anus,  etc.  Sometimes  these  ulcers  spread  and 
so  interfere  with  deglutition  and  respiration  as  to  endanger  life.  The  ul- 
cerations are  accompanied  by  great  prostration  of  the  vital  powers  and  a 
tendency  to  gangrene  of  the  above-named  parts  and  also  of  the  lungs.  This 
irregular  variety  only  occurs  in  those  who  are  poorly  nourished,  live  in  badly 
ventilated  houses,  and  are  surrounded  by  unfavorable  hygienic  influences. 
Again,  there  is  a  form  of  measles  in  which,  at  the  very  onset  of  the 
disease,  there  is  a  very  high  range  of  temperature.  There  will  be  no 
more  severe  catarrhal  symptoms  than  in  the  ordinary  forms — no  more 
bronchitis  ;  but  there  will  be  a  higher  range  of  temperature,  perhaps  rang- 
ing as  high  as  106°  or  107°  F.  Associated  with  this  pyrexia  there  will 
be  restlessness,  a  dry  tongue,  and,  very  soon  after  the  appearance  of 
the  dry  tongue,  a  change  in  the  color  of  the  eruption,  which  will  assume 
a  dusky  purplish  hue.  The  eruption  may  present  this  ]3eculiar  appear- 
ance at  the  very  commencement  of  its  development.  This  type  of  measles 
is  called  "  Mack  measles."  The  color  of  the  eruption  simply  shows  that 
there  have  been  extensive  blood-changes.  In  most  cases,  these  changes 
have  taken  place  prior  to  the  development  of  the  eruption.  By  some  it 
has  been  claimed  that  there  is  at  work  a  peculiar  epidemic  or  endemic  in- 
fluence that  gives  rise  to  the  peculiar  type  of  the  disease  :  but  as  I  have 


MEASLES.  787 

been  brought  in  contact  with  it,  it  has  seemed  to  me  that  it  differed  from 
the  ordinary  type  only  in  the  intensity  of  the  fever.  It  is  the  high  range 
of  temperature  which  stamps  it  as  a  peculiar  type  of  the  disease  ;  but  as 
soon  as  the  eruption  has  made  its  appearance,  although  at  first  it  may  be 
of  a  bright  red  color,  within  a  day  or  two  it  assumes  the  peculiar  dusky 
black  appearance  which  has  given  rise  to  its  name. 

There  is  another  irregular  form  of  measles  in  which  the  eruption  is 
largely  made  up  of  petechial  spots  scattered  over  the  surface  of  the 
body,  due  to  a  hemorrhagic  diathesis.  It  is  really  a  hemorrhagic  form 
of  measles,  and  is  a  very  unfavorable  type  of  the  disease.  At  first  the 
eruption  presents  the  same  appearance  as  the  ordinary  eruption  of  measles; 
but,  after  the  fever  has  continued  a  few  days,  it  assumes  a  dark  color,  the 
patient  becomes  restless,  the  tongue  dry,  there  may  be  vomiting  and 
diarrhoea,  and,  if  death  occur,  at  the  post-mortem  examination  lesions 
very  closely  resembling  those  of  typhoid  fever,  such  as  changes  in  the 
spleen  and  elevation  of  Peyer's  patches,  will  be  found.  These  cases  are 
also  known  by  the  term  ''black  measles."  Hemorrhages  also  occur  from 
nose,  mouth,  urethra,  intestinal  and  other  mucous  tracts. 

There  are  thus  two  forms  of  black  measles — one  in  which  the  eruption 
consists  of  petechial  spots  scattered  over  the  surface,  and  dej)endent  upon 
a  hemorrhagic  tendency  ;  in  the  other  form  the  eruj)tion  assumes  a  dark 
appearance  on  account  of  changes  which  have  occurred  in  the  blood,  the 
result  of  a  very  high  temperature  at  an  early  period  of  the  attack.  There 
is  always  more  or  less  danger  connected  with  any  of  the  more  severe  forms 
of  irregular  development.  Although  measles  is  usually  not  a  disease  of 
much  severity,  yet,  however  mild  the  type  may  be,  it  is  liable  to  complica- 
6ion,  and  the  most  frequent  complications  are  to  be  found  in  the  respira- 
tory organs. 

Complications. — Of  these  the  most  imjDortant  is  capillary  bronchitis. 
Rarely  is  there  a  case  of  measles  without  more  or  less  bronchial  catarrh  ; 
but  the  bronchial  catarrh  which  ordinarily  attends  it  is  not  of  much  con- 
sequence. When,  however,  the  bronchitis  becomes  capillary,  the  patient 
is  in  great  danger.  Upon  auscultation,  if  instead  of  loud,  sonorous  rdles, 
which  indicate  that  the  catarrh  is  confined  to  the  larger  bronchial  tubes, 
there  are  fine  crackling  sounds,  accompanied  by  an  entire  loss  of,  or  an 
extremely  feeble,  vesicular  murmur,  the  catarrhal  inflammation  has  ex- 
tended into  the  finer  bronchial  tubes,  and  there  is  always  danger  of  lobular 
pneumonia  (g.  v.).  A  lobular  pneumonia  which  complicates  measles  is 
always  attended  with  danger,  and  when  depression  of  temperature  fol- 
lows decline  of  the  eruption,  all  the  pulmonary  signs  may  grow  very  in- 
tense. With  serious  lung  complications,  the  eruption  may  recede.  As 
a  rule,  it  attacks  both  lower  lobes  at  the  same  time,  especially  their  dor- 
sal aspect,  while  in  the  upper  lobes  only  a  few  tubes  are  involved.  This 
complication  may  occur  at  any  time  during  the  course  of  measles,  but  it 
is  more  liable  to  occur  Just  after  the  eruptive  stage.  Its  development  is 
attended  by  a  rise  in  temperature,  in  proportion  to  the  extent  of  lung  in- 
volved.    The  urine  is  always  scanty  and  may  be  suppressed. 


788  ACUTE    G ENTERAL   DISEASES. 

Secondary  meningitis  not  infrequently  occurs  as  a  complication  of  measles. 
When  it  does  occur,  it  is  deyeloped  during  the  period  in  which  the  eruption 
is  disappearing.  It  is  more  likely  to  occur  in  this  disease  than  in  scarlet 
fever. 

A  sequela  of  measles  is  a  mild  form  of  ophthalmia.  This  ophthalmia 
may  considerably  inconvenience  the  patient,  and  lead  to  permanent  injury 
of  the  eyes.  It  is  especially  important  to  remember  that  it  appears  during 
the  convalescing  period,  that  it  is  a  conjunctivitis,  and  usually  entirely 
disappears  if  the  eyes  are  frequently  bathed  with  warm  water  and  properly 
protected  from  the  light. 

OtorrhcEa,  or  inflammation  of  the  external  ear,  is  another  sequela  of 
measles.  It  most  commonly  appears  in  those  patients  who  have  what  is 
called  a  strumous  diathesis,  have  phthisical  parents,  are  themselves  badly 
nourished,  or  who  have  suffered  from  a  severe  form  of  measles.  This 
otorrhoea  is  sometimes  very  obstinate,  and  if  it  yields  to  treatment  does  so 
very  tardily  ;  it  may  be  followed  by  permanent  deafness. 

In  adults  acute  miliary  tuberculosis  not  infrequently  occurs  as  a  sequela 
of  measles.  Within  the  past  three  years  I  have  seen  two  cases  of  what, 
previous  to  death,  seemed  to  be  acute  tuberculosis,  and  when  the  autopsy 
was  made,  throughout  the  lung  substance,  here  and  there,  were  little  points 
or  nodules  which  presented  the  usual  appearance  of  miliary  tubercles,  but, 
when  microscopically  examined,  they  were  found  to  be  points  of  vesicular 
pneumonia.  These  patients  really  died  from  pneumonia,  and  not  from 
acute  tuberculosis,  although  the  lungs  presented  the  gross  appearance  of 
acute  tuberculosis.  The  mucous  membrane  of  the  intestinal  canal  may 
also  become  the  seat  of  important  complications  in  measles.  A  mild  form 
of  gastric  catarrh  is  of  quite  frequent  occurrence,  but  is  rarely  serious  in 
character.  Severe  intestinal  catarrhs,  giving  rise  to  troublesome  diarrhoea 
and  dysentery,  are  sometimes  very  serious  complications,  especially  in  very 
young  and  feeble  children.  Occasionally  malignant  epidemics  of  measles 
prevail,  during  which  the  fatal  results  are  chiefly  due  to  intestinal  catarrhs. 

Diplitheria  does  not  so  frequently  complicate  measles  as  it  does  scarlet 
fever.  It  generally  makes  its  appearance  when  the  eruption  is  at  its  height, 
and  when  severe  its  occurrence  is  marked  by  a  rapid  rise  in  temperature. 
The  symptoms  of  the  diphtheria  are  the  same  as  when  it  occurs  as  a 
primary  disease.  It  must  always  be  regarded  as  a  serious  complication. 
Not  infrequently  measles  leaves  the  patient  in  a  state  of  general  ill-health. 
Especially  is  this  the  case  in  scrofulous  and  rachitic  children. 

Differential  Diagnosis. — Ordinarily,  when  the  eruption  is  well  defined, 
the  diagnosis  of  measles  is  not  difficult.  In  some  cases,  however,  the 
eruption  presents  an  appearance  which  closely  resembles  that  of  scarlet 
fever  and  roseola.  In  nearly  every  case  of  measles  the  catarrhal  symptoms 
accompany  the  precursory  stage,  and  increase  in  severity  during  the  period 
of  eruption.  The  presence  or  absence  of  these  catarrhal  symptoms  will 
enable  one  in  the  majority  of  cases  to  make  a  differential  diagnosis. 

In  children,  the  eruption  of  typhus  fever  very  frequently  closely  resem- 
bles that  of  measles,  but  it  does  not  appear  upon  the  face,  and  is  not 


MEASLES.  789 

accompanied  by  catarrhal  symptoms.  In  typhus  feyer,  nervous  symptoms 
are  quite  frequently  present,  such  as  delirium,  prostration,  and  tendency 
to  coma.  Such  symptoms  are  only  met  with  in  the  hemorrhagic  or  typhoid 
variety  of  measles.  Before  the  appearance  of  the  eruption  a  careful  ex- 
amination of  the  mucous  membrane  of  the  pharynx  will  settle  the  question 
of  diagnosis.  In  measles  the  mucous  surface  will  be  more  or  less  intensely 
injected;  in  typhus  fever  it  will  not  be  so  injected. 

The  differential  diagnosis  between  measles  and  small-pox  has  been  con- 
sidered. 

The  eruption  of  measles  differs  from  that  of  roseola.  In  measles  it  is 
partially  confluent,  in  roseola  it  is  non-confluent.  In  roseola  the  mucous 
membrane  of  the  fauces  is  not  intensely  injected,  and  the  fever  does  not 
run  a  characteristic  course,  the  reverse  of  which  occurs  in  measles.  If  the 
temperature  is  normal,  if  the  eruption  on  the  trunk  is  of  a  bright  color, 
if  the  surface  is  smooth,  and  if  catarrhal  symptoms  are  absent,  measles 
may  be  excluded. 

It  is  hardly  possible  to  mistake  syphilitic  exanthemata  for  measles,  for 
there  are  certain  glandular  changes  which  attend  the  development  of 
syphilitic  eruptions  which  establish  the  diagnosis.  In  the  early  period  of 
the  disease,  when  coryza  is  a  prominent  symptom,  before  the  appearance 
of  the  eruption,  measles  may  be  mistaken  for  an  ordinary  influenza. 

Prognosis. — The  prognosis  in  uncomplicated  measles  is  always  good. 
Any  irregularity  in  its  development,  and  dentition  in  children,  may  render 
the  prognosis  unfavorable.  In  the  hemorrhagic,  ulcerative,  and  in  the  ty- 
phoid varieties  the  prognosis  is  grave.  Measles  occurring  in  pregnancy  does 
not  prove  fatal  to  the  extent  that  scarlet  fever  does ;  but  abortion  is  very 
common.  Intra-uterine  measles  may  be  recovered  from,  and  the  child  is 
then  proof  against  a  second  attack.  In  severe  cases,  the  deviations  from 
the  typical  course  of  the  disease  which  render  the  prognosis  unfavorable 
are  a  temperature  of  105°  or  106°  F.  during  the  period  of  initiatory 
fever,  a  retardation  or  an  irregularity  in  the  appearance  of  the  eruption  at 
the  beginning  of  the  eruptive  stage,  and  the  occurrence  of  complications, 
especially  broncho-pneumonia,  croupous  laryngitis  and  diphtheria.  Pro- 
fuse hemorrhages  from  the  mucous  surfaces,  during  any  period  of  the  fever, 
render  the  prognosis  unfavorable.  Eecession  of  the  rash  is  very  unfavor- 
able when  there  are  any  pulmonary  symptoms.  The  hygienic  surroundings 
of  the  patient  greatly  influence  the  prognosis.' 

The  prognosis  also  depends  upon  the  age  of  the  patient ;  the  rate 
of  mortality  is  much  greater  among  adults  than  children,  and  in  very 
young  children  than  in  older  children.  The  character  of  the  prevailing 
epidemic  determines  to  a  very  great  degree  the  prognosis.  When  measles 
is  developed  in  one  who  is  suffering  from  a  severe  chronic  disease,  especially 
some  organic  disease  of  the  lungs,  the  prognosis  is  unfavorable.  The 
patient  will  not  probably  die  during  the  active  period  of  the  measles,  but 
the  chronic  pulmonary  disease  may  terminate  fatally  from  the  effects  of 
the  measles.     For  instance,  a  patient  has  evidences  of  consolidation  about 

1  The  presence  of  sewer-gas  renders  nearly  every  case  fatal.— Quain. 


790  ACUTE    GENEEAL   DISEASES. 

the  apex  of  the  lung,  a  condition  which  justifies  a  favorable  prognosis  ;  let 
measles  be  developed  in  such  a  case  and  capillary  bronchitis,  terminating 
in  more  or  less  extensive  pneumonia,  will  probably  occur,  from  which 
acute  phthisis  may  be  developed. 

In  measles,  death  rarely  occurs  during  the  first  week  of  the  disease  ;  it 
usually  takes  place  during  the  second  week  ;  if  serious  complications  occur, 
it  may  take  place  later  in  the  disease.  The  rate  of  mortality  is  estimated  at 
from  one  to  four  per  cent. 

Treatment. — The  prophylactic  treatment  of  measles  consists  in  isolating 
the  affected  person.  When  measles  run  a  regular  course,  the  principal  duty 
of  the  physician  is  to  watch  for,  and  guard  against  the  occurrence  of  pul- 
monary and  other  complications.  All  that  is  necessary  is  to  place  the 
patient  in  a  large,  well- ventilated,  darkened  room,  with  the  temperature 
of  63°  or  65°  F.,  so  that  the  congested  conjunctivae  may  not  be  exposed  to 
light. 

The  chief  article  of  diet  should  be  milk.  If  the  patient  complains  of 
itching  and  burning  of  the  surface,  he  may  be  frequently  sponged  with 
tepid  water  ;  this  causes  an  alleviation  of  the  itching  and  burning,  and  re- 
duces the  temperature.  In  an  ordinary  case  this  is  all  that  will  be  re- 
quired. Hot  drinks  or  stimulants  have  no  power  to  hasten  the  appearance 
of  the  eruption  ;  the  administration  of  the  latter  may  be  followed  by  very 
injurious  results  ;  convulsions  and  death  may  occur.  In  an  ordinary  case, 
stimulants  should  never  be  administered  during  the  initiatory  period  of 
the  fever,  unless  there  is  some  special  indication  for  their  use,  such  as  great 
prostration  or  bronchial  complication  ;  then  they  may  sometimes  be  used 
with  benefit.  Covering  the  patient  with  heavy  clothing  does  not  hasten 
the  appearance  of  the  eruption.  The'  greatest  cleanliness  should  be  ob- 
served ;  besides,  there  should  be  free  ventilation,  avoiding  all  draughts, 
in  the  sick-room.  If  there  is  thirst,  cold  water  may  be  freely  taken  in 
small  quantities  at  a  time. 

If  the  case  is  severe,  and  the  temperature  rises  to  103  or  104  degrees 
F.,  it  may  be  reduced  by  frequently  sponging  the  surface  with  tepid 
water. ' 

Post-pharyngeal  catarrh  is  liable  to  extend  into  the  larynx  and  bronchial 
tubes  and  give  rise  to  bronchitis.  One  of  the  most  important  duties  of  the 
physician  is  to  watch  for  the  occurrence  of  this  complication  ;  he  should 
frequently  examine  the  chest,  and  when  the  bronchitis  is  found  to  have 
reached  the  capillary  tubes,  should  immediately  commence  treatment  for 
its  relief.  I  have  found  the  inhalation  of  steam  to  afford  the  greatest  re- 
lief, and  to  best  control  the  bronchial  inflammation.  As  soon  as  the  larynx 
has  become  so  involved  as  to  interfere  Avith  the  respiration  of  the  patient, 
and  there  is  danger  of  croupous  laryngitis,  immediately  order  vapor  inhala- 
tions, and  insist  upon  their  continuance  until  the  laryngeal  symptoms  shall 
have  subsided.     Sometimes  this  subsidence  will  take  place  within  two  or 

1  German  writers  recommend  the  cold  bath  in  the  treatment  of  measles.  I  should  hesitate  ro  place  a 
patient  with  measles  in  a  cold  bath,  on  account  of  the  great  tendency  in  this  disease  to  pulmonary  com. 
plications. 


GERMAN   MEASLES.  791 

three  hours,  and,  again,  not  until  after  two  or  three  days.  The  value  of 
vapor  inhalations  in  the  treatment  of  the  laryngeal  and  bronchial  complica- 
tions of  measles,  I  regard  as  very  great.  When  catarrhal  pneumonia  is  de- 
veloped, it  is  to  be  treated  in  the  same  manner  as  catarrhal  pneumonia 
developed  under  any  other  circumstances  ;  the  patient  should  be  sustained 
by  the  free  use  of  stimulants. 

Pulmonary  complications  in  measles  are  often  the  result  of  exposure  to 
sudden  changes  in  temperature  ;  the  severity  of  catarrhal  symptoms  will  al- 
ways be  increased  by  such  exposure,  therefore  it  is  of  great  importance  in 
the  management  of  every  case  of  measles  that  the  patient  should  be  pro- 
tected against  sach  changes.  When  there  is  great  restlessness  during  the 
fever  of  invasion,  or  during  the  early  jseriod  of  the  eruptive  stage,  small 
doses  of  opium,  in  the  form  of  Dover's  powder,  may  be  administered  with 
marked  benefit. 

The  management  of  the  different  varieties  of  measles  will  be  indicated  by 
the  general  condition  of  the  patient.  In  the  ulcerative,  hemorrhagic,  and 
typhoid  varieties,  the  free  administration  of  stimulants  should  be  commenced 
early.  Usually  in  these  varieties  there  is  great  prostration,  and  the  main 
indication  is  the  support  of  the  patient.  Diarrhoea  at  the  close  of  measles 
may  take  the  place  of  lung  complications,  and  should  not  be  too  suddenly 
checked. 

GEEMAlSr   MEASLES. 
(Rotheln.) 

German  measles,  or  epidemic  roseola,  has  been  regarded  by  some  as  a 
modified  form  of  measles ;  by  others  as  a  modified  form  of  scarlet  fever ; 
again,  it  has  been  thought  to  be  a  combination  of  the  two  diseases — a  hy- 
brid disease.  Some  maintain  that  it  is  not  an  independent  and  specific  dis- 
ease, but  that  it  may  embrace  any  blotchy  exanthem.'  I  am  disposed  to 
regard  it  as  a  different  type  of  measles  from  that  which  ordinarily  pre- 
vails, and  by  way  of  distinction  would  call  it  German  measles,  or  epidemic 
roseola. 

Morbid  Anatomy. — It  is  one  of  the  mildest  of  the  eruptive  fevers.  It 
prevails  epidemically  and  endemically.  The  study  of  its  morbid  anatomy 
has  been  almost  exclusively  restricted  to  the  eruption.  This  consists  of  ir- 
regular spots,  or  hypersemic  blotches,  varying  in  size  from  a  pin's  head  to 
a  large  pea,  usually  slightly  elevated,  so  that  when  the  hand  jDasses  over 
the  surface  of  the  skin  it  feels  somewhat  rough.  Sometimes  these  spots  oc- 
casion intense  itching ;  they  are  quite  distinctly  separated  by  healthy  skin, 
and  disappear  under  pressure.  As  a  rule,  even  at  the  acme  of  the  develop- 
ment of  the  eruption,  their  color  is  a  pale  rose-red,  paler  than  the  intense 
red  of  the  eruption  of  scarlet  fever,  or  the  peculiar  bluish  hue  of  the  erup 
tion  in  severe  cases  of  measles.     It  appears  upon  all  parts  of  the  body,  but 

'  Later  German  writers  regard  it  as  an  independent  affection,  a  specific,  acute,  and  contagious  eruptive 
fever,  and  have  given  to  it  tlie  name  of  rubeola. 


792  ACUTE    GENERAL    DISEASES. 

is  most  abundant  upon  the  face  and  trunk.  The  spots  are  usually  discrete, 
are  round  (not  crescentic),  they  often  lie  crowded  closely  together,  but  they 
are  not  confluent. 

Mild  roseola  is  a  punctate  rash.  The  throat  is  red  and  the  glands  in 
the  neck  may  be  enlarged.  The  rash  rarely  lasts  more  than  two  days,  and 
it  is  attended  by  itching.  In  some  cases  there  is  slight  desquamation ; 
it  disappears  and  leaves  no  trace,  except  in  occasional  instances,  when  there 
is  a  transient,  yellowish  discoloration  of  the  skin. 

Some  affirm  that  the  rash  may  disappear  and  reappear  alternately 
for  several  days,  and  when  it  has  finally  disappeared  the  disease  has  ter- 
minated, and  there  is  nothing  to  fear  from  complications  or  sequelee.  In 
certain  rare  cases  vesicles  resembling  miliaria  may  be  developed  upon  the 
hyperaemic  spots,  especially  upon  the  back  ;  these  are  chiefly  due  to  external 
conditions. 

Etiology, — Doubtless  this  disease  is  contagious.  Nothing  is  known  con- 
cerning the  nature  of  its  contagion.  It  is  essentially  a  disease  of  child- 
hood. In  those  over  forty  years  of  age  its  development  is  of  very  rare 
occurrence.  It  is  conveyed  from  one  person  to  another  in  the  same  man- 
ner as  measles.  It  has  been  stated  that  women  are  more  susceptible  to  it 
than  men. 

Symptoms. — Epidemic  roseola  is  so  mild  an  affection,  that  it  is  question- 
able whether  it  has  an  invasive  stage.  The  duration  of  the  stage  of  incuba- 
tion has  not  been  determined.  Generally,  the  symptoms  which  manifest 
themselves  two  or  three  days  before  the  appearance  of  the  eruption  are 
much  less  marked  than  they  are  in  any  other  eruptive  fever.  Perhaps  in 
many  cases  they  escape  notice.  The  period  of  invasion  is  seldom  more  than 
twenty-four  hours.  Quite  frequently  the  eruption  is  the  first  symptom  of 
the  disease. 

In  most  cases  there  may  be  nothing  more  than  a  feeling  of  discomfort. 
In  other  cases  the  disease  may  be  ushered  in  by  vomiting,  diarrhoea,  and 
convulsions.  In  many  cases,  immediately  preceding  the  eruption,  and  ac- 
companying its  appearance,  there  is  well-marked  fever,  headache,  loss  of 
appetite,  and  sometimes  noticeable  prostration.  When  the  eruption  is 
regular  in  its  appearance  it  affects  first  the  neck  and  chest,  then  the  face 
and  scalp,  and  then  gradually  extends  downward  over  the  trunk  and  ex- 
tremities. Usually,  the  development  and  spread  of  the  eruption  are  rapid, 
perhaps  no  more  than  two  or  three  days  being  occupied  in  its  passage  over 
the  entire  body.  Its  duration  upon  any  one  part  of  the  body  before  it  be- 
gins to  disappear  is  not  more  than  twelve  or  twenty-four  hours.  In  the  ma- 
jority of  cases  the  temperature  does  not  rise  more  than  1°  or  3°  F.  It  may 
rise  to  103°  F,  or  104°  F.  During  the  second  day,  the  temperature  begins 
to  fall.  Sometimes  it  reaches  the  normal  within  twelve  hours,  occasion- 
ally not  until  the  third  day.  Sometimes  it  reaches  it  by  crisis,  at  others 
by  lysis.  The  pulse  increases  and  diminishes  in  frequency  according  to 
the  rise  and  fall  of  temperature.  The  tongue  is  usually  covered  with  a 
whitish  coating,  and  is  dotted  here  and  there  with  red  and  swollen  papillae. 
The  mucous  membrane  of  the  fauces  is  generally  congested  and  the  tonsils 


GERMAN   MEASLES. 


793 


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Fig.  166. 

Temperature  Record  in  ^  case  of  German 
Measles. 


moderately  swollen  ;  there  may  be  some  soreness  of  the  throat.  The 
mucous  membrane  of  the  air-passages  is 
usually  in  a  condition  of  mild  catarrh, 
consequently,  at  the  onset  of  the  disease, 
sneezing  and  coughing  are  frequently 
present,  but  they  are  less  marked  and  are 
of  shorter  duration  than  in  measles.  Suf- 
fusion of  the  eyes  with  congestion  of  the 
conjunctival  vessels  is  rarely  present ;  there 
may  be  a  slight  degree  of  photophobia. 
The  face  and  eyelids  are  usually  slightly 
swollen  at  the  time  the  eruption  makes  its 
appearance,  but  this  swelling  rapidly  dis- 
appears. 

In  most  cases,  there  is  moderate  swell- 
ing of  the  lymphatic  glands  of  the  neck, 
and  enlargement  of  the  glands  at  the  nape 
of  the  neck.  Moderate  enlargement  of  the 
occipital  glands  may  continue  for  a  num- 
ber of  days  The  disease  is  so  mild  in  char- 
acter that  children  are  with  difficulty  kept 
in  bed. 

Differential  Diagnosis. — One  of  the  promi- 
nent features  of  this  disease  is  the  close  resemblance  which  its  eruption 
bears  to  that  of  measles.  In  certain  cases  it  may  be  impossible  by  the  erup- 
tion alone  to  make  a  differential  diagnosis.  When  the  eruption  of  measles 
is  not  typically  developed,  a  complete  history  of  the  case  must  be  taken 
into  consideration.  When  this  has  been  done,  there  is  usually  no  great 
difficulty  in  arriving  at  a  correct  diagnosis.  Perhaps  that  which  will  best 
aid  in  making  a  differential  diagnosis  between  roseola  and  measles  is  the 
fact  that  an  attack  of  one  does  not  protect  against  the  other,  any  more  than 
does  an  attack  of  varicella  protect  an  individual  from  an  attack  of  variola. 
This  fact  certainly  establishes  the  non-identity  of  the  two  diseases.  The 
short  period  of  invasion,  the  eruption  appearing  first  on  the  chest  and  neck, 
the  very  mild  nose  and  throat  symptoms,  and  the  low  temperature  are  in 
contrast  with  the  symptoms  of  measles. 

It  has  been  questioned  whether  a  person  may  not  have  a  second  attack 
of  epidemic  roseola.  The  latest  observations  go  to  prove  that  a  second  attack 
is  of  as  rare  occurrence  as  a  second  attack  of  measles  or  scarlet  fever. 
Again,  one  attack  does  not  protect  an  individual  against  the  contagion  of 
scarlet  fever ;  nor  does  an  attack  of  scarlet  fever  protect  one  against  the 
contagion  of  roseola.  An  individual  may  have  an  attack  of  epidemic 
roseola  very  soon  after  he  has  been  ill  with  measles  or  scarlet  fever. 

Prognosis. — The  prognosis  is  always  good.  Complications  rarely  occur  , 
when  they  do,  they  are  usually  pulmonary. 

Treatment. — The  treatment  of  this  affection  consists  in  protection  against 
exposure.     Tepid  sponging  will  relieve  troublesome  itching,  and  reduce 


794  ACUTE    GENERAL   DISEASES. 

fever.     Regulate  the  diet,  and  carefully  watch  the  catarrh  of  the   air-pas 
sages.     As  a  rule,  convalescence  is  rapid. 

MILIARY    FEVEK. 

This  form  of  fever  cannot  strictly  be  regarded  as  a  contagious  disease, 
but  it  so  frequently  prevails  in  connection  with  measles  and  scarlet  fever, 
and  has  apparently  so  many  elements  of  contagion,  that  it  is  included  in 
the  list  of  contagious  fevers.  Some  deny  its  existence  as  a  distinct  fever. 
Writers  have  described  it  under  the  names  of  sudamina,  sudoral  exanthema, 
and  miliaria  alba,  etc.  Several  diseases  which  are  accompanied  by  sweat- 
ing, and  which  exhibit  a  tendency  to  the  formation  of  miliary  vesicles,  have 
been  called  miliary  fever. 

Until  the  occurrence  of  the  severe  epidemic  of  the  disease  known  as  the 
''English  Sweating  Sickness,"  its  specific  type  was  not  recognized.  It  has 
prevailed  epidemically  over  limited  areas,  in  Belgium,  France,  England, 
Germany,  Italy,  and  Austria.  In  some  of  these  epidemics  eleven  to  twenty 
per  cent,  of  the  whole  population  of  the  invaded  district  has  been  attacked. 
The  average  duration  of  the  epidemics  has  been  from  three  to  four  weeks  • 
occasionally  they  have  lasted  from  three  to  four  months. 

Morbid  Anatomy. — Few  post-mortem  examinations  have  been  made,  and 
those  few  have  failed  to  reveal  any  characteristic  lesion.  The  miliary 
vesicles  which  are  seen  upon  the  surface  of  the  body,  and  the  cutaneous 
eruption,  are  developed  because  the  secretion  of  the  sudoriferous  glands 
cannot  escape.  The  escape  of  the  contents  of  these  glands  may  be  pre- 
vented by  two  causes  :  (1)  the  gland-ducts  may  become  obstructed  ;  or,  (2) 
the  secretion  may  be  so  abundant  that  it  cannot  be  transmitted  by  the 
gland-duct.  In  either  case,  the  secretion  emerges  under  the  epidermis 
around  the  sweat-duct,  and  as  the  scales  are  lifted  up,  a  small  clear  vesicle 
is  formed.  The  liquid  contained  in  the  vesicle  at  first  is  transparent,  has 
an  acid  reaction,  and  is  said  to  contain  free  nuclei  and  cells  which  have 
three  or  more  nuclei  ;  these  nuclei  remain  visible  after  the  cell  membrane 
has  been  destroyed  by  the  addition  of  acetic  acid.  The  contents  of  the 
vesicle  becomes  milky  and  yellowish  from  pus  (m.  alba).  It  has  been 
claimed  that  the  virus  of  the  disease  is  contained  in  these  polynucleated 
cells.  After  death,  the  skin  becomes  oedematous,  and  very  soon  the  odor 
of  decomposition  is  perceptible. 

Etiology. — It  has  been  supposed  that  miliary  fever  was  indirectly  induced 
by  scarlatina,  the  puerperal  condition,  variola,  vaccinia,  typhus  fever  and 
like  diseases,  and  that  it  was  not  a  distinct  disease  arising  from  some  con- 
stitutional cause.  The  prevalence  of  this  fever  in  connection  with  these 
diseases  gave  rise  to  this  supposition.  Epidemics  of  this  disease  have 
generally  prevailed  during  the  spring  and  summer  months  ;  from  this  fact 
one  would  be  led  to  think  that  there  is  some  atmospheric  condition  pecul- 
iar to  these  months.  Again,  the  disease  has  most  frequently  appeared  in 
ivarm,  moist  weather,  and  from  this  fact  it  has  been  supposed  that  some 
peculiar  condition  of  the  soil  is  necessary  to  its  development.     Certain 


MILIARY  PEVER.  795 

epidemics  have  shown  a  close  connection  with  contaminations  of  the  soil, 
such  as  arise  from  neglect  of  drainage,  collections  of  refuse,  etc.  Doubt- 
less, such  conditions  of  the  soil  may  increase  its  severity,  and  cause  it  to 
prevail  more  extensively,  but  facts  do  not  prove  that,  directly  or  indirectly, 
they  cause  its  development. 

The  disease  usually  attacks  healthy  adults,  and  occurs  more  frequently 
among  females  than  males.  It  attacks  all  classes,  and  its  spread  does  not 
seem  to  be  affected  by  crowding. ' 

Symptoms. — The  average  duration  of  the  disease  is  from  five  to  eight 
days.  It  has  three  stages:  (1)  tlie  stage  of  invasion ;  (2)  the  stage  of 
sweating  ;  and,  (3)  the  stage  of  erupiion  and  desquamation. 

The  Stage  of  Invasion. — The  average  duration  of  this  stage  is  from 
forty-eight  to  seventy-two  hours.  It  is  characterized  by  an  excessive  irri- 
tation of  the  skin,  thirst,  general  lassitude  and  headache.  There  is  also 
more  or  less  febrile  movement.  Some  writers  mention  a  feelinsr  of  suf- 
focation,  which  is  usually  preceded  by  a  sense  of  oppression  at  the  epigas- 
trium.    These  are  the  characteristic  symptoms  of  the  stage  of  invasion. 

The  Stage  of  Swezting. — This  stage  is  usually  ushered  in  by  rigors  ; 
rarely,  by  a  well-marked  chill.  The  characteristic  symptom  of  this  stage 
is  profuse  and  persistent  sweating.  The  sweating  is  accompanied  by  a 
prickling  sensation  of  the  skin,  distress,  and  a  sense  of  compression  at  the 
epigastrium,  and  by  more  or  less  violent  palpitation  of  the  heart,  with  pre- 
cordial pain.  Usually  the  sweat  appears  on  all  parts  of  the  body  at  the 
same  time.  Sometimes  it  appears  first  upon  the  head  and  breast,  then 
gradually  descends,  and  soon  becomes  so  abundant  that  every  article  of 
clothing,  bed-clothes  and  bedding,  becomes  saturated.  The  pulse  some- 
times reaches  140  beats  per  minute,  the  temperature  rises  to  103°  F.,  104° 
F.,  or  even  105°  F.,  and  the  skin,  notwithstanding  the  profuse  perspiration, 
feels  extremely  hot.  During  this  stage  the  headache  and  the  sense  of 
suffocation  increase ;  the  epigastric  and  precordial  pain  and  the  palpita- 
tion increase  in  severity,  and  sometimes  become  alarming,  although  the 
most  careful  physical  examination  fails  to  discover  any  lesion  in  the 
heart  or  lungs  to  account  for  them.  The  respiration  becomes  rapid,  often 
irregular  and  intermittent. 

Irregular  exacerbations,  or  even  intermissions,  in  these  symptoms  may  oc- 
cur, but,  as  a  rule,  they  continue  without  abatement  until  the  vesicle  ap- 
pears, on  the  third  or  fourth  day  of  the  disease. 

The  Stage  of  Eruption. — This  stage  is  characterized  by  the  appearance  of 
a  rash.     It  is  first  seen  upon  the  neck  and  breast,  then  upon  the  back  and 

'  It  can  hardly  be  regarded  as  a  contagious  disease,  in  the  sense  that  it  can  be  communicated  directly 
from  the  sick  to  the  well.  It  does  not  seem  to  be  well  established  that  the  disease  can  be  developed  by 
inoculation  with  the  contents  of  the  vesicle,  notwithstanding  it  has  been  supposed  that  certain  cells  in 
the  fluid  hold  the  contagion  of  the  disease.  The  infrequency  of  the  simultaneous  occurrence  of  miliary 
fever  with  epidemics  of  measles  or  scarlet  fever,  is  unfavorable  to  the  theory  that  there  is  a  specific  rela- 
tionship between  the  poisons  of  these  diseases.  The  view  that  there  is  an  intimate  relationship  between 
cholera  and  miliary  fever  has  been  accepted  by  some  writers,  and  the  accession  of  the  latter  during 
the  course  of  the  former  has  been  supposed  to  exert  a  favorable  influence  over  the  course  of  the  disease  ; 
the  opposite,  however,  docs  not  appear  to  hold  good,  but  on  the  contrary,  favors  a  fatal  termination. 
Much  remains  to  be  learned  in  regard  to  the  relationship  existing  between  miliary  fever  and  the  other 
diseases  whicli  've  have  mentioned. 


796  ACUTE  ge:n"eeal  diseases. 

extremities,  sometimes  upon  the  mucous  membrane  of  the  mouth,  nose,  and 
conjunctiva,  sometimes  upon  the  abdomen  and  scalp.  This  eruption  con- 
sists of  irregularly  shaped  spots,  1-8  to  1-16  in.  in  diameter.  In  some 
cases  they  stud  the  skin  so  thickly  that  it  appears  like  an  uniform  sheet  of 
vivid  redness.  After  the  lapse  of  a  few  hours,  vesicles  can  be  seen  in  the 
centre  of  these  spots  ;  perhaps  at  first  they  are  so  small  as  to  necessitate 
the  aid  of  a  lens  to  discover  them.  These  vesicles  rapidly  increase  in  size, 
and  may  reach  the  size  of  a  millet-seed  or  a  small  pea.  The  contents  of 
these  vesicles  have  already  been  described.  Occasionally,  as  the  eruption 
appears,  all  the  constitutional  symptoms  are  increased  in  severity,  but  usu- 
ally they  are  modified  and  disappear  either  suddenly  or  gradually  after  its 
development.  In  the  milder  cases  the  vesicles  only,  without  the  efflores- 
cence, are  seen.  Vomiting  is  rarely  present,  although  nausea  is  a  common 
symptom,  as  is  also  constipation. 

The  urine  is  usually  scanty  and  high  colored  ;  in  some  cases  there  is  sup- 
pression of  urine.  Occasionally,  during  the  stage  of  eruption,  profuse 
secretion  of  urine  takes  place.  This  has  been  regarded  as  a  favorable 
symptom.  The  vesicles,  clear  at  first,  soon  become  opaque  and  yellowish, 
remain  for  two  or  three  days,  then  burst  and  begin  to  fall  off  in  scales. 
Desquamation  is  usually  completed  within  forty-eight  hours,  but  convales- 
cence is  often  quite  protracted  on  account  of  the  debility  and  emaciation. 

Such  is  a  brief  description  of  miliary  fever,  when  it  runs  a  regular  course, 
but  there  are  certain  variations  in  the  development  of  the  symptoms  which 
should  be  noticed.  In  the  severest  form  of  the  disease,  the  temperature  may 
rise  to  107°  or  108°  F.,  and  there  may  be  delirium  and  a  sense  of  suffocation. 
Again,  even  in  fatal  cases,  the  eruption,  sweating  and  convulsions  may 
be  absent.  Occasionally  sudden  and  fatal  collapse  follows  the  sweating 
sta^e.  The  typhoid  condition  may  be  developed  in  the  sweating  stage, 
and  may  be  attended  by  black  sordes  upon  the  teeth  and  tongue,  epistaxis 
and  uterine  hemorrhage,  and  may  terminate  fatally,  without  any  consid- 
erable anatomical  changes  recognizable  after  death. 

Complications  are  not  of  frequent  occurrence.  Occasionally  there  is 
bronchitis,  pneumonia,  and  diarrhoea. 

Relapses  are  of  common  occurrence,  but  recovery  generally  takes  place 
after  a  short  relapse. 

DiflFerential  Diagnosis. — Miliary  fever  may  be  confounded  with  measles, 
with  malarial  fever,  and  with  typhoid  fever. 

The  profuse  sweating,  the  prickling  of  the  skin,  the  intense  oppression 
at  the  epigastrium,  the  sense  of  suffocation,  with  precordial  pain,  and  the 
peculiarity  of  the  eruption,  are  sufficient  to  distinguish  it  from  measles, 
from  intermittent  fever  (although  a  decidedly  intermittent  type  of  the  dis- 
ease sometimes  prevails),  and  from  typhoid  fever.  When  the  disease  pre- 
vails epidemically,  the  diagnosis  cannot  be  difficult. 

Prognosis. — When  the  disease  runs  a  regular  course,  with  only  a  moderate 
degree  of  severity,  the  prognosis  is  good  ;  whereas  great  severity  of  the  fe- 
brile symptoms,  exceptionally  profuse  sweating,  and  increasing  sense  of 
constriction  of  the  chest,  with  suffocation,  render  the  prognosis  unfavora- 


INFLUENZA.  797 

ble.  The  accession  of  profuse  hemorrhages,  coma,  convulsions,  active  de- 
lirium, or  symptoms  of  collapse,  render  the  prognosis  unfavorable.  The 
severity  of  the  symptoms  is  usually  mitigated  when  the  eruption  makes  its 
appearance,  and  death  rarely  occurs  after  that  stage  is  reached.  If  a  fatal 
termination  is  reached,  it  usually  takes  place  during  an  exacerbation,  prior 
to  the  appearance  of  the  eruption.  In  some  epidemics,  the  mortality  has 
been  very  great ;  in  other  epidemics  the  disease  has  been  mild  in  character  ; 
eight  or  nine  per  cent,  is  the  average  death-rate.  The  character  of  the 
epidemic  affects  the  prognosis. 

Treatment. — At  one  time  diaphoretics  were  employed  in  the  treatment  of 
this  disease,  on  the  supposition  that  the  sweating  and  eruption  were  criti- 
cal manifestations,  and  must  be  aided  by  all  possible  means.  The  sense  of 
suffocation,  with  that  of  constriction  of  the  chest,  was  thought  to  indicate 
blood-letting  ;  but  it  was  soon  decided  that  loss  of  blood  aggravated  rather 
than  improved  the  patient's  condition.  Antispasmodics,  nervines,  quin- 
ine, emetics  and  counter-irritants  at  different  times  have  formed  the  basis 
of  various  plans  of  treatment.  Of  late,  subcutaneous  injections  of  mor- 
phine have  been  used  with  advantage.  Sinapisms  and  blisters  have  been 
employed  for  the  relief  of  the  sense  of  constriction  in  the  chest,  and  for  the 
ej)igastric  and  precordial  distress,  with  benefit  to  the  patient.  It  is  now 
acknowledged  that  the  administration  of  purgatives  in  large  doses  should 
be  carefully  avoided,  as  well  as  blood-letting,  general  or  local. 

At  present  the  expectant  plan  of  treatment  is  regarded  with  most  favor. 
It  chiefly  consists  in  the  use  of  cooling  drinks,  aromatic  teas,  acidulated 
water,  sponging  with  warm  water,  or  the  employment  of  warm  baths.  It 
has  been  thought  that  the  addition  of  alum  or  vinegar  to  the  water  used  for 
sponging  or  bathing  is  beneficial.  In  the  treatment  of  this  affection,  quin- 
ine seems  to  be  regarded  with  almost  universal  favor.  If  restlessness  is 
persistent,  opium,  ether,  valerian,  and  antispasmodics  may  be  employed  in 
moderate  doses,  carefully  watching  the  effect  produced.  The  patient  should 
be  surrounded  by  proper  hygienic  influences,  the  diet  should  be  moderately 
nutritive,  and  in  those  cases  in  which  convalescence  is  tedious  a  steady  and 
continued  tonic  treatment  is  indicated.  In  the  severest  form  of  the  disease 
stimulants  may  be  employed  with  benefit. 

INFLUENZA. 

{Epidemic  Cata/rrJl.) 

Influenza  is  a  specific  continued  fever,  generally  widely  epidemic,  and  at- 
tended by  catarrh  of  the  respiratory  and  digestive  tracts.  It  has  received  a 
great  variety  of  names.  In  1830  and  '31  a  severe  influenza  epidemic  swept 
over  the  whole  civilized  world. 

Morbid  Anatomy.  — There  are  no  special  pathological  lesions  of  influenza. 
There  is  generally  more  or  less  extensive  inflammation  of  the  respiratory 
organs  ;  the  lungs  are  usually  inflated  so  that  when  the  chest  is  opened  they 
protrude  from  the  cavity  instead  of  collapsing.  Sometimes  they  are  very 
dry,  at  others  oedematous.     Spots  of  lobular  consolidation  appear  as  de- 


798 


ACUTE    GEKEEAL   DISEASES. 


pressions  between  the  inflated  portions.  The  mucous  membrane  of  the 
trachea  and  larger  bronchi  is  red  and  covered  with  frothy  or  viscid  muco- 
pns.  The  injection  is  usually  most  marked  in  the  smaller  tubes.  The 
bronchial  glands  are  enlarged  and  softened.  Pale,  firm  clots  are  found  in 
the  right  heart.  The  gastric  and  intestinal  mucous  membrane  is  congested  ; 
the  stomach  is  usually  more  congested  than  the  intestines.  Hence  the  name 
gastric  influenza. 

Etiology. — All  conditions  and  ages  suffer  alike;  but  children  are  some- 
times remarkably  exempt.  The  disease  travels  very  rapidly  ;  it  has  passed 
over  the  whole  of  Europe  in  six  weeks.  It  passes  quickly  from  one  country 
to  another,  visiting  whole  continents  in  a  short  time.  It  rarely  continues 
in  one  locality  more  than  two  months.  There  is  no  doubt  that  influenza 
is  due  to  some  powerful  special  morbific  agent,  which  is  given  off  by  the 
mouth  of  the  infected,  and  which  acts  specifically  upon  the  respiratory 
mucous  membrane  and  also  upon  the  nervous  system.' 

Symptoms. — Influenza  comes  on  suddenly,  A  feeling  of  chilliness, 
sometimes  distinct  rigors,  flashes  of  heat,  and  a  feeling  of  lassitude  are  fol- 
lowed by  symptoms  of  a  severe  naso-pharyngeal  catarrh,  with  frontal 
headache,  pains  in  the  limbs  and  back,  soreness  of  the  throat,  hoarseness, 
and  a  frequent  racking  cough,  difficult  breathing  and  constriction  across 
the  chest.  The  sputa  are  first  mucous  and  then  scanty,  later  copious  and 
muco-purulent.  The  respirations  are  accelerated  ;  there  is  great  prostra- 
tion, lassitude,  apathy,  muscular 
weakness,  and  precordial  oppres- 
sion. The  fever  assumes  a  remittent 
type,  attended  by  profuse  perspira- 
tion. Sudamina  appear  on  the  sur- 
face and  herpes  on  the  lips.  The 
pulse  is  rarely  over  90  ;  yet  a  tem- 
perature of  104°  has  been  observed, 
and  the  pulse  has  been  feeble,  ir- 
regular, and  130  per  minute.  The 
tongue  is  moist  and  covered  with  a 
white  fur  ;  it  may  be  dry  and  brown. 
There  is  anorexia.  Nausea  and 
vomiting  may  be  early  symptoms 
and  continue  throughout  the  whole 
course  of  the  disease.  The  bowels 
at  first  are  constipated,  later  there 
is  diarrhcea.  There  may  be  hepatic  tenderness  and  slight  jaundice.  As 
the  disease  advances  the  face  gets  congested  and  livid,  the  frontal  head- 
ache becomes  more  severe,  the  pulse  increases  in  frequency  and  becomes 
feeble,  the  tongue  becomes  brown  and  dry.  There  are  muscular  tremors 
and  subsultus,  the  patient  becomes  dull  and  listless,  and  delirium  is  often 
present. 


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Fig.  167. 
Temperature  Record  in  a  case  of  Influenza. 


1  Brimer  (in  Virchow's  Handbnch)  thinks  it  is  a  miasmatic  disease,  caused  by  a  living  miasm  capable  of 
being  transmitted  by  the  air  and  having  an  independent  existence.    It  is  probably  contagious. 


INFLUENZA.  799 

On  auscultation  sibilant  and  sonorous  rales  are  heard  over  some  portions 
of  the  chest,  while  at  others  the  inspiratory  sounds  are  dry  and  harsh.  The 
Tesicular  murmur  is  always  indistinct.  Measle-like  spots  are  often  seen  on 
the  palatal  mucous  membrane.  In  mild  cases  the  disease  is  at  its  height 
on  the  third  day  and  then  gradually  declines.  In  the  severe  cases  where  the 
pulmonary  symptoms  are  prominent,  convalescence  does  not  commence  until 
the  tenth  or  twelfth  day  ;  convalescence  is  protracted  and  relapses  are  fre- 
quent. The  urine  is  less  in  quantity  than  normal ;  sometimes  there  is 
complete  suppression.  It  is  high-colored  and  deposits  a  sediment  on  stand- 
ing. The  different  "  varieties"  of  influenza  as  described  by  writers  are  due 
to  the  different  complications. 

Differential  Diagnosis. — The  large  number  of  persons  attacked,  the  nerv- 
ous debility  which  accompanies  it,  and  its  short  uniform  course  are  gener- 
ally sufficient  for  its  diagnosis. 

The  Prognosis  is  good  except  in  the  very  old,  very  young,  and  in  those  al- 
ready subjects  of  pulmonary  or  renal  disease.  Whenever  there  is  a  high 
mortality-rate,  the  fatality  is  due  to  complications  which  have  been  en- 
grafted on  the  influenza.  Its  complications  are  chiefly  of  the  respiratory 
tract,  the  more  frequent  of  which  are  laryngitis,  bronchitis,  pulmonary 
congestion  and  oedema,  pneumonia,'  which  is  usually  lobular,  and  pleurisy  ; 
these  complications  have  given  to  the  disease  the  name  of  epidemic  catarrhal 
fever.  Pharyngitis,  parotitis,  salivation,  hypersemia  of  the  liver,  and  sub- 
acute gastritis  are  rare  complications  of  the  digestive  apparatus.  Herpes 
labialis  occurs  often.  The  duration  of  influenza  varies  from  four  to  twelve 
days ;  and  an  epidemic  rarely  continues  more  than  from  four  to  six  weeks 
in  one  locality. 

Treatment. — When  influenza  is  prevailing  all  exposure  to  cold  must  be 
carefully  avoided,  and  in  its  treatment  the  general  hygienic  measures  of 
the  acute  infectious  fevers  are  to  be  employed ;  medicinal  treatment  is  not 
very  efficacious.  Quinine  sometimes  aborts  it,  if  given  in  large  doses  at  its 
very  onset.  In  the  early  stages  liquor  ammonii  acetatis  and  pulvis  ipe- 
cacuanhse  (one  grain  of  the  latter  in  one-half  ounce  of  the  former)  every 
two  or  three  hours  is  all  that  is  required.  The  bowels  should  be  kept 
freely  open  with  salines ;  milk  combined  with  alkaline  waters  is  the  only 
food  w^hich  should  be  allowed  for  the  first  forty-eight  hours.  If  patients 
are  restless,  Dover's  powders  may  be  given  in  small  doses.  Steam  inhala- 
tions will  relieve  the  laryngeal  and  bronchial  symptoms,  and  may  be  con- 
stantly employed  during  the  acute  stage.  The  prostration  which  occurs 
in  the  old,  young,  or  feeble  must  be  combated  early  with  stimulants. 

All  revulsives,  blood-letting  and  depressing  remedies  are  contraindi- 
cated.  Colchicum,  carbonate  of  potash,  and  opiates  are  of  service  in  those 
cases  of  influenza  where  pain  and  rheumatic  symptoms  are  predominant. 
When  convalescence  commences  the  patient  should  begin  to  take  quinine 
and  iron  in  small  doses  with  a  nourishing  diet ;  a  change  of  air  is  often  of 
great   service,  especially  if  there  have  been  pulmonary  complications.     It 

'  In  one  hundred  and  eighty-three  patients  at  H6tel  Dieu  over  twenty  per  cent,  had  lobar  pneumonia. 
—Copland. 


800  ACUTE    GE]S"ERAL   DISEASES. 

must  be  remembered  that  influenza  is  often  the  exciting  cause  of  a  phthi- 
sical development  m  subjects  who  are  so  predisposed. 

PEETUSSIS. 
(  Whooping -Cough. ) 

Whooping-cough  is  an  acute  contagious  disease,  attended  by  a  peculiar 
spasmodic  cough.  It  should  be  classed  among  the  diseases  of  children, 
although  it  may  occur  at  any  age. 

Morbid  Anatomy. — The  principal,  if  not  the  only,  morbid  changes  in 
this  affection  are  those  of  catarrhal  bronchitis.  Those  who  regard  the 
disease  as  of  nervous  origin  claim  that  there  are  evidences  of  inflammation 
of  the  vagus  nerve,  or  congestion  of  the  medulla  oblongata.  I  am  dis- 
posed to  regard  it  as  a  specific  catarrh  of  the  respiratory  mucous  membrane, 
which  differs  from  other  forms  of  catarrh  in  being  contagious  and  attended 
by  peculiar  laryngeal  and  bronchial  spasms.  Its  complications  are  cerebral 
oedema  and  congestion,  lobular  collapse,  lobular  emphysema,  bronchial 
dilatation,  or  capillary  bronchitis  and  catarrhal  pneumonia. 

The  specific  catarrh  is  located  chiefly  in  the  bronchi,  although  some  re- 
gard it  as  at  first  limited  to  the  pharyngeal  mucous  crypts,  and  still 
others  regard  it  as  confined  to  the  larynx.  The  bronchial  and  mediastinal 
glands  may  undergo  softening,  the  pleurae  and  pericardium  may  be  ecchy- 
motic.  The  mucous  membrane  of  the  stomach  is  congested  and  sometimes 
studded  with  petechial  extravasations.  Follicular  enteritis  is  not  uncom- 
mon. The  liver  and  the  spleen  are  often  enlarged  and  fatty.  Letzreich 
claims  to  have  found  a  fungoid  vegetation  in  the  epithelium  of  the  air 
tubes.     Buhl,  Oertel,  and  Hiiter  also  found  them. 

Etiology. — Whooping-cough  depends  upon  a  specific  poison  which  is 
given  off  in  the  breath  of  the  affected,  and  conveyed  through  the  air  to 
the  healthy.  A  second  attack  is  rare.  The  period  of  incubation  varies 
from  five  days  to  two  weeks ;  micrococci  are  sometimes  found  in  the  sputum. 
Teething  and  measles  predispose  to  the  reception  of  the  infection.  It  may 
be  carried  in  clothes.  It  may  prevail  epidemically,  attacking  nearly  all 
the  children  of  a  neighborhood  or  township. 

Symptoms. — There  are  three  recognized  stages  in  whooping-cough,  a 
catarrhal,  a  spasmodic,  and  a  stage  of  decline. 

The  catarrhal  stage  is  marked  by  the  ordinary  symptoms  of  a  severe  naso- 
pharyngeal and  bronchial  catarrh.  It  rarely  commences  with  a  chill,  but 
fever,  restlessness,  and  languor  are  marked.  The  fever  in  the  early  stage 
is  intermittent.  It  commences  with  coryza,  and  a  severe  dry  paroxysmal 
cough,  which  is  soon  attended  by  an  abundant,  tenacious,  viscid,  transparent 
mucus.  The  respirations  are  shallow  and  the  pulse  is  rapid.  The  dura- 
tion of  this  stage  is  from  two  days  to  three  weeks ;  nine  to  ten  days  is  the 
average. 

The  spasmodic  stage  is  attended  by  a  characteristic  spasmodic  cough. 
This  cough  is  very  severe  and  distressing ;  the  face  grows  red,  and  then 
begins  a  long,  clear,  piping  sound,  followed  by  a  series  of  rapid,  convulsive 


PERTUSSIS.  801 

and  forcible  expiratory  puffs,  which  are  succeeded  by  a  prolonged,  shrill 
inspiratory  sound  or  whoop.  If  the  fit  lasts  any  length  of  time,  the  cough 
becomes  inaudible,  and  a  considerable  quantity  of  clear,  yiscid  mucus  is 
expectorated  or  vomited  with  the  contents  of  the  stomach.  During  the 
paroxysm  the  patient  grows  red  or  purplish  in  the  face,  the  eyes  pro- 
trude, the  tongue  assumes  a  dark  appearance,  and  he  seems  on  the  verge 
of  suffocation.  Bleeding  from  the  mouth,  nose,  ears,  and  lungs  often 
occurs  during  a  violent  paroxysm.  The  face  becomes  puffy,  and  ulcers 
form  on  the  tongue,  and  hemorrhages  occur  into  the  conjunctivae.  The 
subsidence  of  the  paroxysm  is  usually  followed  by  a  sense  of  exhaustion, 
with  soreness  about  the  muscles  of  the  chest,  and  expectoration  of  whitish, 
viscid  mucus. 

A  physical  examination  of  the  chest  during  a  paroxysm  of  whooping 
cough  shows  a  feeble  or  absent  respiratory  murmur  over  the  whole  chest, 
with  sibilant  and  sonorous  rales  ;  during  the  interval  mr.cous  rales  are 
usually  heard.  The  frequency  and  duration  of  the  paroxysm  vary  greatly 
in  different  cases.  There  may  be  one  hundred  in  twenty-four  hours.  They 
are  most  frequent,  or  occur  only  at  night.  As  a  rule  the  more  violent  the 
paroxysm  the  sooner  it  is  followed  by  another.  The  disease  usually  attains 
its  height  by  the  end  of  the  fourth  or  fifth  week.  In  mild  cases  the  pa- 
tient is  well  in  the  interval  between  the  paroxysms,  but  m  severe  cases 
there  may  be  languor  and  debility,  loss  of  appetite,  headache,  and  more  or 
less  fever.  Moist  or  dry  crepitations  and  a  weak  inspiratory  sound  are  often 
heard  during  the  interval. 

The  stage  of  decline  is  marked  not  by  any  sudden  transition,  but  by  a 
gradual  diminution  in  the  frequency  and  severity  of  the  paroxysms.  The 
j)eculiar  whoop  ceases,  the  expectoration  is  less  difficult  and  becomes  more 
purulent  in  character,  and  finally,  after  a  period  of  about  nine  weeks,  the 
characteristic  cough  ceases  altogether,  and  the  patient  passes  into  a  rapid 
convalescence.  Whenever  the  coughing  fits  lose  their  characteristic  feat- 
ures and  become  dry  and  hacking,  and  the  dyspnoea  is  greatly  increased 
and  continues  through  the  intervals  with  a  marked  rise  in  the  temperature, 
it  indicates  some  pulmonary  complication.  Another  complication  which 
is  particularly  to  be  feared  in  this  disease  is  cerebral  congestion.  When, 
during  a  paroxysm,  the  countenance  becomes  flushed  and  swollen,  the 
jugular  veins  turgid,  with  a  gush  of  blood  from  the  nose,  there  is  danger 
of  such  an  occurrence.  When  the  face  is  continually  flushed,  the  head 
hot,  the  patient'  drowsy  or  restless  in  his  sleep,  moaning  and  grinding  his 
teeth,  there  is  danger  of  convulsions  and  coma,  and  the  disease  often  termi- 
nates fatally. 

Differential  Diagnosis. — In  its  earlier  stages,  it  is  not  possible  to  diagnos- 
ticate whooping-cough  with  certainty  ;  but  its  existence  may  be  suspected 
if  the  cough  is  of  a  violent  spasmodic  character,  and  if  the  disease  is  prev- 
alent. When  the  disease  is  fully  established,  the  peculiar  cough  and  ex- 
pectoration distinguish  it  from  all  other  catarrlis. 

Prognosis. — Whooping-cough  is  always  a  serious  disease,  although  it  is 
rarely  directly  fatal  ;  yet  indirectly  it  frequently  causes  death.  It  is  dan- 
51 


803  ACUTE    GENEKAL   DISEASES. 

gerous  in  proportion  to  the  number  and  severity  of  the  paroxysms,  the  in^ 
tensity  of  the  fever,  and  the  character  and  severity  of  the  complications. 
Cerebral  or  pulmonary  complications  are  always  dangerous.  Teething 
children  are  liable  to  convulsions  during  paroxysms  of  the  coughing. 
Death  may  result  from  laryngeal  spasm  independent  of  complications.  A 
condition  of  general  debility,  rickets,  poverty  and  destitution,  a  residence 
in  a  city  in  badly  ventilated  apartments,  and  epidemic  influences,  tend  to 
render  the  prognosis  unfavorable. 

Treatment. — The  chief  indications  in  the  treatment  of  whooping-cough 
are,  first,  to  diminish  the  severity  of  the  paroxysms  ;  secojid,  to  prevent 
and  treat  as  far  as  possible  the  complications  ;  third,  to  attend  to  the  gen- 
eral health  of  the  patient.  There  are  no  known  means  by  which  this  affec- 
tion may  be  averted.  The  paroxysms  cannot  be  altogether  prevented,  but 
their  severity  may  be  lessened. 

All  of  the  internal  and  external  specifics  for  the  prevention  of  the  parox- 
ysms of  whooping-cough,  which  have  been  proposed,  and  in  some  instances 
strongly  advocated,  are  of  very  doubtful  benefit.  The  most  important  and 
reliable  remedies  for  relieving  the  paroxysms  of  coughing  are  the  sedatives 
and  antispasmodics,  the  most  efficient  of  which  are  belladonna,  hydrocyanic 
acid,  hydrate  of  chloral,  hyoscyamus,  cannabis  indica,  the  bromides,  chloro- 
form and  musk  ;  all  of  these  remedies  must  be  given  in  minute  doses,  and 
their  effects  closely  watched.  The  dilute  mineral  acids,  arsenic,  nux  vomica, 
cochineal,  bromide  of  potassium,  and  repeated  emetics — emetics  are  no 
longer  given — have  each  in  turn  been  highly  recommended  as  specifics  for 
the  control  of  the  paroxysms  in  whooping  cough.  Alum  is  recommended 
by  Golding  Bird  (gr.  i-v  every  four  hours)  and  Meigs  ^  says  it  is  the  best 
remedy.  No  form  of  opium  or  belladonna  is  to  be  used  till  after  the 
catarrhal  stage  is  past.  Infusion  of  chestnut  leaves  is  regarded  highly. 
Inhalation  of  coal  gas  is  recommended  by  the  French  Academy  of  Medi- 
oine.  Ergot,  the  carioUc  acid  spray,  asafoetida,  arsenic  and  quinine  are 
iighly  efficacious,^  the  second  and  last  especially.  The  nitrite  of  amyl  and 
jaborandi  are  drugs  that  I  would  not  give  to  very  young  children.  Local 
;applications  to  the  larynx,  such  as  solution  of  nitrate  of  silver,  etc.,  ac- 
.cording  to  my  experience,  do  more  harm  than  good  ;  and  the  same  is  true 
of  counter-irritants,  such  as  liniments  and  plasters. 

I  desire  to  impress  this  fact,  that  whooping-cough  is  a  self -limiting  dis- 
ease, and,  like  all  other  diseases  of  that  class,  must  be  treated  expectantly. 
The  patient,  by  warm  clothing,  should  guard  against  undue  exposure.  In 
bad  weather,  he  should  be  confined  to  the  house  in  a  room  of  uniform 
temperature  ;  but  there  is  no  reason,  if  the  weather  is  favorable,  why  he 
should  not  go  out  into  the  open  air.  The  diet  should  be  simple,  and  the 
state  of  the  alimentary  canal  carefully  looked  after.  Adults  and  older 
children  should  be  taught  to  suppress  the  cough  as  much  as  possible. 

Complications  must  be  watched  for,  and  treated  as  soon  as  they  occur. 
Bronchitis  is  the  most  frequent  complication  ;  when  it  occurs  it  should  re- 
ceive prompt  attention,  according  to  the  rules  already  given  for  the  man- 

1  Dis.  of  Children.  *  Binz  and  Squire. 


HYDROPHOBIA.  803 

agement  of  bronchitis,  great  care  being  taken  tliat  it  does  not  become  a 
broncho-pneumonia.  If  the  symptoms  of  congestion  of  the  brain  or  of 
pneumonia  are  developed,  they  should  be  met  by  the  most  prompt  and  effi- 
cient remedies  adapted  to  these  conditions,  and  their  earliest  appearance 
should  be  watched  for.  It  is  important  to  remember  that  in  any  or  all  of 
the  complications  of  whooping-cough,  the  treatment  should  be  supporting 
in  character. 

During  convalescence,  tonics,  such  as  iron,  quinine  and  cod-liver  oil,  are 
indicated  ;  in  fact,  in  a  large  proportion  of  cases  these  remedies  are  service- 
able throughout  the  whole  course  of  the  disease.  Astringents  and  restora- 
tives are  called  for  in  the  third  stage  and  at  the  commencement  of  conva- 
lescence. Sometimes  this  affection  assumes  a  chronic  form,  continuing  after 
several  relapses  much  beyond  the  usual  period.  In  these  cases,  the  great 
remedy  is  change  of  air.  In  all  stages  of  whooping-cough,  benefit  is  de- 
rived from  a  short  sea-voyage  and  a  temporary  residence  in  a  warm  climate. 
It  has  been  recently  stated  by  some  very  judicious  observers,  that  large 
doses  of  the  sulphate  of  quinine  have  the  power  of  aborting  this  disease. 
My  experience  in  this  direction  is  not  sufficient  to  deny  or  sustain  the  state- 
ment ;  but  my  impression  is  that  this,  like  many  other  so-called  specifics, 
after  a  more  extended  trial,  will  be  found  unavailing. 

HYDEOPHOBIA. 

Hydrophobia,  or  rabies,  is  a  specific  contagious  disease  special  to  animals 
of  the  canine  and  feline  species,  which  may  be  communicated  to  man  and 
to  all  warm-blooded  animals. 

Morbid  Anatomy. — There  are  no  constant  pathological  changes.  The 
mucous  membranes  of  the  alimentary  and  respiratory  tracts,  especially  of 
the  fauces  and  pharynx,  are  congested,  (Edematous,  and  possibly  show  points 
of  hemorrhage.  The  tongue,  tonsils,  and  the  salivary  glands  are  enlarged 
and  softened,  and  the  lungs  and  other  internal  organs  are  congested. 

Eecent  investigations  have  shown '  congestion  of  the  nervous  centres,  most 
marked  about  the  basal  ganglia,  the  medulla  and  the  gray  matter  of  the 
cervical  cord.  This  is  accompanied  by  a  diffuse  cellular  infiltration  of  the 
adventitia  of  the  veins,  with  venous  injection  and  thrombosis.  Miliary  an- 
eurisms and  minute  hemorrhages  have  also  been  noted  in  the  medulla,  cer- 
vical and  dorsal  regions  of  the  cord.^ 

The  blood  is  dark,  forming  soft  clots,  and  putrefactive  changes  appear 
early  after  death. 

Etiology. — The  cause  of  the  disease  is  unquestionably  a  specific  virus 
which  is  most  abundant  and  concentrated  in  the  saliva  and  secretions  of 
the  mouth  and  pharynx. 

The  poison  retains  its  vitality  for  some  time  after  the  death  of  the 
affected  animal.  Although  not  proven,  it  is  probable  that  the  disease  is 
never  of  spontaneous  origin,  but  spreads  among  animals  by  contagion.     It 

1  Fitz  and  Shattuck. 

2  Benedict  considers  the  essential  pathological  change  in  the  nerve  centres  to  be  "an  acute  exudative 
inflammation  attended  by  hyaloid  degeneration." 


804  ACUTE    GENERAL   DISEASES. 

certainly  is  communicated  to  man  solely  by  inoculation,  which  can  take 
place  only  through  some  break  in  the  surface.  Applied  to  the  skin  or  swal- 
lowed the  virus  is  inert.' 

Symptoms. — As  in  other  infectious  diseases,  there  is  a  period  of  latency 
following  the  inoculation,  during  which  the  wound  heals  readily  and  pre- 
sents no  peculiarities.  This  period  of  incubation  varies  from  a  few  days  to 
several  months,  and  in  some  cases  even  to  years.  It  is  seldom,  however, 
that  the  disease  appears  after  five  months,  and  usually  within  two  to  six 
weeks  the  stage  of  invasion  begins. 

This  may  or  may  not  have  been  preceded  by  slight  reddening  about  the 
seat  of  the  inoculation,  with  pain  which  radiates  from  the  wound  along  the 
nerve  trunks.  In  a  few  cases  the  inflammation  causes  suppuration  and  re- 
opening of  the  wound. 

The  period  of  invasion,  or  melancliolic  stage,  is  attended  by  marked  de- 
pression of  spirits  and  change  in  the  disposition.  The  patient  is  feverish 
and  shivering  alternately,  is  restless,  uneasy  and  sleepless,  and  speaks  in 
a  sharp,  quick  manner.  The  pupils  are  dilated  and  the  eyes  bright,  and 
the  countenance  has  a  look  of  anxious  anticipation  of  some  unknown 
danger.  The  pulse  is  increased  in  frequency,  the  skin  dry,  and  there  is 
constipation,  with  perhaps  nausea  and  vomiting.  In  this  stage  the  respi- 
ration is  oppressed,  and  shows  evidences  of  the  approaching  spasms.  There 
is  epigastric  heaviness,  and  with  inspiration  the  shoulders  are  elevated  and 
the  epigastrium  protuberant. 

There  may  be  also  slight  constriction  of  the  throat  and  hesitancy  in 
swallowing,  with  general  hypera^sthesia  and  sexual  excitement. 

These  symptoms  increase  in  severity  for  two  or  three  days,  when  the 
patient  passes  into  the  C07ivulsive  stage. 

The  restlessness  and  undefined  dread  are  more  marked,  the  eyes  have  a 
wild  look,  are  bright,  staring,  and  constantly  moving  ;  the  brows  are  con- 
tracted, the  surface  pale,  and  the  patient  not  only  often  appears  like  one 
with  acute  mania,  but  the  fear  and  horror  may  pass  on  to  halluciations  and 
delirium. 

The  mouth  and  fauces  are  dry,  congested,  and  covered  with  thick, 
tenacious  saliva,  which  gathers  about  the  lips  in  frothy  masses.  Thirst  is 
intense,  but  every  effort  the  patient  makes  to  drink,  and  later  the  sight 
of  water  or  thought  of  drinking  is  followed  by  increase  of  the  pharyngeal 
constriction  at  first,  and  later  by  violent  spasms  of  the  muscles  of  deglu- 
tition and  respiration,  attended  by  general  tremors  and  most  terrific  mental 
distress. 

At  first  the  convulsions  only  follow  attempts  at  drinking,  but  the  general 
hypersesthesia  increases  rapidly  and  becomes  so  intense  that  the  weight  of 
the  clothes,  loud  harsh  sounds,  bright  lights,  or  a  draught  of  cold  air  will 
excite  general  convulsions  that  leave  the  patient  utterly  exhausted  and  with 
the  most  agonizing  horror  of  their  repetition. 

In  some  cases  death  occurs  early  in  the  disease  from  asphyxia  during  a 

1  Pasteur's  experiments  show  that  inoculation  with  a  diluted  virus  affords  protection  from  the  actual 
disease.  Not  over  seventy  per  cent,  of  tliose  bitten  by  rabid  animals  become  hydrophobic,  owing,  doubt- 
less, in  many  cases  to  the  cleansing  which  the  fangs  receive  as  they  pass  through  the  clothing. 


HYDROPHOBIA.  805 

spasm,  but  more  commonly  as  the  symptoms  increase  in  severity  the  patient 
is  rapidly  exhausted  ;  the  pulse  becomes  feeble,  frequent,  and  irregular, 
and  as  the  spasms  are  more  prolonged,  he  may  die  from  gradual  asphyxia 
or  exhaustion. 

In  rare  cases  a,  paraplegic  stage  is  said  to  occur,  in  which  the  paralysis  is 
most  marked  in  the  under  jaw  and  lower  limbs. 

The  '*  hydrophobia  "  which  is  so  characteristic  of  the  disease  as  to  give 
it  a  name,  is  due  entirely  to  fear  of  the  distressing  spasm  which  every  effort 
at  swallowing  produces,  and  is  generally  absent  in  dogs  and  other  animals. 
For  the  same  reason  the  patient  is  continually  hawking  and  spitting  out 
the  thick,  ropy  mucus  which  is  so  abundantly  secreted. 

The  peculiar  characteristics  of  the  dis-^ase  are  the  intense  hyperaesthesia 
of  the  skin  and  organs  of  special  sense ;  the  exalted  reflex  irritability  of 
the  nervous  centres,  which  results  in  the  peculiar  spasms ;  and  the  parox- 
ysmal rabid  impulses  that  lead  the  patient  to  injure,  it  may  be,  his  dearest 
friends,  even  when  he  is  conscious  of  the  nature  of  his  frenzy  and  is  strug- 
gling against  it. 

Differential  Diagnosis. — Hydrophobia  may  be  confounded  with  tetanus, 
but  in  tetanus  the  mind  is  clear  throughout,  there  is  no  fear  of  liquids, 
the  spasms  are  tonic  and  the  hyperaesthesia  is  not  so  acute,  nor  does  it  in- 
volve the  special  senses. 

In  hysteria  the  difficulty  in  swallowing  is  the  only  symptom  of  hydro- 
phobia, and  the  expressions  of  fear  are  out  of  all  proportion  to  the  other 
symptoms.  A  spurious  rabies  may  be  developed  by  the  imagination  in 
patients,  who  suppose  they  have  been  bitten  by  a  rabid  animal,  but  the 
course  of  the  disease,  its  milder  symptoms  and  favorable  termination,  will 
readily  distinguish  it. 

Prognosis. — Most  authors  regard  the  disease  as  absolutely  fatal,  and  in 
tables  of  cases  which  record  a  small  per  cent,  of  recoveries  the  possible 
hysterical  nature  of  these  cases  must  be  considered.  I  have  never  known 
a  case  to  recover. 

The  duration  of  the  disease  is  from  two  to  ten  days,  but  in  rare  cases  may 
be  extended  to  two  or  three  weeks.  Death  usually  occurs  from  asphyxia, 
rarely  from  exhaustion  or  inanition. 

Treatment. — When  it  can  be  done  immediately,  if  the  injury  is  upon  a 
limb,  a  tight  ligature  should  be  applied  above  the  wound,  which  is  then  to 
be  widely  excised  and  the  part  cupped.  Venous  hemorrhage  should  be 
encouraged. 

Of  the  many  remedies  proposed,  curare  offers  the  most  encouragement. 
It  should  be  given  hypodermically,  in  doses  of  one-third  grain  every  fifteen 
minutes,  increasing  until  the  spasms  are  controlled.  Recovery  has  been 
reported  in  one  case  where  it  was  used. 


806  ACUTE   GEIfTERAL   DISEASES. 

MALABIAL   FEVEE. 

Introduction. 

The  different  varieties  of  malarial  fever  are  like  different  branches  of 
the  same  tree  ;  they  have  many  things  in  common,  yet  differ  from  each 
other  so  widely  in  the  phenomena  which  attend  their  development, 
that  they  may  be  regarded  as  distinct  diseases.  They  have  a  common 
origin  in  a  poison  which  has  received  the  name  of  miasm. '  All  varie- 
ties of  malarial  fever  depend  upon  one  and  the  same  poison,  which  is- 
subject  to  certain  variations  in  quantity.  The  concentration  of  this  poison 
determines  the  severity  and,  to  a  certain  extent,  the  type  of  the  fever.  It 
is  possible  to  arrange  the  different  types  in  a  progressive  scale,  from  the 
mildest  to  the  most  severe,  beginning  with  simple  intermittent  and  passing 
on  to  pernicious  fever.  The  extent  of  the  morbid  processes  and  the  rapid- 
ity with  which  they  are  developed  depend  npon  the  intensity  of  the  malarial, 
poison,  the  length  of  time  the  individual  has  been  under  its  influence, 
and,  to  some  extent,  upon  individual  idiosyncrasies. 

Many  theories  have  been  advanced  as  to  the  nature  of  this  miasm 
or  malarial  poison.  By  some  it  is  regarded  as  gaseous  in  its  nature  ;  others 
believe  it  to  be  a  living  vegetable  organism  ;  and  again,  others  think  it  a. 
specific  poison,  having  no  tangible,  chemical  or  microscopical  constituents. 
No  one  of  these  theories,  nor  any  of  the  many  others  which  at  different 
times  have  been  advanced,  has  been  sustained  either  by  fact  or  by  reliable 
chemical  or  microscopical  analysis.  Thus  far  we  have  no  pof^Uive  knowledge 
in  regard  to  its  true  nature,  but  we  do  know  something  of  the  circum- 
stances which  are  necessary  for  its  production  and  the  laws  which  regulate 
its  development. 

First. — There  must  be  a  certain  amount  of  vegetable  matter,  either  on 
the  surface  or  in  the  substance  of  the  soil  where  the  malarial  poison  is  gen- 
erated. It  is  not  necessary  that  the  quantity  be  large,  but  a  certain  amount 
is  a  necessity. 

Second. — A  certain  amount  of  moisture  must  be  on  the  surface  or  in  the 
substance  of  the  soil ;  it  need  not  be  excessive ;  but  some  is  indispensable. 

Third.  — A  certain  average  degree  of  temperature  is  necessary  for  its  pro- 
duction. It  cannot  be  developed  below  an  average  temperature  of  58°  F. 
for  the  twenty-four  hours,  and  will  not  prevail  as  an  epidemic  unless  the 
average  temperature  ranges  as  high  as  65°  P.  for  the  twenty-four  hours. 

In  regions  where  these  fevers  prevail,  their  type,  form  and  intensity,  to 
a  great  degree,  depend  upon  the  height  of  the  temperature.  As  a  rule, 
malarial  fevers  are  endemic,  rarely  extending  over  large  sections  of  coun- 
try in  the  form  of  an  epidemic.  We  also  have  some  knowledge  concerning 
the  regions  in  which  malarial  fevers  are  most  likely  to  prevail,  and  which 
seem  most  favorable  to  the  development  of  malarial  poison. 

First.—  Marshes  are  especially  favorable  to  the  development  of  this  poi- 
son, and  may  generate  it  for  an  indefinite  period.     The  Pontine  marshes 

I  "  Telluric  poison  "  is  a  term  which  has  recently  come  into  vogue. 


MALARIAL   FEVEE.  80? 

have  been  malarial  for  more  than  two  thousand  years.  Yet  all  marshes 
are  not  malarial ;  their  power  to  generate  the  malarial  poison  varies  with 
the  amount  of  water  they  contain.  Where  there  is  an  abundance  of  water, 
malarial  fevers  are  rare  ;  when  they  are  covered  only  with  a  thin  sheet  of 
water,  and  are  exposed  to  the  direct  rays  of  the  sun,  malarial  poison  will 
abound.  Marshes  that  have  dried  up  are  especially  favorable  to  the  de- 
velopment of  this  poison,  yet  as  soon  as  heavy  rains  submerge  the  previously 
parched  surface,  the  power  to  generate  the  poison  is  for  a  time  diminished 
or  entirely  arrested.  Scattered  here  and  there  over  our  own  continent  are 
districts  which  have  been  malarial  ever  since  the  white  man  has  held  pos- 
session of  them ;  whether  such  was  the  case  in  earlier  times,  history  is  too 
uncertain  to  determine. 

As  a  rule,  salt-water  marshes  are  especially  free  from  malaria,  but  when 
salt  and  fresh  water  are  mixed  in  the  marsh,  the  most  favorable  conditions 
for  the  abundant  development  of  malaria  occur.  Marshes  that  rest  on  a 
substratum  of  sand  are  far  less  malarial  than  those  resting  on  limestone, 
clay,  or  mud.  There  are  marshes  in  the  higher  latitude  of  New  York  and 
other  States  which  often,  during  the  heat  of  summer,  become  dry,  yet  no 
malarial  poison  is  generated  (although  during  the  day  the  thermometer 
may  reach  90°  F.),  since  during  the  night  the  temperature  falls  below  50° 
F.  There  are  some  quite  extensive  marshes  in  which,  apparently,  every  con- 
dition of  development  of  malaria  exists,  and  yet  none  is  generated.  We 
cannot  account  for  this  fact  unless  we  accept  the  theory  that  the  ozone 
which  is  claimed  to  be  present  in  such  marshes  arrests  or  prevents  its  gene- 
ration. Damp  "  bottom  lands  "  that  are  exposed  to  an  annual  overflow, 
such  as  are  found  along  the  southern  shores  of  the  Mississippi  River,  are  as 
fruitful  as  swampy  regions  in  the  generation  of  this  poison. 

Second. — Another  condition  which  seems  to  favor  the  development  of 
malaria  is  the  upheaval  of  new  alluvial  soils,  such  as  obtains  when  new 
lands  are  first  brought  under  cultivation.  This  same  state  of  things  also 
occurs  throughout  the  middle  and  southern  portions  of  this  State,  and  in 
the  New  England  States.  Where  railroad  excavations  are  made,  malarial 
fever  is  very  frequently  developed.  In  New  York  City,  while  the  Fourth 
Avenue  improvements  were  being  made,  the  entire  region  along  the 
avenue  was  rendered  highly  malarious  by  the  excavations.  Such  excava- 
tions bring  decomposing  vegetable  matters  to  the  surface  ;  these,  under 
the  influence  of  heat  and  moisture,  generate  miasm, 

The  fact  that  fevers  of  this  type  appear  in  regions  previously  free  from 
them,  as  soon  as  the  conditions  favorable  to  their  development  exist,  is 
confirmed  by  the  testimony  of  many  careful  observers. 

Third. — Eegions  otherwise  non -malarial  may  have  malarial  poison 
brought  to  them  by  the  waters  of  rivers  which  have  their  source  in,  or 
flow  through,  malarial  districts.  Examples  of  this  kind  are  found  along 
the  banks  of  our  Western  rivers,  where  some  of  the  most  pernicious  types 
of  this  fever  are  developed;  while  in  places  only  a  short  distance  from 
these  rivers  it  is  unknown. 

Fourth. — Non-malarial  regions  may  be  rendered  malarial  from  poison 


808  ACUTE    GEITERAL   DISEASES. 

transmitted  by  the  wind.  There  has  been  considerable  discussion  as  to 
whether  this  poison  can  be  transmitted  in  such  a  manner,  and  if  it  can  be, 
to  what  distance;  there  is  no  reliable  account  of  its  transmission  over  a 
greater  distance  than  four  and  three-quarter  miles. '  The  wind  may  also 
carry  malarial  poison  up  along  the  sides  of  mountains,  to  an  elevation  of 
one  thousand  feet ;  some  writers  say  no  higher  than  six  hundred  feet. 
American  writers  give  an  account  of  its  being  carried  higher  than  six  hun- 
dred feet,  while  some  German  writers  give  well  authenticated  cases,  which 
show  that  it  must  have  been  carried  to  the  height  of  one  or  two  thousand 
feet.  * 

The  circumstances  which  are  inimical  to  its  production  are: 

First. — Hig}i  latitude.  In  this  country  malarial  poison  is  not  generated 
in  higher  latitude  than  that  of  Quebec.  The  limit  of  its  development  is 
63°  north  and  57°  south  latitude.  Between  these  two  parallels  of  latitude, 
both  on  the  eastern  and  western  hemispheres,  malarial  fevers  may  be 
developed  ;  the  nearer  the  approach  to  the  equator,  the  more  severe  the 
type.  They  do  not  prevail  over  the  entire  region  embraced  between  these 
parallels  of  latitude,  but  it  is  possible  for  them  to  be  developed  at  any 
point  where  the  altitude  is  not  too  great. 

Second. — Higli  elevation  is  another  condition  inimical  to  its  development. 
As  a  rule  it  is  not  generated  above  an  elevation  of  one  thousand  feet  above 
the  sea.  There  are,  however,  some  remarkable  exceptions  to  this  rule. 
We  find  recorded  cases  of  malarial  fever  which  have  been  developed  upon 
plateaus  among  the  Pyrenees,  at  an  altitude  of  five  thousand  feet,  and  in 
South  America  at  ten  and  eleven  thousand  feet  above  the  sea-level. 
Among  the  Pyrenees,  there  is  a  marsh  which  has  a  clay  bottom,  and  there 
malarial  poison  is  developed  which  is  very  persistent. 

Third. — Drainage  is  another  means  which  diminishes,  and  in  certain 
conformations  of  soil  entirely  destroys,  malarial  generation.  In  the  ma- 
jority of  marshes,  this  generation  can  be  arrested  or  prevented  by  free 
drainage.  Yet  there  are  marshes  upon  which  millions  have  been  expended 
in  drainage  and  which  still  remain  pestiferous.  Perhaps  it  is  possible  to 
drain  the  Jei'sey  flats  so  as  to  render  them  non-malarial  in  their  character, 
out  it  is  hardly  probable  that  this  change  can  be  effected,  for  they  have  a 
clay  bottom,  and  contain  both  salt  and  fresh  water,  conditions  which  are 
most  favorable  to  malarial  generation.  Years  of  labor  and  large  expend- 
itures of  money  have  been  bestowed  upon  the  Pontine  marshes  to  render 
them  non-malarial,  yet  they  are  as  pestiferous  as  they  were  twenty  cen- 
turies ago. 

Fourth. — Cold  is  a  powerful  agent  in  arresting  malarial  generation.  If, 
in  a  pestiferous  region,  the  temperature  should  fall  below  the  freezing 
point,  only  for  one  night,  nothing  more  need  be  feared  in  that  region  from 

1  Malarial  fever  broke  out  in  the  crew  of  a  ship,  which  was  anchored  just  four  and  three-quarter  miles 
from  shore  where  this  fever  was  prevailing.  No  cases  were  on  board  when  the  anchor  was  cast,  nor  did 
any  of  the  crew  go  on  shore.  So  long  as  the  wind  blevi^  from  the  ship  towards  shore,  the  crew  remained 
well,  but  when  the  wind  changed  its  direction  and  blew  from  the  shore  towards  the  ship,  within  six  days 
from  the  time  of  change,  cases  of  well  developed  malarial  fever  appeared  on  board.  This  seemed  to  prove 
conclusively  that  the  fever  was  brought  to  the  ship  by  the  wind. 


MALARIAL   FEVER.  809 

malaria,  until  the  average  temperature  shall  have  again  reached  60"  F. 
This  law  holds  in  all  malarial  districts^.  In  these  districts,  after  the 
temperature  has  fallen  below  the  freezing  point,  persons  may  have  the 
fever,  but  it  is  the  result  of  previous  poisoning.  Again,  the  generation 
is  less  rapid  and  the  poison  is  less  virulent  during  the  day  than  at  night. 
This  is  the  uniform  testimony  of  those  who  have  seen  most  of,  and  written 
most  on  malarial  diseases.  It  is  also  almost  universally  conceded  that  mala- 
rial districts  are  most  j)estif  erous  during  months  when  the  atmosphere  is  hot 
and  dry,  with  little  or  no  wind,  especially  when  this  state  of  atmosphere 
has  been  preceded  by  long,  heavy  rains,  and  that  the  virulence  of  the 
poison  is  greatly  diminished  as  soon  as  fresh,  strong  winds  clear  the  atmos- 
phere. 

The  question  arises  :  How  does  malarial  poison  gain  entrance  into  the  hu- 
man body  ?  The  most  reasonable  view  is  that  this  is  effected  through  the 
respired  air.  Certain  facts  seem  to  show  that  it  maybe  introduced  through 
the  intestinal  tract  with  the  food  and  water.  There  seems  to  be  scarcely 
a  doubt  but  that  it  may  be  taken  into  the  stomach  with  foul  drinking- 
water.  When  this  poison  has  once  been  introduced  into  the  circulation,  it 
undoubtedly  has  the  power  of  reproducing  itself.  From  this  fact,  which 
must  be  regarded  as  well  established,  these  who  regard  this  jjoison  as  a  liv- 
ing organism,  claim  that  these  organisms  may  reproduce  themselves  in- 
definitely, but  this  has  never  yet  been  demonstrated.' 

It  has  also  been  claimed  that  certain  races  are  more  exempt  than  others 
from  malarial  fever,  also  that  there  are  idiosyncrasies  of  constitution  which 
render  certain  individuals  exempt  from  diseases  of  this  type,  for  in  dis- 
tricts where  these  fevers  prevail  there  are  persons  who  never  have  the 
fever.  This  exception,  both  in  races  and  individuals,  is  due  to  the  greater 
physical  power  of  the  individual,  which  enables  him  to  resist  these  noxious 
atmospheric  influences.  In  a  district  where  malarial  influences  prevail, 
the  weak  and  anaemic  are  the  most  liable  to  be  attacked,  and  aU  those  in- 
fluences which  tend  to  lower  vitality,  and  to  render  feeble  the  powers  of 
resistance,  must  be  regarded  as  special  predisposing  causes.  A  strong  man 
may  resist  for  a  long  time,  while  the  old  and  children  very  quickly  suc- 
cumb to  the  influence  of  the  poison.  Women  are  more  susceptible  than 
men.  We  can  no  more  account  for  the  fact  that  one  person  can  take  in 
large  doses  of  malarial  poison  without  being  affected  by  it,  while  another 
is  affected  by  a  very  small  quantity,  than  we  can  account  for  the  fact 
that  one  person  can  take  large  quantities  of  alcoholic  stimulants  without 
showing  any  signs  of  intoxication,  while  a  very  small  quantity  will  intox- 
icate another,  supposing,  in  both  instances,  the  individuals  to  have  ap- 
parently an  equally  vigorous  constitution.     Some  claim  that  when  a  jjerson 

'  1880.  Recently  Crudeli  (of  Romel  and  Klebs  of  Prague)  examined  the  lower  strata  of  air,  the  soil,  and 
the  stagnant  water,  and  in  the  two  former  they  found  a  "  microscopic  fungus,"  consisting  of  numerous 
movable  shining  spores,  long  and  oval,  nine  micro-millimeters  in  diameter.  This  fungus  was  cultivated 
and  when  inoculated  into  animals  they  all  had  a  regular  typical  chills  and  fever  with  an  enlarged  spleen- 
They  call  this  the  hacillm  malaria.  Roman  physicians  now  claim  that  they  have  found  this  in  the  human 
subject.  It  is  said  to  be  always  in  the  blood  during  the  period  of  invasion.  The  spleen  and  the  marrow  of 
the  bones  are  its  favorite  seats. 


810  ACUTE    GENERAL   DISEASES. 

has  been  poisoned  witli  malaria,  complete  recovery  never  takes  place  ;  others 
that  even  in  the  worst  cases  recovery  is  possible.  My  own  experience  leads 
me  to  believe  that  when  an  individual  has  once  suffered  from  malarial 
poisoning,  he  is  much  more  susceptible  to  the  poison  than  one  who  has 
never  been  so  poisoned.  Some  unknown  physical  change  has  taken  place 
which  renders  him  a  fit  subject  for  malarial  manifestations  upon  the 
slightest  exposure. 

The  doctrine  of  latency  of  malarial  poison  in  the  human  body  is  an  in- 
teresting and  at  the  same  time  a  very  obscure  subject.  That  there  is  a 
period  of  incubation,  or  rather  that  a  certain  time  elapses  between  the  ex- 
posure and  the  development  of  malarial  fever,  seems  to  be  settled.  For  a 
certain  period,  often  a  long  one,  always  elapses  before  new-comers  in  a 
malarial  district  have  their  first  attack  of  the  fever ;  sometimes  the  poison 
remains  latent  until  after  they  have  removed  from  the  district.  It  is  on  the 
basis  of  the  latency  of  the  malarial  poison  that  the  relapses  can  be  ac- 
counted for  which  occur  in  those  who,  having  lived  in  a  malarial  district, 
remove  and  remain  in  a  non-malarial  one.  This  reawakening  of  the  mala- 
rial poison  may  depend  upon  a  variety  of  causes,  such  as  taking  cold,  over- 
fatigue, sudden  changes  of  temperature,  etc.  From  my  own  observation,  I 
am  convinced  that  it  is  impossible  to  bring  one  wholly  from  under  the 
infiuence  of  the  poison  while  remaining  in  a  malarial  district,  though  he 
may  become  exempt  from  its  influence  if  he  remains  beyond  the  malarial 
belt.  Undoubtedly,  an  individual  may  become  so  acclimated  as  to  resist 
malarial  influences,  and  live  for  a  long  time  in  a  malarial  district  without 
suffering  any  evil  effects  from  it.  There  can  be  no  question  but  that  those 
living  in  such  districts  suffer  less  from  the  acute  manifestations  of  the 
poisoning  than  new-comers.  But  those  changes  which  are  called  chronic 
malarial  manifestations  are  constantly  going  on  in  those  who  are  supposed 
to  be  acclimated. 

Malaria  acts  like  any  other  poison  :  after  a  time  the  system  reaches  a  cer- 
tain degree  of  tolerance.  This  tolerance;  or  immunity  from  its  manifesta- 
tions, amounts  to  nothing  more  than  the  accommodation  of  the  system  to 
its  influence.  Let  the  acclimated  person,  as  he  is  called,  be  taken  sick 
with  any  active  form  of  disease,  such  as  diphtheria  or  pneumonia,  and  it 
usually  proves  fatal,  not  that  there  is  anything  unusually  severe  in  the 
diphtheria  or  pneumonia,  but  death  is  due  to  the  fact  that  the  system  is 
"depressed  by  the  malarial  poison,  and  its  power  of  resistance  to  disease  is 
lessened. 

rN^TEKMITTENT   FEVEE. 

Like  typhoid  fever,  intermittent  fever  is  met  with  in  all  parts  of  the 
world,  although  the  region  of  its  development  may  be  said  to  be  limited 
by  63°  north  and  57°  south  latitude.  Within  these  parallels  it  is  the 
more  prevalent  nearer  the  equator. 

Morbid  Anatomy. — Its  anatomical  changes  are  few.  None  of  those 
changes  in  the  blood  which  are  present  in  the  more  severe  forms  of  in- 
fectious diseases  are  found,  nor  those  which  are  present  in  the  pernicious 


IlsTERMITTENT   FEVER. 


811 


type  of  malarial  fever,  such  as  ijigmentation  and  marked  diminution  in 
the  red  globules.  But  the  blood  clots  imperfectly,  and  is  of  an  abnormally 
dark  color,  and  if  the  fever  has  continued  for  a  long  time  there  may  be 
slight  diminution  in  the  number  of  the  red  globules  and  a  decrease  in  the 
fibrin-factors ;  but  these  changes,  to  a  great  extent,  are  due  to  the  high 
temperature  which  attends  its  paroxysms. 

The  only  constant  pathological  lesion  of  intermittent  fever  is  congestion 
of  the  internal  organs.  The  spleen  and  liver  are  always  more  or  less  en- 
larged, but  the  enlargement  is  due  to  simple  hyperasmia;  no  structural 
changes  occur  in  these  organs  until  the  intermittent  paroxysms  have  been 
often  repeated,  and  the  malarial  poisoning  has  been  of  long  duration. 
There  is  also  more  or  less  hyperaemia  of  the  kidneys  and  the  mucous  mem- 
brane of  the  intestines,  but  it  is  not  attended  by  any  signs  of  gastric  or 
intestinal  catarrh.  As  yet  no  one  has  been  able  to  prove  that  any  structural 
change  takes  place  either  in  the  nerve  tissue  or  in  any  other  tissue  of  the 
body ;  nor  from  the  structural  or  functional  disturbances  that  occur  during 
the  fever  has  any  one  been  able  to  find  satisfactory  answer  to  the  question: 
why  is  it  a  paroxysmal  and  not  a  continued  fever?  During  a  paroxysm  of 
the  fever  the  white  blood-globules  are  very  rapidly  increased  in  number. 

Etiology. — This  subject  has  just  been  considered.  All  agree  that  simple 
intermittent  fever  is  due  to  malarial  poisoning,  and  that  the  poison  is  in- 
troduced into  the  body  either  through  the  lungs  or  through  the  intestinal 
tract.  Whatever  tends  to  depress  the  mental  or  physical  powers  of  an  in- 
dividual renders  him  more  susceptible  to  malarial  influences,  and  con- 
sequently these  depressing  influences  must  be  regarded  as  predisposing 
causes.  Among  these  may  be  included 
intemperance,  exposure  to  night  air,  exces- 
sive fatigue,  bad  hygiene,  and  a  long  list 
of  like  debilitating  causes. 

Symptoms. — This  fever  is  paroxysmal, 
and  differs  in  its  types  according  to  the 
period  of  time  which  intervenes  between 
the  paroxysms.  The  first,  and  most  com- 
mon, is  the  quotidian  type,  in  which  the 
paroxysm  occurs  every  day,  and  there  is 
an  interval  of  twenty-four  hours  between 
the  paroxysms. 

The  second  is  the  tertian  type,  in  which 
the  paroxysm  occurs  every  third  day,  with 
an  interval  of  forty-eight  hours  between  the 
paroxysms. 

The  third  is  the  quartan^  type,  in  which 
the  paroxysm  occurs  every  fourtli  day, 
with  an  interval  of  three  days  or  seventy- 
two  hours  between  the  paroxysms.  These 
are  the  regular  and  more  common  types. 


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5. 

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Fig.  168. 
Fever  Curve  in  Quotidian  Intermittent. 


1  III  98,237  cases  iu  tlie  U.  S.  army,  only  1,757  were  quartan. 


812 


AOFTE   GElsTERAL   DISEASES. 


Pig.  169. 
Fever  Curve  in  Tertian  Intermittent. 


Other  types  exist,  which,  altliough  irregular,  are  unquestionably  modi- 
fications of  those  already  mentioned.    Among  these  is  the  double  quotidian, 

in  which  two  paroxysms  occur  daily.  Usu- 
ally one  paroxysm  is  scYere,  the  other  mild  ; 
the  severer  one  generally  occurs  in  the 
morning,  the  milder  in  the  afternoon  or 
evening.  There  is  also  double  tertian,  in 
which  a  paroxysm  occurs  daily,  but  it 
differs  from  the  quotidian  as  the  paroxysms 
that  resemble  each  other  occur  at  intervals 
of  forty-eight  hours.  For  instance,  the 
paroxysm  of  to-day  is  characterized  by  the 
occurrence  of  a  severe  chill  and  mild  fever  ; 
to-morrow  it  is  characterized  by  a  short 
chill  and  severe  fever ;  the  following  day 
there  occurs  the  severe  chill  and  mild  fever, 
as  on  the  first  day. 

A  form  of  intermittent  fever  is  met  with 
in  which  the  paroxysm  occurs  on  the 
seventh,  fourteenth,  twenty-first  day,  etc., 
with  an  interval  of  seven  days  between  the 
paroxysms.  The  types  most  frequently  met 
with  are  the  quotidian,  tertian  and  quar- 
tan. In  the  quotidian  variety  the  paroxysm  occurs  in  the  morning,  in 
the  tertian  it  occurs  about  noon,  while  in  the  quartan  it  occurs  in  the 
afternoon  or  evening.  The  duration  of  the 
paroxysm  varies  with  the  type  of  the  fever. 
In  the  quotidian  it  lasts  from  eight  to  ten 
hours,  in  the  tertian  it  lasts  from  six  to 
eight  hours,  in  the  quartan  from  four  to  six 
hours.  There  are  many  exceptions  to  these 
rules,  but  it  is  a  question  whether  there 
would  be  any  if  the  disease  was  permitted 
to  run  its  course  without  treatment. 

Paroxysms. — A  paroxysm  of  intermit- 
tent fever  has  three  stages  —the  cold  stage, 
the  hot  stage,  and  the  stage  of  sweating. 
In  most  cases  these  are  readily  distinguished 
from  one  another.  In  the  true  type  of 
intermittent  fever  regular  intervals  between 
the  paroxysms  of  fever  occur.  The  phenom- 
ena which  usually  precede  the  cold  stage 
are  pain  in  the  head,  a  sense  of  languor, 
and  some  nausea. 

Cold  Stage. — Passage  into  this  stage  is 
first  marked  by  a  sensation  of  coldness 
along  the  back,  which  soon  extends  to  the  extremities,  and  an   uncom- 


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Pig.  170. 
Fever  Curve  in  Quartan  Intermittent. 


IISTTEKMITTENT   FEVEK.  813 

fortable  sensation  of  coldness  gradually  creeps  over  the  entire  body.  The 
skin  becomes  shrivelled,  the  finger  ends  and  lips  become  blue,  the  face 
is  pale,  the  eyes  are  sunken,  chills  rapidly  follow  each  other,  the  teeth 
begin  to  chatter,  any  voluntary  motion  is  attended  by  trembling,  until 
finally,  as  one  chill  after  another  in  quick  succession  jiasses  over  the  body, 
the  teeth  chatter  so  that  the  noise  can  be  heard  some  distance  from 
the  patient,  and  there  is  a  shaking  of  the  entire  body.  The  surface  of 
the  body  becomes  rough,  the  blood  seems  to  recede  from  it,  and  it  as- 
sumes the  appearance  of  goose-shin  or  cutis  anserina.  The  temperature 
of  the  surface  of  the  body  is  lower  than  normal,  but  if  the  thermometer 
be  placed  in  the  axilla  or  under  the  tongue  the  tcmiierature  marks  104° 
or  105°  F.  The  voice  of  the  patient  is  weak  and  husky  ;  the  respirations 
are  rapid,  short  and  sighing,  but  the  mind  remains  clear.  The  urine  is 
increased  in  quantity  and  paler  than  normal,  and  there  is  frequent  desire 
to  empty  the  bladder.  Usually  these  symptoms  last  from  half  an  hour  to 
two  or  three  hours  ;  the  length  of  time  depends  upon  the  severity  of  the 
case.  Children  do  not  have  a  regular  chill ;  they  merely  grow  cold,  blue 
and  livid. 

After  the  cold  stage  has  continued  for  a  longer  or  a  shorter  period,  the 
patient  begins  to  have  flashes  of  heat  alternating  with  the  chilly  sensa- 
tions. Usually  these  are  first  felt  at  the  extremities,  but  they  rapidly  ex- 
tend over  the  whole  body,  and  the  hot  stage  is  established. 

Hot  Stage. — The  skin  is  now  no  longer  shrivelled,  but  becomes  red, 
swollen  and  turgid,  and  there  is  a  recession  of  the  blood  from  the  central 
organs  to  the  surface  of  the  body.  That  the  temperature  is  elevated  can- 
not be  ascertained  simply  by  laying  the  hand  upon  the  surface.  If, 
however,  the  thermometer  is  placed  in  the  axilla,  in  most  cases  the  tem- 
perature marks  106°  or  107°  F.  Thirst  is  intense.  The  uncomfortable  sen- 
sation which  the  patient  experienced  while  passing  from  the  cold  to  the 
hot  stage,  has  given  place  to  great  restlessness,  the  patient  tossing  from 
side  to  side,  with  face  flushed  and  eyes  red  and  fiery.  Sometimes  her- 
petic vesicles  appear  about  the  mouth.  The  tongue  becomes  dry,  the  caro- 
tids pulsate,  the  radial  pulse  becomes  firmer  and  more  rapid  than  in  the 
cold  stage,  and  nausea  is  marked.  It  may  have  been  present  in  the  cold 
stage,  but  in  the  hot  stage  nausea  and  vomiting  become  the  prominent 
symptoms.  As  a  rule  these  symptoms  last  from  half  an  hour  to  two  hours. 
In  exceptional  cases  they  may  continue  for  a  much  longer  time,  the  ordi- 
nary duration  of  a  paroxysm  of  a  quotidian  intermittent  being  from  eight 
to  ten  hours  ;  that  of  a  tertian,  from  six  to  eight  hours  ;  and  that  of  a 
quartan,  from  four  to  six  hours.  It  is  possible,  especially  in  those  forms 
of  malarial  fever  in  which  the  poisoning  is  intense,  for  the  hot  stage  of 
a  quotidian  to  continue  twelve  hours. 

There  is  no  condition  in  which,  for  the  time,  there  is  more  intense  fever 
than  in  the  hot  stage  of  intermittent  fever.  The  urine,  which  during  the 
cold  stage  was  abundant  and  of  a  pale  color,  now  becomes  highly  colored 
and  scanty.  Not  infrequently  it  is  almost  suppressed  during  the  hot  stage. 
Complete  suppression  of  urine  occurs  only  in  the  pernicious  type  of  the  dis- 


814  ACUTE   GENEEAL   DISEASES. 

ease.  When  the  fever  has  continued  for  a  longer  or  shorter  time,  a  slight 
moisture  appears  upon  the  forehead,  which  gradually  spreads  over  the  en- 
tire body,  and  the  patient  becomes  bathed  in  a  profuse  perspiration.  He 
is  now  in  the  sweating  stage.  In  children,  just  before  the  sweat,  coma  or 
convulsions  may  occur. 

Sioeating  Stage. — As  this  stage  comes  on,  restlessness  and  uneasiness  de- 
cline, and  a  feeling  of  comfort  is  experienced  as  the  perspiration  makes  its 
appearance.  The  temperature  rapidly  falls  ;  the  pulse  rapidly  diminishes 
in  frequency  and  force  ;  the  pulsation  of  the  carotids  ceases  ;  the  face  as- 
sumes its  normal  appearance  ;  the  congestion  of  the  conjunctivaB  disap- 
pears ;  and  the  patient  rapidly  passes  from  a  high  state  of  fever  into 
one  in  which  he  falls  asleep,  and  awakens  after  a  period  ranging  from  one 
to  three  hours,  with  a  sense  of  exhaustion. 

Interval. — During  the  interval  between  the  paroxysms  at  first  the 
patient  may  feel  perfectly  well,  but  if  there  is  a  frequent  repetition  of 
the  paroxysms,  there  will  very  soon  be  a  marked  loss  of  vitality  ;  he  be- 
comes pale  and  feeble,  and  all  the  symptoms  of  malarial  cachexia  are  pres- 
ent. There  will  be  more  or  less  of  a  Jaundiced  hue  to  the  skin,  enlarge- 
ment of  the  spleen  and  liver,  and  pigmentation  of  the  tissues.  It  is 
true  that  many  paroxysms  of  simple  intermittent  may  occur  before  any 
such  general  disturbance  of  the  health  of  the  patient  manifests  itself  ; 
yet,  in  the  interval  between  the  paroxysms,  we  cannot  call  the  patient's 
condition  one  of  perfect  health.  Usually,  in  the  quotidian  type,  the  day 
previous  to  the  development  of  the  first  paroxysm,  unnoticed  by  the  pa- 
tient, there  is  a  slight  rise  in  temperature,  perhaps  to  101°  F.  At  the 
same  time  he  experiences  a  sense  of  lassitude,  and  is  disinclined  to  make 
any  exertion,  either  mental  or  physical.  The  temperature  commences  to 
rise  in  the  morning,  and  by  noon  it  has  reached  its  maximum  ;  then  it  be- 
gins to  fall,  and  by  evening  it  may  have  fallen  to  nearly  its  normal  stand- 
ard. Thus  the  course  of  the  temperature  is  quite  characteristic,  and  may 
be  summed  up  as  a  rapid  ascent,  a  short  and  intense  stationary  period, 
and  a  critical  defervescence  constituting  the  paroxysm,  with  a  perfectly 
normal  temperature  in  the  interval.  The  following  day  another  rise  in 
temperature  will  be  noticed  ;  now  the  rise  does  not  occur  in  the  morning, 
but  after  midday,  perhaps  as  late  as  in  the  evening.  IJsually  in  the  quo- 
tidian type  of  intermittent  fever  the  highest  temperature  is  reached  a  little 
earlier  each  day  ;  if  it  is  reached  a  little  later,  the  fever  is  being  modified 
or  controlled  by  treatment. 

When  the  paroxysm  comes  on  a  little  earlier  each  day,  it  is  called  antici- 
pating, and  indicates  that  the  fever  is  not  being  controlled  ;  when  it  comes 
on  later  each  day  it  then  indicates  that  the  fever  is  being  controlled,  and  is 
called  a  postponing  intermittent .  The  types  of  intermittent  fever  which 
occur  most  frequently  in  temperate  climates  are  the  quotidian  and  the 
tertian.  In  those  whio  have  suffered  repeatedly  from  intermittent  fever, 
the  disease  is  liable  to  run  an  irregular  course,  the  paroxysms  occurring  on 
irregular  days,  and  with  irregular  intervals.  In  children  this  fever  shows 
certain   deviations  from  the  ordinary  course.     The  paroxysms  may  be 


INTEEMITTENT   FEVER.  815 

Tisliered  in  by  convulsions,  or  by  a  period  of  stupor.  Children  rarely  have 
the  distinct  chill  ;  after  a  period  varying  from  ten  minues  to  half  an  hour, 
we  have  the  hot  stage  of  regular  intermittent  fever  coming  on,  with  all  its 
attendant  phenomena.  The  intermissions  are  rarely  complete.  The  child 
loses  his  appetite  and  flesh,  becomes  irritable,  and  has  a  pale,  waxen  look, 
suffers  from  gastric  and  intestinal  disturbances,  and  the  intermittent  very 
soon  lapses  into  the  remittent  form. 

Differential  Diagnosis. — The  differential  diagnosis  of  simple  intermittent 
fever  is  never  very  difficult.  There  are  only  tAvo  diseases  which  are  liable 
to  be  mistaken  for  it,  namely,  remittent  fever ,  and  pymmia. 

It  is  readily  distinguished  from  remittent  fever,  for  in  remittent  fever 
there  is  never  a  complete  intermission,  whereas  in  intermittent  there  is 
always  a  period  in  which  there  is  no  fever.  A  careful  thermometrical  ob- 
servation for  twenty-four  hours  settles  all  questions  in  regard  to  it.  There 
is  also  a  regular  development  of  the  paroxysm  in  intermittent,  which  does 
not  occur  in  remittent.  In  remittent,  there  is  usually  but  one  chill,  while 
in  intermittent  a  chill  precedes  each  paroxysm  of  fever.  When  the  chill 
and  sweat  are  absent,  but  a  sense  of  heat,  malaise,  headache  and  lassitude 
come  on  at  pretty  regular  periods  in  a  malarial  district,  the  thermometer 
showing  a  pyrexia  of  102°  to  104°  F.,  the  patient  is  said  to  have  '^dumb- 
ague." 

Prognosis. — The  prognosis  in  simple  intermittent  fever  is  good.  The 
possibility  of  the  development  of  malarial  cachexia  must  enter  into  the 
prognosis.  When  this  occurs  the  case  is  more  than  one  of  simple  inter- 
mittent fever  ;  there  is  enlarged  spleen  and  liver,  with  pigmentation  of 
the  tissues. 

Treatment. — The  treatment  of  intermittent  fever  is  divided  into  that  for 
the  paroxysm  and  that  for  the  interval. 

The  treatment  for  the  paroxysm,  in  most  cases,  is  simply  to  render  the 
patient  as  comfortable  as  possible  while  passing  through  its  various  stages. 
At  one  time  it  was  proposed  to  tourniquet  the  limbs,  so  as  to  prevent  con- 
gestion of  internal  organs,  and  thus  arrest  the  paroxysms.  Again,  it  has 
been  proposed  to  apply  cold  to  the  surface  for  the  purpose  of  giving  a 
shock  to  the  nervous  system,  and  in  that  manner  to  arrest  the  paroxysm. 
Some  propose  to  cover  the  surface  of  the  body  with  sinapisms,  in  order  to 
irritate  the  cutaneous  surface.  Some  have  claimed  that  if  an  individual  is 
brought  fully  under  the  influence  of  alcohol  the  regular  development  of  a 
paroxysm  can  be  prevented.  It  has  also  been  claimed  that  opium,  given 
in  full  doses  at  the  usual  time  for  the  recurrence  of  the  paroxysm,  has 
power  to  prevent  it.  Experience  does  not  lead  me  to  accept  any  of  these 
statements.  It  is  true  that,  in  some  instances,  a  sudden  shock  to  the 
neiwous  system  may  prevent  the  development  of  an  intermittent  paroxysm 
when  the  paroxysms  have  become  a  habit. 

If  there  is  anything  in  the  entire  list  of  means  (either  remedial  or 
hygienic)  which  has  power  to  prevent  the  full  development  of  a  paroxysm, 
it  is  opium.  When  this  is  administered  hypodermically,  early  in  the  cold 
stage,  it  will  diminish  the  severity  of  the  cold  and  hot  stages.     Whether, 


816  ACUTE  GESTEEAL  DISEASES. 

in  the  treatment  of  the  milder  forms  of  intermittent  fever  the  combination 
of  opium  with  quinine  is  advisable,  is  still  an  unanswered  question,  though 
it  seems  to  me  that  in  such  cases  much  comfort  can  be  afforded,  and  the 
patient  be  much  less  injuriously  affected  by  the  paroxysm  if  opium  be  ad- 
ministered in  moderate  doses.  Patients  with  intermittent  fever  should  be 
kept  in  bed  during  the  entire  paroxysm,  however  mild  it  may  bo. 

During  the  cold  stage,  cover  them  with  blankets,  surround  them  with 
bottles  of  hot  water,  and  let  them  drink  freely  of  hot  water.  All  these 
means  will  hasten  the  hot  stage  of  the  disease. 

During  the  hot  stage,  the  extra  clothing  and  external  heat  should  be 
gradually  removed  and  cold  instead  of  hot  drinks  should  be  administered. 
If  nausea  and  vomiting  are  present  in  this  stage,  opium,  administered  hypo- 
dermically,  affords  great  relief.  When  the  patient  reaches  the  sweating 
stage,  let  him  alone  ;  within  a  few  hours  he  will  be  entirely  relieved  and 
in  a  state  of  convalescence. 

The  treatment  of  the  interval  is  to  prevent  the  occurrence  of  another 
paroxysm.  A  patient  should  never  be  allowed  to  have  a  second  intermit- 
tent paroxysm  ;  for  if  the  system  once  becomes  accustomed  to  these  parox- 
ysms, they  will  be  repeated  upon  the  slightest  provocation.  This  will  be 
found  to  be  the  case  with  those  who  for  a  long  time  have  not  been  sub- 
jected to  malarial  influence,  and  yet  upon  the  least  nervous  excitement  or 
fatigue  will  have  a  paroxysm.  The  great  remedy  at  this  time  is  the  sul- 
phate of  quinine.  Skilfully  used,  it  is  all-powerful  to  accomplish  this  re- 
sult. How  and  why  it  arrests  the  development  of  these  paroxysms  is  still 
unknown.  Our  knowledge  of  its  antiperiodic  power  is  purely  empirical. 
There  is  much  difference  of  opinion  as  to  the  mode  in  which  it  should  be 
administered.  In  commencing  the  treatment  of  a  case  of  intermittent 
fever,  after  the  occurrence  of  the  first  paroxysm  it  is  always  safe  to  assume 
that  the  fever  is  of  the  quotidian  type.  At  least  thirty  grains  of  quinine 
should  be  administered  between  the  termination  of  one  paroxysm  and  the 
hour  when  another  is  to  be  expected.  The  first  dose  of  ten  grains  should 
be  given  toward  the  close  of  the  sweating  stage,  and  twenty  grains  about 
two  hours  before  the  time  of  the  expected  paroxysm.  If  possible,  give  the 
quinine  in  solution.  If  irritability  of  the  stomach  causes  rejection  of  the 
quinine,  it  may  be  administered  hypodermically,  or  by  enema.  Three 
grains  administered  hypodermically  has  about  the  same  antiperiodic  power 
as  ten  grains  administered  by  the  stomach.  If  one  succeeds  in  preventing 
the  occurrence  of  a  second  paroxysm  much  has  been  accomplished.  Hav- 
ing prevented  the  occurrence  of  a  second  paroxysm,  it  is  important  that  a 
moderate  degree  of  cinchonism  should  be  maintained  for  a  number  of  days, 
by  the  daily  administration  of  quinine  in  moderate  doses.  About  two 
hours  before  the  time  of  day  at  which  the  first  paroxysm  occurred,  from 
ten  to  fifteen  grains  of  quinine  should  be  daily  administered. 

A  patient  should  visit  his  physician  one  month  from  the  date  of  the  first 
paroxysm,  for  although  he  may  not  have  had  a  fresh  malarial  exposure, 
there  will  be  a  strong  tendency  at  this  time  to  a  repetition  of  the  paroxysm, 
and  it  is  important  that  at  that  time  he  should  be  again  brought  fully 


INTERMITTENT   FEVEE.  817 

under  the  influence  of  quinine.  If  it  is  possible  for  him  to  remove  from  a 
malarial  district  a  second  paroxysm  will  almost  certainly  be  prevented.  If, 
however,  the  patient  is  not  seen  in  his  first  paroxysm,  and  if  he  lives  in  a 
malarial  district,  sulphate  of  quinine,  administered  in  the  manner  I  have 
just  recommended,  may  only  prevent  for  a  time  the  return  of  the  parox- 
ysm, and  even  complete  cinchonism  may  fail  to  control  it.  The  case 
should  now  be  carefully  examined  in  order  to  ascertain  if  there  is  not  some 
condition  present  which  interferes  with  the  antiperiodic  action  of  the  qui- 
nine, such  as  hepatic  or  splenic  hypersemia.  When  careful  percussion  shows 
that  the  liver  and  spleen  are  increased  in  size,  even  after  the  administra- 
tion of  full  doses  of  quinine,  the  administration  of  full  doses  of  calomel 
with  the  quinine  will  increase  the  antiperiodic  power  of  the  latter,  and 
diminish  the  percussion  areas  of  these  organs. 

Occasionally,  when  full  doses  of  quinine  combined  with  calomel  have 
failed  to  prevent  a  recurrence  of  a  paroxysm,  I  have  noticed  an  unusual 
excitement  attending  its  development,  and  believing  from  this  circumstance 
that  owing  to  individual  idiosyncrasies  the  malarial  poison  had  a  more 
than  usual  irritating  effect  upon  the  nervous  system,  I  have  accomplished 
the  desired  result  by  administering  full  doses  of  opium  with  the  quinine. 
In  fact,  if  the  patient  is  of  a  highly  sensitive,  nervous  organization,  I 
never  allow  a  second  paroxysm  to  pass  without  administering  a  full  dose  of 
opium  before  the  time  when  its  return  is  to  be  expected.  In  all  those  cases 
which  are  called  obstinate,  we  must  ascertain  why  we  fail  to  control  the  dis- 
ease by  the  use  of  quinine.  I  rarely  have  administered  arsenic  in  simple 
intermittent  fever.  If  I  fail  to  control  the  fever  with  quinine,  after  I  have 
reduced  splenic  and  hepatic  congestion,  controlled  nervous  irritability,  and 
increased  nutrition  by  the  administration  of  iron  and  the  moderate  use  of 
stimulants,  I  never  succeed  with  arsenic.  In  some  of  the  chronic  forms  of 
malarial  manifestation,  I  have  found  arsenic  of  great  service,  but  never  in 
simple  intermittent  fever.  Salicin,  strychnia,  piperine,  eucalyptus,  and 
hydrastia  sometimes  act  antiperiodically  when  quinine  fails. 

Mashed  Intermittent. — In  this  connection  should  be  mentioned  a 
form  of  intermittent  fever  which  has  been  designated  as  masked  inter- 
mittent fever.  For  example,  to-day  a  patient  has  a  regular  intermittent 
paroxysm,  but  to-morrow,  instead  of  its  recurrence,  perhaps  he  suffers 
from  the  most  intense  neuralgia.  This  neuralgia  may  have  its  seat  in 
an  intercostal  or  in  the  sciatic  nerve,  or,  perhaps,  more  frequently  in  the 
frontal  branch  of  the  ophthalmic  division  of  the  trigeminus.  Some  one 
nerve  becomes  involved  and  no  other  seems  to  be  affected.  In  some  cases, 
an  intense  hemicrania  takes  the  place  of  the  paroxysm.  As  a  rule,  these 
neuralgise  have  distinct  intermissions,  and  so  come  to  be  regarded  as  masked 
forms  of  intermittent  fever.  Instead  of  a  neuralgia,  the  patient  may  have 
an  attack  of  asthma,  or  an  attack  of  indigestion.  Diarrhoea,  dysentery, 
and  sometimes  hgematuria  and  apparent  suppression  of  the  urine  may  take 
the  place  of  a  distinct  intermittent  fever  paroxysm.  Again,  a  patient  may 
have  a  single  well-defined  chill,  or  even  two  chills,  followed  by  most  intense 
hemicrania,  and  then  have  no  more  for  a  long  time  ;  but  sooner  or  later  he' 
52 


818 


ACUTE   GENERAL   DISEASES. 


will  have  a  well-defined  intermittent  paroxysm  which  will  reveal  the  real 
nature  of  the  disease. 

EEMITTEJSTT    FEVEE. 


This  is  a  continued  fever,  with  diurnal  exacerbations.  It  is  known  by 
different  names,  such  as  Southern,  Western,  African,  continued,  bilious, 
acclimative,  and  remittent  fever.  The  term  remittent  fever  is  the  one 
more  generally  accepted. 

Morbid  Anatomy. — The  anatomical  lesions  of  remittent  fever  resemble 
those  of  intermittent  fever  ;  and  the  differences  are  in  degree  rather  than 
in  kind. 

Unquestionably,  both  these  types  of  fever  are  the  result  of  malarial 
poisoning,  and  the  same  diminution  of  the  red  globules  and  the  same 
changes  in  the  fibrin  factors  occur  in  remittent  as  in  intermittent.  Yet 
there  are  other  changes  in  the  blood  which  are  usually  present  in  the 
former,  and  quite  rare  in  the  latter,  namely,  the  presence  of  free  pigment- 
granules.  These  pigment-granules  are  met  with  in  some  of  the  pernicious 
forms  of  intermittent  fever  ;  but  in  all  cases  of  well-develojjed  remittent 
fever  they  are  present  at  some  time  during  the  progress  of  the  disease. 
This  pigmentation  is  due  to  haemoglobin  which  has  been  liberated  from  the 
blood-corpuscles  within  the  blood-vessels,  and  the  coloring  matter  may  re- 
main either  within  the  blood-corpuscles,  which,  after  a  time,  become  trans- 
formed into  pigment-granules,  or  remain  free  in  the  fluid  portion  of  the 

blood,  or  infiltrate  the  adjacent 
cells  and  tissues.  It  may  be 
transformed  into  granular  or 
crystalline  hsematoidin. 

The  spleen  is  not  so  much 
enlarged  in  remittent  as  in 
intermittent  fever,  and  the 
increase  in  size  seems  to  be  of 
a  different  nature.  The  enlarge- 
ment is  evidently  the  result  of 
congestion,  and  the  organ  some 
times  presents  very  nearly  the 
same  appearance  as  it  presents 
in  typhoid  fever,  except  that 
there  is  more  pigmentation. 
There  are  also  structural  lesions 
^^  j^  found    in    the    liver,    in    the 

Section  of  the  Liver  from  a  case  of  Remittent  Fever,  showing  stomach  and   in   the  intcstinCS, 

.  „  ,    ,    .        P^rt"f  a  Lobule.  which  are  uot  present  in  inter- 

A  -  Central  vein  of  the  lobule.  -"^ 


5,  B.  Intralohvlar  capillarief!  densely  pi(/mented. 
C.  Hepatic  cells,  also  containing  pigmeni. 


mittent  fever.  The  liver  is 
not  very  much  increased  in 
size,  and  is  of  a  hronze  hue.  The  principal  change  is  in  color,  which 
is  uniform  throughout  its  entire  substance.  This  varies  in  degree  in 
•different  types  of  the  disease,  and  in  different  cases  of  the  same  type. 


REMITTENT   FEVEE.  819 

The  peculiar  color  is  due  to  pigmentation  of  the  liver-tissue,  and  varies 
according  to  the  amount  of  pigment  deposited.  Pigmentation  may  occur 
in  other  tissues  of  the  body,  but  not  to  the  same  extent  as  in  the  liver.  On 
a  microscopical  examination  of  the  liver,  pigment  is  found  throughout  its 
entire  structure — not  only  in  the  hepatic  cells,  but  in  the  nuclei  of  these 
cells,  and  in  the  walls  of  the  blood-vessels.  This  discoloration  is  of  such 
uniform  occurrence  that  it  has  been  recognized  as  the  characteristic  path- 
ological lesion  of  remittent  fever.  Consequently,  the  "  h'0)ized  liver"  is 
spoken  of  as  the  characteristic  lesion  of  this  fever.  Occasionally  this  lesion 
occurs  in  intermittent  and  pernicious  fever,  but  this  is  so  seldom,  and  its 
presence  is  so  constant  in  remittent  fever,  that  if  met  with  at  an  autopsy 
remittent  fever  may  be  suspected. 

The  mucous  membrane  of  the  stomach  is  more  or  less  congested,  thick,- 
ened,  and  softened.  Changes  similar  to  those  in  typhoid  are  found  in  the 
mucous  membrane  of  the  intestines  ;  it  is  more  or  less  congested,  and  pre- 
sents very  much  the  appearance  seen  when  a  moderately  severe  catarrhal 
inflammation  is  present.  The  Peyerian  patches  are  usually  enlarged,  and 
quite  frequently  present  the  shaven  beard  appearance.  In  some  cases 
there  are  ulcerations,  not,  however,  as  extensive  or  of  the  same  nature  as 
the  ulcerative  processes  of  typhoid  fever.  The  mesenteric  glands  are  not 
enlarged,  and  there  is  none  of  that  granular  infiltration  so  noticeable  in  ty- 
phoid fever. 

Etiology. — The  great  predisposing  and  exciting  cause  of  this  fever  is  ma- 
larial poisoning.  There  can  be  no  question  but  that  the  same  malarial  poi- 
son which  gives  rise  to  intermittent  fever  can  produce  a  remittent  fever.  In 
other  words,  a  remittent  can  pass  into  an  intermittent  fever,  and  an  inter- 
mittent into  a  remittent  fever.  While  it  is  possible  for  this  to  occur,  the 
two  diseases  do  not,  as  a  rule,  prevail  in  the  same  locality  at  the  same  time. 
Endemics  of  one  form  may  occur  and  be  followed  by  endemics  or  sporadic 
cases  of  the  other  form.  In  some  localities  remittent  fever  is  almost  the 
only  form  of  malarial  disease,  intermittent  fever  only  occasionally  occur- 
ring. 

There  is  probably  no  form  of  endemic  disease  the  geographical  bounda- 
ries of  which  are  more  extensive  than  those  of  remittent  and  intermittent 
fever.  In  general  terms  they  may  be  said  to  encircle  the  earth  parallel  with 
the  equator,  circumscribing  a  broad  belt,  limited  by  GS""  north  and  by  57° 
south  latitude.  The  boundaries  of  this  belt  are  quite  irregular,  now  ap- 
proaching the  line  of  the  tropics,  now  receding  from  it.  The  remittent 
fever  which  occurs  within  the  temperate  portions  of  this  belt  is  much  less 
severe  than  that  which  occurs  in  the  tropical  regions.  From  the  localities 
in  which  this  fever  prevails,  it  would  seem  that  a  higher  average  tempera- 
ture is  required  for  its  development  than  is  required  for  the  development  of 
intermittent  fever.  As  already  stated,  a  remittent  fever  during  its  con- 
valescence may  become  an  intermittent,  and,  conversely,  an  intermittent, 
either  from  new  exposure  to  malarial  influences  or  to  the  influence  of  high 
temperature,  may  become  a  remittent.  Prom  this  fact,  the  conviction  is 
forced  upon  us  that  both  types  of  fever  are  developed  from  a  common  poi- 


820  ACUTE    GENERAL   DISEASES. 

son.  Usually  certain  atmospheric  changes  will  have  taken  place  to  change 
the  type  of  the  fever.  Intermittent  fever  may  prevail  early  in  the  season, 
but  as  the  season  advances,  and  the  temperature  ranges  higher,  the  fever 
which  prevails  will  assume  the  remittent  type.  Those  who  go  from  a  non- 
malarial  district  into  one  where  remittent  fever  is  prevailing  are  likely  to 
have  it,  while  the  old  inhabitants  only  suffer  from  the  milder  form  of  inter- 
mittent. 

Sjrmptoms. — Its  ushering-in  symptoms  are  usually  well  marked.  The 
most  constant  as  well  as  the  most  urgent  of  the  premonitory  symptoms  is 
oppression  in  the  epigastrium.  This  may  be  present  for  forty-eight  hours, 
or  even  a  longer  time,  prior  to  the  development  of  the  fever.  There  is 
also  a  certain  lassitude,  nausea,  and  loss  of  appetite  ;  and  with  these  feel- 
ings uneasiness  and  perhaps  pain  in  the  head  and  limbs.  It  does  not  come 
on  gradually,  like  typhoid  fever,  but  abruptly,  usually  with  a  chill.  It  is 
not  difficult  to  determine  when  the  patient  began  to  be  sick.  The  chill  is 
neither  so  complete  nor  so  long  continued  as  in  intermittent  fever  or  pneu- 
monia. During  the  chill  the  thermometer  will  indicate  a  temperature  two 
or  three  degrees  above  the  normal.  With  the  chill  there  is  a  most  intense 
headache,  and  pain  in  the  back  and  limbs.  As  a  rule  the  chill  is  not  of  so 
long  duration  as  the  chill  of  intermittent,  neither  does  it  begin  like  it,  by 
creeping  down  the  back  and  gradually  extending  over  the  body,  but  there 
is  general  coldness  over  the  entire  surface  at  the  very  commencement  of 
the  chilly  sensation.  Again,  there  is  not  that  tremulousness  and  shaking 
of  the  body,  nor  that  chattering  of  the  teeth,  which  are  so  frequently  ex- 
perienced in  intermittent  fever.  Following  the  chill  there  is  fever,  during 
which  the  temperature  rises  very  rapidly.  The  fever  increases  in  severity, 
and,  within  twelve  hours  from  the  time  of  its  commencement  the  tempera- 
ture may  reach  105°  or  106°  F.  As  soon  as  the  temperature  commences  to 
rise,  the  pulse  is  increased  in  frequency,  and  perhaps  beats  100  or  120  a 
minute.  The  face  becomes  flushed,  the  eyes  are  usually  suffused,  and  the 
conjunctivse  are  somewhat  congested.  The  patient  is  restless,  tossing  in 
bed,  in  the  vain  search  of  an  easy  posture.  As  the  hot  stage  advances, 
nausea  and  vomiting  are  always  present,  and  the  sense  of  oppression  in  the 
epigastrium  increases,  and  is  not  relieved  by  vomiting,  which  is  persistent 
and  distressing. 

In  the  febrile  stage  of  remittent  fever  the  patient  suffers  from  pain  in 
the  epigastrium,  to  such  an  extent  that  quite  commonly  it  is  the  only  thing 
of  which  he  complains.  The  epigastric  distress  is  often  accompanied  by 
the  most  extreme  tenderness  upon  pressure.  The  material  first  vomited 
simply  consists  of  the  contents  of  the  stomach,  next  follows  the  vomit- 
ing of  a  greenish  matter,  and  finally,  in  severe  cases,  there  may  be  a 
slight  amount  of  black  vomit.  The  quantity  of  fluid  vomited  is  greater 
than  the  quantity  taken  into  the  stomach.  Vomiting  of  stringy  mucus 
tinged  with  green  is  always  present.  Sometimes  the  patient's  stomach 
rejects  everything  taken  into  it,  and  the  vomiting  is  accompanied  by  intense 
pain  in  the  head.  Usually  at  the  commencement  of  the  fever,  the  bowels 
are  constipated. 


KEMITTEKT   FEVER. 


821 


The  febrile  symptoms  increase  in  severity  for  ten  or  twelve  hours, 
when  a  slight  perspiration  appears  upon  the  forehead.  In  a  short  time,  it 
extends  over  the  entire  body,  not  profuse,  but  a  slight  moisture  upon  the 
surface.     With  the  perspiration  there  will  be  a  fall  of  one  or  two  degrees 


Fig.  172. 
Temperature  Kecord  in  a  case  of  Remittent  Fever  ending  in  recovery. 

in  temperature,  and  a  fall  in  the  pulse  of  ten  or  twenty  beats  in  the  minute. 
The  thirst  will  diminish,  the  vomiting  grow  less,  there  may  now  be  ability 
to  retain  fluids  in  the  stomach,  and  the  patient  falls  into  a  quiet,  refresh- 
ing sleep,  and  is  relieved  from  all  the  severer  symptoms  of  the  paroxysm. 
If,  however,  the  thermometer  is  placed  in  the  axilla,  it  will  indicate  fever, 
and  although  the  temperature  may  show  a  marked  decline,  it  is  still  above 
the  normal  standard.  At  no  time  is  there  a  complete  interruption  ;  the 
fever  is  continuous.  This  is  termed  the  period  of  remission.  At  the  same 
hour  on  the  following  day  all  the  active  febrile  symptoms  return,  the  range 
of  temperature  is  higher,  the  gastric  disturbance  is  more  marked,  the 
countenance  assumes  an  anxious  expression,  and  all  the  symptoms  are  more 
severe. 

This  return  of  the  severe  febrile  symptoms  constitutes  what  is  called  the 
exacerbation,  and  the  period  between  the  time  when  the  fever  abates  and 
the  development  of  the  exacerbations  is  called  the  j)eriod  of  remission. 
Remissions  and  exacerbations  are  the  characteristic  symptoms  of  a  remit- 
tent fever  when  it  is  fully  developed,  at  which  time  a  morning  remission 
is  the  rule,  though  the  time  of  the  first  paroxysm  varies.  The  morning 
remission  is  so  invariable  that  it  is  regarded  by  many  as  a  diagnostic  sign. 
If  the  exacerbation  begins  at  noon  it  will  usually  decline  about  midnight, 
and  the  remission  will  last  until  about  noon  the  next  day.  In  very  severe 
cases  there  may  be  a  double  exacerbation,  one  at  noon,  the  other  at  mid- 
night, the  remissions  being  in  the  evening  and  morning.  The  second 
exacerbation  is  similar  to  the  primary  in  its  attendant  phenomena,  except 
that  it  is  more  severe  and  of  longer  duration,  ends  in  a  less  profuse  per- 
spiration, and  the  remission  is  not  so  well  marked  as  the  first.  On  the 
third  day  at  about  the  same  hour,  or  a  little  earlier,  there  is  another 


822  ACUTE   GE2^ERAL   DISEASES. 

exacerbation,  which  has  a  sfill  longer  duration,  is  of  greater  severity,  and 
is  followed  by  a  more  incomplete  remission. 

If  the  disease  continues,  the  remission  from  day  to  day  becomes  less  and 
less  distinct.  By  the  end  of  the  first  week  the  remission  can  no  longer  be 
detected,  and  the  fever  becomes  continuous,  without  any  marked  daily  va- 
riation in  temperature  or  pulse.  As  the  remissions  become  less  and  less 
distinct,  with  each  returning  exacerbation,  the  tongue  becomes  more  and 
more  parched,  sordes  collect  upon  the  teeth,  the  countenance  becomes  dull 
and  heavy,  distress  and  pain  in  the  epigastrium  continue,  and  are  accom- 
panied by  tenderness,  although  the  senses  of  the  patient  are  so  dulled  that 
he  may  scarcely  complain  of  it ;  and  the  Vomiting  is  not  so  constant,  and 
is  of  a  less  distressing  character  ;  constipation,  which  was  present  at  the  com- 
mencement of  the  fever,  has  now  given  way  to  diarrhoea,  the  discharges  usu- 
ally being  of  a  brownish  color.  With  tlie  diarrhoea  there  is  some  fulness  of 
the  abdomen,  and  some  local  tympanitis.  Hiccough  is  often  obstinate  and 
distressing.  The  pulse  is  increased  in  frequency,  and  will  reach  120  or  130  ; 
it  is  small,  thready,  and  feeble— at  the  onset  of  the  disease  it  was  full  and 
compressible.  The  patient  slips  down  in  bed,  picks  at  the  bed-clothes  ; 
there  is  subsultus  and  difficulty  in  deglutition,  and  the  tongue  is  protruded 
with  difficulty,  as  in  the  severer  forms  of  typhoid  fever.  The  urine  is 
scanty,  acid,  dark  colored,  but  very  rarely  is  it  albuminous.  It  may  be 
bloodj.  The  patient  passes  into  a  condition  closely  resembling  that  of  one 
in  the  third  week  of  typhoid  fever,  with  the  exception  that  there  is  no  erup- 
tion. 

The  diarrhoea,  abdominal  disturbance,  and  tympanitis,  and  often  the 
tenderness  over  the  ileo-caecal  region,  the  typhoid  tongue,  and  the  low  mut- 
tering delirium,  closely  ally  this  stage  of  remittent  fever  to  typhoid  fever. 
After  these  symptoms  have  continued  a  week  or  ten  days,  if  the  case  is  to 
terminate  in  recovery,  remissions  occur  and  become  more  and  more  dis- 
tinct, until  finally  there  is  no  exacerbation,  and  the  patient  passes  into  a 
state  of  convalescence.  If,  however,  a  fatal  termination  is  to  take  place, 
the  remissions  will  not  recur,  but-  the  typhoid  symptoms  become  more 
marked,  and  the  patient  finally  dies  from  exhaustion  or  from  complica- 
tions. Of  all  the  symptoms  which  attend  remittent  fever,  nausea  and 
vomiting  are  the  most  constant  and  the  most  distressing.  I  have  seen  pa- 
tients, after  the  temperature  has  fallen  to  its  normal  standard,  suffer  for 
weeks  from  gastric  disturbance,  attended  by  more  or  less  jaundice. 

If,  in  the  progress  of  a  remittent  fever,  the  exacerbation  occurs  a  little 
earlier  each  day,  then  treatment  is  not  controlling  it ;  the  fever  is  then  said 
to  be  anticipating,  and  the  disease  is  almost  certainly  passing  from  a  dis- 
tinct remittent  to  a  continued  remittent.  If,  on  the  other  hand,  the  ex- 
acerbation occurs  a  little  later  each  day,  the  fever  is  said  to  be  postponing, 
and  it  is  under  control,  the  remissions  become  longer,  the  exacerbations  be- 
come shorter  and  less  severe,  until  the  patient  reaches  complete  convales- 
cence. The  thermometer  will  indicate  to  what  extent  the  disease  is  being 
controlled. 

Bilious  Remittent  Fever. — In  a  certain  proportion  of  cases  in  all  endem- 


REMITTEKT  FEVEE.  S'i'd 

ics  of  remittent  fever,  vomiting  of  "  bilious  "  material,  and  jaundice  are 
prominent  symptoms,  the  skin  often  becoming  so  yellow  that  the  patients 
present  an  appearance  similar  to  that  of  those  suffering  from  yellow  fever  ; 
with  this  yellow  discoloration  of  the  skin  there  is  an  unusual  tenderness  on 
pressure  over  the  hepatic  region.  Under  such  circumstances  this  fever 
has  been  named  "  bilious  remittent."  By  some  of  the  older  writers  it  has 
been  described  as  an  idiopathic  fever,  distinct  from  remittent  or  any  other 
form  of  malarial  fever.  Medical  literature,  however,  contains  no  facts  in 
support  of  such  a  view.  The  pathology  and  symptomatology  of  the  fever 
described  by  writers  under  the  head  of  bilious  remittent  fever  differ  in  no 
respect  from  those  of  simple  remittent,  except  that  the  fever  is  accompa- 
nied by  symptoms  of  more  than  usual  hepatic  and  gastric  disturbance.  My 
own  experience  leads  me  to  regard  it  as  a  form  of  simple  remittent,  accom- 
panied by  a  more  than  usually  severe  gastro-hepatic  catarrh,  and  that  it 
is  not  entitled  to  a  separate  place  in  the  nosology  of  fevers. 

Infantile  Remittent  Fever. — It  is  a  matter  of  every-day  experience  that 
children  are  subject  to  certain  gastric  and  intestinal  derangements,  which 
are  attended  by  more  or  less  fever,  which  is  very  apt  to  assume  a  remittent 
type.  Such  fevers  cannot,  however,  be  regarded  as  specific  diseases,  for 
they  are  developed  independent  of  any  specific  fever  poison,  and  are  only 
symptomatic  of  some  local  irritation.  There  is  a  form  of  mild  typhoid  fe- 
ver which  is  often  met  with  in  children,  especially  in  the  autumn,  which 
has  also  incorrectly  received  the  name  of  infantile  remittent  fever.  In 
this  class  of  cases,  the  usual  symptoms  of  typhoid  fever  are  so  modified  by 
age  that  the  fever  assumes  a  remittent  type.  The  presence  of  rose-colored 
spots,  and  the  characteristic  typhoid  lesion  of  the  intestines,  will  determine 
the  true  nature  of  these  fevers.  Simple  malarial  remittent  in  children  does 
not  differ  from  the  remittent  of  adults.  Remittent  fever  in  children  is  more 
liable  to  be  followed  by  malarial  cachexia  than  in  the  adult. 

Differential  Diagnosis. — The  rules  by  which  a  remittent  is  distinguished 
from  an  intermittent  fever  have  already  been  given. 

The  differential  diagnosis  between  remittent  and  typhoid  fever  is  often 
attended  with  difficulty,  if  the  patient  is  not  seen  until  the  second  week  of 
the  disease,  but  if  he  is  seen  at  the  very  onset  of  the  fever,  it  is  hardly  pos- 
sible to  confound  these  two  forms  of  fever.  The  sudden  advent  of  a  remit- 
tent is  in  marked  contrast  to  the  slow  development  of  a  typhoid  fever.  Be- 
sides, they  widely  diff'er  in  the  range  of  temperature  during  the  first  week 
of  their  development.  In  remittent  there  is  a  distinct  remission,  and  there 
can  be  no  doubt  as  to  the  type  of  fever  after  the  first,  certainly  not  after  the 
second  remission  has  occurred.  Gastric  symptoms  are  much  more  severe  in 
remittent  than  in  typhoid.  By  these  symptoms  alone  a  differential  diag- 
nosis can  be  made.  If,  however,  the  fever  has  been  protracted  to  the  third 
week,  and  the  remissions  are  slight  or  altogether  absent,  although  many  of 
the  symptoms  of  typhoid  fever  are  present,  the  absence  of  the  rose-colored 
spots,  taken  in  connection  with  the  previous  history  of  the  patient,  is  suf- 
ficient to  establish  the  diagnosis. 

Remittent  fever  may  be  distinguished  from  yellow  fever  by  its  high  range 


834  ACUTE   GENERAL   DISEASES. 

of  temperature,  by  its  daily  exacerbation  and  remission,  by  the  presence  o: 
pigment  in  the  blood,  and  by  the  absence  of  albumen  in  the  urine,  which 
is  present  in  yellow  fever.  In  remittent  fever,  hemorrhage  from  the  mu- 
cous  surfaces,  especially  from  the  mucous  membrane  of  the  stomach,  indeed 
from  any  source,  is  of  rare  occurrence,  while  in  yellow  fever  it  frequently 
occurs  from  mouth,  nose,  eyes,  ears,  bowels,  and  urinary  passages.  Death 
often  occurs  on  the  third  day  in  yellow  fever,  but  in  the  severest  cases  of 
remittent  fever  not  before  the  seventh  day.  Yellow  fever  is  portable  and 
contagious  ;  remittent  is  neither.  Eemittent  fever  may  be  confounded  with 
pygemia  and  septicaemia,  but  their  differential  diagnosis  has  already  been 
sufficiently  considered. 

Prognosis. — The  prognosis  in  simple  remittent  fever  is  good.  Even  cases 
of  the  severe  types  of  this  fever  should  terminate  in  recovery,  if  skilfully 
managed,  especially  if  they  are  seen  in  the  early  stages.  Its  type  varies  very 
much  according  to  locality.  The  remittent  fever  in  New  York  City  is  of  a 
mild  type.  In  that  form  which  prevails  in  our  Western  and  Southern 
States  a  fatal  termination  is  of  frequent  occurrence.  There  is  a  type  which 
soon  loses  its  remission,  and  becomes  a  pernicious  malarial  fever,  the  prog- 
nosis of  which  is  unfavorable.  The  complications  which  may  render  the 
prognosis  unfavorable  are  meningitis,  pneumonia,  gastritis,  enteritis,  diar- 
rhoea, dysentery,  and  splenitis.  The  prognosis  will  also  be  modified  by  the 
condition  of  the  patient  at  the  time  of  the  attack,  and  by  the  character  of 
the  endemic  which  is  prevailing. 

The  symptoms  which  indicate  that  recovery  is  to  take  place  are  the  fact 
that  the  exacerbation  is  delayed  or  rendered  less  severe,  the  early  subsidence 
of  gastric  symptoms  and  headache,  and  a  decrease  in  the  frequency  of  the 
pulse,  and  the  appearance  of  vesicles  about  the  lips.  Distinct  remissions, 
accompanied  by  moderately  free  perspiration,  indicate  an  approaching  fa- 
vorable change.  On  the  other  hand,  if  the  fever  is  more  continuons  than 
paroxysmal,  with  a  pulse  becoming  daily  more  feeble  and  more  frequent,  if 
there  is  a  tendency  to  collapse  at  the  close  of  the  exacerbations,  and  sup- 
pression of  urine,  with  signs  of  extreme  exhaustion,  danger  is  indicated. 
The  average  duration  of  this  fever  is  two  weeks. 

As  this  fever  varies  so  greatly  in  severity  at  different  times  and  in  dif- 
ferent localities,  it  is  impossible  to  accurately  determine  its  average  rate  of 
mortality. 

Treatment. — In  this  disease,  we  have  means  at  our  command  by  which, 
in  the  majority  of  cases,  it  can  be  controlled,  and  by  which,  in  most  in- 
stances, its  duration  may  be  much  shortened.  It  is  hardly  necessary  to 
refer  to  such  remedial  agents  as  blood-letting,  emetics,  cathartics  and 
diaphoretics,  which  have  all  been  employed  in  the  treatment  of  this  fever, 
for  they  have  all  been  supplanted  by  a  single  remedy.  Experience  has 
proved  that  the  poison  which  causes  the  fever  cannot  be  removed  from  the 
system  by  any  of  the  so-called  eliminative  methods  of  treatment.  If  this 
class  of  patients  are  depleted  to  any  extent,  the  development  of  those 
typhoid  symptoms  which  are  especially  to  be  avoided  will  be  hastened. 
Those  living  in  malarial  districts  are  never  up  to  the  normal  standard  of 


EEMITTENT    FEVER.  835 

vigor,  and,  consequently,  are  in  a  condition  to  be  affected  unfavorably  oy 
any  plan  of  treatment  or  by  any  remedial  agents  which  shall  enfeeble  the 
vital  powers. 

The  first  thing  to  be  done  in  the  successful  management  of  this  fever  is 
to  place  the  patient  under  the  best  possible  hygienic  surroundings.  The 
same  care  should  be  exercised  in  the  arrangment  of  the  sick-room  as  has 
already  been  proposed  in  the  management  of  tyjjhoid  fever.  Those  who 
have  seen  most  of  remittent  fever  in  its  severer  form  recommend  that  the 
treatment  of  each  case  be  commenced  by  administering  a  mercurial  purge. 
They  claim  that  there  is  always  more  or  less  engorgement  of  the  liver, 
spleen,  and  mucous  membrane  of  the  stomach  and  intestines,  and  that, 
so  long  as  these  organs  remain  in  this  condition,  no  plan  of  treatment 
will  be  successful.  However  great  may  be  the  differences  of  opinion 
in  regard  to  this,  all  agree  that  the  sulphate  of  quinine  should  be  used 
in  its  treatment.  Practitioners  differ  as  to  the  mode  of  its  administra- 
tion, but  all  advocate  its  use.  Some  maintain  that  it  has  greater  power 
over  the  disease  when  administered  in  small  doses,  rejoeated  at  short  in- 
tervals ;  others,  that  it  should  be  given  in  one  or  two  large  doses  during 
the  remission,  an  hour  or  two  before  the  commencement  of  the  expected 
exacerbations.  Others,  again,  claim  that  the  quinine  has  its  greatest 
power  over  the  fever  when  administered  during  the  activity  of  the  febrile 
excitement.' 

From  these  reports,  and  from  my  own  experience,  I  do  not  hesitate  to 
administer  quinine  at  any  time  during  the  period  of  the  exacerbation  or 
remission.  My  rule  is  to  give  ten  or  twenty  grains  at  a  dose,  according 
to  the  severity  of  the  fever,  and  repeat  it  every  two  hours  until  cinchonism 
is  produced.  When  cinchonism  is  reached,  although  the  fever  may  not 
be  controlled,  it  is  well  to  stop  its  administration  until  twenty-four  hours 
have  elapsed  ;  by  doing  this  one  can  better  determine  the  antiperiodic 
power  of  the  drug.  If  the  exacerbations  do  not  disappear,  but  are  de- 
layed and  are  less  severe,  the  fever  is  being  controlled.  If,  notwithstand- 
ing this  free  use  of  quinine,  the  exacerbations  are  more  severe  and  longer 
in  duration,  and  the  remissions  less  frequent,  and  typhoid  symptoms  are 
manifesting  themselves,  stimulants  may  be  demanded.  Even  large  doses 
of  stimulants  may  be  required  to  sustain  the  patient  while  he  is  passing 
through  this  period  of  the  disease.'* 

Remittent  fever  is  not,  like  typhoid  fever,  a  disease  of  days  or  weeks. 

1  This  subject  was  carefully  studied  by  those  engaged  in  the  English  Medical  Service  in  India.  Under 
the  direction  of  the  Surgeon-General  in  that  department  quinine  was  administered  at  different  periods  in 
the  course  of  the  fever,  one  surgeon  giving  quinine  at  the  commencement  of  the  exacerbation,  another 
immediately  after  the  exacerbation  had  passed  its  height  and  as  the  sweating  stage  was  coming  on,  an- 
other immediately  preceding  the  exacerbation,  and  still  others  giving  it  during  the  remission.  This  plan 
was  adopted  to  determine  with  positiveness  when  the  smallest  amount  of  quinine  would  have  the  greatest 
controlling  eflfecl  over  the  fever.  Prom  the  various  branches  of  the  department  reports  were  made, 
whence  the  conclusion  was  arrived  at  that  quinine,  administered  during  the  time  of  the  exacerbation, 
had  not  only  a  greater  influence  in  diminishing  the  severity  of  the  disease,  but  it  also  more  completely  con- 
trolled the  fever,  and  more  markedly  shortened  its  duration  than  when  it  was  administered  during  the  re- 
mission. 

"Livingstone  and  other  African  travellers  advise  bitter  ale  as  about  the  best  stimulant,  and  the  one  best 
borne  by  the  irritable  stomach  in  this  fever. 


826  ACUTE    GENERAL   DISEASES. 

In  its  severer  forms  no  time  should  be  lost  while  waiting  for  the  action  of 
cathartics  or  other  remedial  agents  which  are  supposed  to  be  of  importance, 
but  the  administration  of  quinine  should  be  at  once  commenced.  When 
the  disease  has  reached  its  second  or  third  week,  and  there  is  no  evi- 
dence that  the  patient  is  passing  on  toward  recovery,  administer  a  sec- 
ond time  large  doses  of  quinine ;  in  this  way  the  progress  of  the 
fever  may  be  arrested.  If,  after  a  second  cinchonism  is  produced, 
the  fever  is  not  arrested,  omit  again  for  a  few  days  the  administration, 
of  quinine  ;  then  repeat  the  large  doses  a  third  time.  Ifc  is  much  better 
to  proceed  in  this  way  than  to  keep  the  patient  in  a  continued  state 
of  cinchonism.  It  is  not  necessai:y  to  enumerate  the  long  list  of  drugs 
which  at  different  times  have  been  proposed  as  specifics  in  this  fever,  all 
of  which,  by  common  consent,  are  now  regarded  as  far  less  reliable  than, 
quinine.  The  important  thing  is  to  know  how  and  when  to  administer 
quinine. 

There  are  certain  palliative  measures  which  it  is  sometimes  important 
to  employ.  If  the  exacerbations  are  very  intense,  the  headache  very 
severe,  and  the  restlessness  or  other  febrile  symptoms  are  not  relieved  by 
full  doses  of  quinine,  cold  may  be  employed  for  its  antipyretic  effect,  as 
in  typhoid  fever.  Full  doses  of  the  bromide  of  potassium  promote  sleep. 
Frequently,  in  mild  cases,  sponging  the  surface  with  tepid  water  is  not 
only  grateful  to  the  patient,  but  it  has  a  controlling  influence  over  the 
fever.  If  vomiting  is  constant,  severe,  and  exhausting,  hypodermics  of 
morphine  will  be  found  of  service.  Some  advise  Fowler's  solution  to  check 
the  distressing  vomiting.  The  treatment  of  this  fever  is  expectant,  save 
in  the  use  of  quinine. 

CONTIIS^UED    MALAEIAL    FEVER. 

I  have  included  this  fever  in  the  list  of  the  malarial  fevers,  although  it 
is  not  altogether  malarial  in  its  origin ;  malarial  poison,  however,  is  es- 
sential to  its  development.  As  i'*:  has  many  elements  in  common  with 
typhoid,  and  many  which  ally  it  to  remittent  fever,  it  has  been  called 
"typho-malarial."  '  During  the  late  civil  war  it  was  called  camp  and 
Chickahominy  fever. 

In  its  etiological  aspect  it  partakes  more  of  the  character  of  typhus  than 
of  typhoid.  The  name  typho-malarial  fever  has  been  employed  by  one 
class  of  observers  to  indicate  the  presence  of  malaria,  and  the  specific  poison 
of  typhoid  fever.  By  another  class  the  term  has  been  employed  to  indi- 
cate the  presence  of  malaria  and  a  septic  poison.  Many  doubt  the  exist- 
ence of  such  a  form  of  fever,  and  regard  the  so-called  typhoid  element  as 
nothing  more  than  a  typhoid  condition,  liable  to  be  developed  in  con- 
nection with  remittent  fever,  as  well  as  with  many  other  diseases.  The 
term  typho-malarial  is  a  convenient  one  for  the  first  class  of  observers,  and 
is  one  which  can  be  employed  by  them  without  confusion  ;  whereas  to  the 

1  Wood  (Prac.  of   Med.)  calls  it  entero-miasmatic,  and  Drake  (Dis.  of  Mississippi  Valley)  gives  it  the 
name  Remitto-Typtius. 


CONTINUED   MALARIAL   FEVER.  827 

second  class  of  observers  it  is  exceedingly  objectionable,  and  gives  rise  to 
confusion. 

This  fever  is  produced  by  the  combined  action  of  a  septic  and  a  malarial 
poison.  In  some  the  septic  element  predominates,  and  in  others  the 
malarial.  The  preponderance  of  the  one  or  the  other  will  determine  with 
a  good  degree  of  certainty  the  course,  prognosis,  and  treatment  of  each 
individual  case.  The  distinguishing  lines,  however,  between  these  two 
elements  are  not  always  sharply  drawn  ;  both  may  be  modified  in  their 
manner  of  development  and  in  their  morbid  anatomy,  by  the  development 
of  intercurrent  complications,  such  as  scurvy,  pneumonia,  etc. 

Morbid  Anatomy. — The  changes  which  take  place  in  the  constituents  of 
the  blood  are  a  decrease  in  the  albumen  and  fibrin-factors,  and  an  increase 
in  white  blood-globules.  In  connection  with  these  blood  changes  there  are 
more  or  less  extensive  parenchymatous  changes  in  the  internal  organs  simi- 
lar to  those  met  with  in  other  forms  of  acute  infectious  diseases. 

The  liver  is  increased  in  size,  and  its  cut  surface  presents  an  appearance 
which  closely  resembles  that  known  as  nutmeg  liver.  Sometimes  it  presents 
the  peculiar  bronzed  color  of  the  liver  in  remittent  fever  ;  at  other  times  it 
very  closely  resembles  the  liver  of  yellow  fever.  A  microscopical  examina- 
tion shows  free  fat  and  pigment  granules,  as  well  as  lymphoid,  fusiform 
and  stellate  cells — which  are  perhaps  derived  in  great  measure  from  the 
spleen  ;  no  pigment  is  found  in  the  hepatic  cells,  but  they  are  stained  with 
bile,  as  is  also  the  inter-lobular  tissue. 

In  most  cases  the  spleen  is  enlarged,  softened,  and  of  an  almost  black 
color.  The  Malpighian  bodies  are  prominent,  and  present  the  appearance 
on  the  torn  surface  of  the  spleen  of  little  tumors,  varying  in  size  from  a 
pin's  head  to  that  of  a  pea.  The  organ  is  rarely  as  much  enlarged  or  'soft- 
ened as  in  typhoid  or  remittent  fevers.  It  is  always  the  seat  of  more  or  less 
pigmentation.  The  pigment  is  in  the  lymphoid  cells  of  the  spleen  chiefly, 
but  it  also  accumulates  about  the  veins. 

No  uniform  change  will  be  noticed  in  the  kidneys,  except  hyperaemia, 
which  will  be  most  marked  in  their  cortical  substance. 

The  lungs  are  the  seat  of  more  or  less  extensive  hypostatic  congestion. 
Splenization  of  the  lungs  is  not  frequent. 

The  lieart  is  pale  and  flabby.  Its  muscular  fibres  are  the  seat  of  granular 
or  vitreous  degeneration  similar  to  that  which  takes  place  in  the  heart  in 
typhoid  fever.  Exsanguinated  clots  more  or  less  firm  may  be  found  in  its 
cavities,  but  they  have  nothing  peculiar  about  them.  They  closely  re- 
semble those  found  in  persons  who  have  died  from  failure  of  heart  power. 
They  are  rarely,  if  ever,  the  direct  cause  of  death. 

The  intestinal  changes  resemble  those  of  typhoid  fever ;  by  some  they 
have  been  regarded  as  identical,  but  if  carefully  observed  some  very  marked 
differences  can  be  recognized,  especially  when  attempts  are  made  to  divide 
the  stages  of  their  development  into  periods  so  as  to  correspond  to  the  days 

■In  1847,  Wood  stated  that  "remittent  or  bilious  fever,  as  it  was  then  popularly  called,  was  some- 
times of  a  low  adynamic  character,  from  co-operation  of  a  typhoid  epidemic  influence  with  miasmata." 
Forty  years  ago  the  term  gastric  fever  was  given  to  that  variety  of  marsh  fever  where  the  stomach  was 
deranged  and  irritable  from  the  onset. 


828  ACUTE   GENEEAL  DISEASES. 

and  weeks  of  the  fever.  The  closed  follicles  of  the  intestinal  tract  are  enlarged 
and  more  or  less  pigmented.'  At  the  post-mortem  examination  of  one  who 
has  died  of  this  fever  these  glands  will  usually  be  found  in  all  stages  of 
this  pathological  process,  from  slight  enlargement  and  softening  to  ulcera- 
tion of  the  entire  follicle.  The  summit  of  the  enlarged  follicle  is  the  first 
seat  of  the  ulcer.  These  ulcers  may  involve  a  single  follicle,  or  they  may 
invade  the  adjacent  mucous  membrane  and  produce  ulcers  from  one-half 
an  inch  to  an  inch  in  diameter.  The  largest  and  most  extensive  ulcerations 
are  to  be  found  in  the  ileum,  involving  the  Peyerian  patches.  The  edges 
of  these  ulcers  are  irregular  and  everted  ;  their  base  is  usually  of  a  grayish 
color,  often  mottled  with  black  points.  There  is  little  to  distinguish  these 
intestinal  changes  from  similar  ones  which  develop  in  typhoid  fever,  ex- 
cept, perhaps,  the  tendency  to  the  deposit  of  black  pigment  in  the  enlarged 
follicles.  The  mucous  membrane  between  the  follicles  presents  the  ordinary 
appearance  of  catarrhal  inflammation.'^ 

The  minute  anatomical  changes  which  attend  the  development  of  these 
intestinal  lesions  do  not  essentially  differ  from  those  already  described  as 
occurring  in  typhoid  fever,  except  that  they  have  no  regular  stage  of  de- 
velopment, the  processes  are  slower  and  the  presence  of  pigment  in  the 
enlarged  and  ulcerating  follicles  stamps  it  as  depending  upon  an  essentially 
different  exciting  cause.  Intestinal  perforation  and  consequent  peritonitis, 
the  result  of  the  intestinal  ulceration,  may  occur,  but  such  accidents  are 
rare.  Usually,  the  mesenteric  glands  are  more  or  less  enlarged.  They  are 
of  a  livid  color,  and  more  or  less  pigmented.  The  principal  changes  in  the 
glands  are  similar  to  those  which  occur  in  a  purely  inflammatory  process. 
Occasionally  the  mucous  membrane  of  the  stomach  and  large  intestine,  if 
there  have  been  any  manifestations  of  scurvy  during  the  progress  of  the 
fever,  will  be  thickened  and  softened,  perhaps  extensively  ulcerated,  pre- 
senting an  appearance,  in  some  instances,  closely  resembling  that  found 
after  death  in  malarial  dysentery.^ 

While,  therefore,  no  pathological  lesions  which  can  be  regarded  as  char- 
acteristic of  this  type  of  fever  are  found,  and  while  the  lesions  very  closely 
resemble  those  of  typhoid  fever  on  the  one  hand,  and  remittent  fever  on 
the  other,  still  there  are  differences  which  are  sufficient  to  distinguish  it 
from  both  and  to  stamp  it  as  a  distinct  type  of  fever. 

Etiology. — It  is  difficult  to  determine  the  true  etiology  of  this  fever. 
That  malarial  poison  is  necessary  for  its  development  there  can  be  no 
question.  It  is  equally  certain  that  some  other  poison  besides  malaria  is 
in  operation  whenever  it  prevails.     This  poison  is  not  the  specific  poison  of 

1  Maclean,  in  Quain's  Die,  p.  1334,  says  that  the  adynamic  form  of  remittent  is  called  typho -malarial 
by  many  English  physicians  resident  in  India ;  but  that  Italian  and  French  physicians  prefer  the  term 
"  pernicious."    At  the  jiosi-mortem,  ulceration  of  the  Peyerian  patches  is  found. 

2  Wood  mentions  certain  cases  of  bilious  remittent,  with  ulceration  of  the  intestines  ;  evidently  writers 
before  1860-1870  found  lesions  that  struck  them  as  peculiar  in  malarial  fever,  for  we  find  them  saying 
that  "some  cases  of  typhoid  were  during  life  wrongly  called  remittent,  as  ulcers  were  found  in  the  intes- 
tines at  the  autopsy.''^ — (1847,  Wood's  Prac.  Med.) 

3  In  1821  there  occurred  in  Philadelphia  a  f  e\'er  among  the  negroes,  where  symptoms  of  a  septic  or 
typhus  fever  were  united  with  those  of  marsh  poisoning.  Dissection  revealed  inflammation  of  stomach 
and  intestines  and  almost  complete  disorganization  of  the  blood. — Account  of  an  Epidem.,  by  Dr.  Emer- 
son, Phil.  Jour,  of  Med.  and  Phys.  Sci. ,  iii  ,  1831. 


COKTINUED   MALARIAL   FEVER,  829 

typhoid  fever ;  nor  are  its  development  and  spread  in  any  way  connected 
with  the  excrements  of  one  suffering  from  tlie  fever.  There  are  a  few 
facts  connected  with  its  development  which  are  now  well  established  : 

First.  It  is  met  with  only  in  malarial  districts. 

Second.  In  the  majority  of  instances,  when  this  fever  has  prevailed,  its 
development  has  been  preceded  or  attended  by  marked  and  easily  recognized 
anti-hygienic  conditions,  such  as  overcrowding,  bad  sewerage,  and  other 
conditions  favorable  to  the  development  of  septic  poison. 

Third.  That  it  is  a  7ion-contagious  disease,  and  is  never  propagated  from 
the  affected  to  the  healthy,  either  directly  by  personal  contagion,  or  indi- 
rectly by  morbid  excretions. 

Fourth.  In  its  morbid  anatomy  and  symptomatology  it  is  a  combination 
of  malarial  and  septic  fever.  The  special  symptoms  and  lesions  of  one  or 
the  other  of  these  fevers  stamp  its  character.  In  large  cities  in  which 
malarial  diseases  are  prevalent,  seiuer  gases  seem  to  furnish  the  septic  element 
which  is  so  essential  for  its  development.  The  history  of  disease  in  New 
York  City  during  the  past  few  years  furnishes  striking  examples  of  the 
combination  of  these  two  poisons  in  develoj)ing  a  type  of  fever  which  must 
be  classed  under  the  head  of  non-specific  continued  fever,  attended  by 
typhoid  symptoms  and  intestinal  ulceration.' 

Symptoms. — It  is  difficult  to  present  a  typical  picture  of  this  fever.  To 
give  even  an  outline  of  its  symptoms  which  shall  be  approximately  true  of 
all,  or  even  the  majority  of  cases,  is  impossible.  Its  clinical  history  varies 
as  the  malarial  or  septic  element  predominates.  Besides,  there  is  a  large 
number  of  cases  in  which  neither  of  these  elements  predominates,  for  the 
patient  almost  insensibly  passes  from  a  malarial  into  a  typhoid  condi- 
tion. There  are  also  certain  anti-hygienic  conditions  which  may  be  pres- 
ent, which  give  to  the  fever  an  unusual  and  peculiar  type.  For  examjole, 
when  those  conditions  exist  which  favor  the  development  of  scurvy,  as  the 
patient  enters  upon  the  second  week  of  the  fever  the  scorbutic  phenomena 
will  become  prominent.  At  times  the  dysenteric  element  may  be  engrafted 
on  this  fever,  and  greatly  modify  its  course,  and  lead  to  a  train  of  symp- 
toms and  morbid  changes  which  closely  ally  it  to  epidemic  dysentery.  The 
course  of  this  fever  may  also  be  greatly  modified  by  certain  local  complica- 
tions which  are  especially  liable  to  occur  during  the  second  or  third  week. 
The  presence  of  any  of  these  conditions  will  greatly  change  its  clinical  his- 
tory, bub  the  phenomena  which  attend  its  early  development  will  always  be 
sufficient  to  determine  its  true  character. 

In  considering  the  symptoms  in  detail,  that  class  of  cases  in  which  the 
malarial  element  is  predominant  will  first  be  described.  This  type  of  fever 
is  usually  ushered  in  by  a  distinct  chill."    In  some  instances  no  premonitory 

^  When  Dr.  Drake  (Dis.  of  Inter.  Valley  of  N.  A.)  called  this  disease  remitto-typhus.  he  came  nearer 
than  any  other  observer  in  giving  it  a  name  corresponding  to  its  etiology.  That  it  partakes  of  re- 
mittent characteristics,  no  one  can  deny;  that  it  has  a  septic,  a  "crowd-poison,"  a  ''sewer-gas,"  a 
"typhus  "  character,  seems  to  me  to  be  incontestable, hence  "  remitto-tjrphus  "  would  be  unobjectionable, 
were  not  the  word  typhus  now  restricted  to  the  specific,  contagious  fever  of  that  name,  whose  poison  can 
only  cause  one  disease,  and  cannot  mingle  with,  or  be  modified  by  any  other. 

2  In  Gibb's  account  of  a  malignant  epidemic  in  Nicaragua,  Central  America,  none  of  the  cases  began 
with  a  chill. 


830 


ACUTE   GENERAL   DISEASES. 


symptoms  are  present ;  in  others  the  chill  is  preceded  by  wandering  pains 
in  the  limbs  and  back,  headache,  loss  of  appetite,  and  a  feeling  of  great 
exhaustion.  In  a  large  proportion  of  cases  m  the  early  stage,  the  counte- 
nance has  a  peculiar  waxy,  clay-colored  or  yellowish  tinge.  The  chill  yaries 
in  duration  from  half  an  hour  to  an  hour,  and  in  character  closely  resem- 
bles the  chill  of  simple  remittent  fever.     It  is  immediately  followed  by 


3<y:   I    2.    3.   4.    5.    6.  7.     8.    9.   10.  II.  12.  IS.  14.  16.  Id  17.   18.  19.  20.  U  22, 

'»<^'l  1  1  H 1   1  1 N  H~h["H"l11"^Hi  1  1   1    i  ll/frl 

105' ' c 

.04°__=__g  =  ^^^= =  ___ =  _  =  ___=__ 

2 s^ ■± — ^4 

'"EEEEEEEEEEEEEEEE?EEEEEEEEEE=i=E^^EdEi::EE= 

.oJHMHHyiyuiyEiiyipyyB^EEE|im 

1  m^  1  M  1    1    1  1  1  1  1    1  1  M  1  M  1  1  1  1  1  1  1  1  1  1  1  1  1  1  M  i  M    Mil 

Fig.  173. 
Temperature  Record  in  a  case  of  Continued  Malarial  Fever,  Remittent  type. 

active  febrile  symptoms,  the  temperature  rising  in  a  few  hours  to  103°  or 
104°  F.  The  pulse  reaches  100,  and  is  full  and  forcible.  The  excretions 
are  all  checked,  and  there  is  mental  disturbance  and  sometimes  delirium. 

When  once  established,  the  fever  pursues  a  variable  course.  At  its  onset, 
and  for  the  first  few  days,  its  phenomena  often  closely  resemble  those  of 
simple  remittent  fever,  though  the  remissions  are  never  so  well  defined,  and 
there  is  at  the  very  onset  of  the  fever  an  amount  of  intestinal  disturbance 
which  Th  rarely  present  in  simple  remittent.  The  existence  of  abdominal 
tenderness,  especially  in  the  right  iliac  fossa,  is  a  strong  point  in  its 
diagnosis.  As  the  temperature  rises,  nausea,  vomiting,  and  epigastric 
tenderness  are  present  in  a  greater  or  less  degree.  These  gastric  symp- 
toms bear  a  close  resemblance  to  those  which  attend  the  development  of 
remittent  fever,  while  the  intestinal  and  abdominal  symptoms  are  similar 
to  those  of  typhoid.  Diarrhoea  may  precede  the  chill ;  in  most  cases  it  is 
present  during  some  portion  of  the  fever.  At  first  the  tongue  presents  a 
pale,  flabby  appearance,  with  a  smooth  surface  ;  soon  it  becomes  covered 
with  a  white  or  yellowish-white  coating  ;  later  it  becomes  red,  and  the 
coating  becomes  brownish  ;  in  severe  cases  it  may  suddenly  become  clean, 
red  and  shining,  and  sordes  may  collect  upon  the  teeth  and  lips. 

In  those  cases  in  which  a  scorbutic  element  exists,  the  tongue  is  enlarged, 
pale,  and  flabby,  its  surface  smooth  and  covered  with  a  white  fur,  which  is 
thickest  on  its  edges,  the  gums  are  swollen  and  present  the  characteristic 
appearance  of  scurvy  ;  the  skin  is  covered  with  petechias  and  irregular  dis- 
colorations,  and  mental  and  bodily  prostration  is  early  marked. 


CONTIlfrUED    MALARIAL   FEVER.  831 

In  those  cases  in  which  a  dysenteric  element  is  present,  as  the  fever  de- 
velops, the  dysenteric  symptoms  become  prominent,  the  discharges  from 
the  bowels  are  blood-stained  and  watery.  The  tongue  soon  becomes  dry  and 
brown,  and  the  patient  shows  signs  of  extreme  exhaustion,  with  a  few  of 
the  gastric  symptoms  which  are  usually  so  well  marked  in  the  early  period 
of  the  fever.  Throughout  the  whole  course  of  the  disease  there  is  a  marked 
tendency  to  periodicity,  the  exacerbations  usually  assuming  a  tertian  type/ 
In  fatal  cases,  as  the  patient  reaches  the  second  or  third  week  the  symptoms 
are  very  like  those  of  fatal  typhoid  fever  ;  the  prostration  becomes  more  and 
more  complete,  the  pulse  reaches  130  or  140,  is  feeble,  compressible  and 
irregular,  the  skin  is  hot  and  cold  in  patches,  the  patient  gradually  passes 
into  a  state  of  stupor  and  coma,  involuntary  evacuations  take  place,  there 
is  subsultus,  deafness,  a  blackened  and  rigid  tongue,  and  death  ensues.  In 
cases  that  recover,  symptoms  of  amendment  may  be  noticed  between  the 
tenth  and  twentieth  days.  The  tongue  begins  to  become  clean,  the  abdom- 
inal symptoms  subside,  the  pulse  becomes  less  frequent  and  fuller,  the  dis- 
turbance of  the  nervous  system  disappears,  the  appetite  gradually  returns, 
and  the  patient  enters  upon  a  tedious  convalescence,  which  is  attended  by 
more  or  less  diarrhoea,  mental  stupor,  cardiac  irritability,  and  a  slow  return 
of  mental  and  physical  vigor. 

The  train  of  symptoms  thus  briefly  sketched  may  be  greatly  modified  by 
a  variety  of  complications.  ISTot  infrequently  pulmonary  complications 
develop  during  its  second  week,  and  so  change  its  phenomena  that  the  fever 
element  may  be  overlooked  and  the  pulmonary  element  alone  engages  the 
attention  of  the  physician.  Suppurative  inflammation  of  the  cervical  and 
inguinal  glands  sometimes  complicates  it,  and  leads  one  to  the  mistake  of 
regarding  it  as  a  purely  suppurative  fever.  Enlargement  and  suppura- 
tion of  one  or  both  parotids  are  not  uncommon  events.  Again,  scurvy 
under  certain  anti-hygienic  conditions  may  so  modify  its  phenomena  as  to 
lead  one  to  regard  it  as  an  entirely  new  type  of  fever.  The  scorbutic  ele- 
ment in  this  class  of  cases  is  developed  in  connection  with  the  malarial 
exposure. 

The  prominent  symptoms  present  in  the  septic  type  of  this  fever,  such  as 
lassitude,  headache,  pains  in  the  back  and  limbs,  resemble  those  of  typi- 
cal typhoid  fever  ;  either  a  distinct  chill  or  a  complete  intermittent  or 
remittent  paroxysm  ushers  in  the  febrile  symptoms.  The  rise  in  tempera- 
ture following  the  ushering-in  chill  has  no  typical  range  ;  in  some  cases 
the  rise  is  gradual,  not  reaching  its  maximum  before  the  middle  of  the 
second  week  ;  in  other  cases  the  rise  is  sudden,  reaching  104°  or  105°  F. 
within  twenty-four  hours  after  the  occurrence  of  the  chill.  In  typhoid 
fever  during  the  first  week,  there  are  indistinct  forenoon  remissions  and 
afternoon  exacerbations,  but  in  this  fever  the  remissions  are  well-marked, 
especially  on  every  second  or  third  day,  causing  the  fever  to  assume  a  more 
or  less  distinct  tertian  or  quartan  type.     One  of  its  earliest  symptoms  is 

1  As  the  disease  progrefses  the  exacerbations  become  shorter ;  the  remissions  longer,  and  at  times  a 
normal  or  even  a  subnormal  temperature  may  be  reached,  temporarily,  as  the  adynamic  condition  becomes 
pronounced. 


832 


ACUTE    GENEEAL   DISEASES. 


well-marTced  hepatic  tenderness  ;  with  the  hepatic  tenderness  there  is  en- 
largement of  the  spleen,  which,  as  the  fever  progresses,  reaches  a  much 
larger  size  than  is  ordinarily  met  with  in  typhoid  fever.  During  the  first 
week  the  pulse  is  full  and  rarely  more  than  100,  but  during  the  second  and 


3aij'. 

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4. 

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13.  14.  15.  16.  17.  18. 

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Fig.  174. 

Temperature  Record  in  a  case  of  Continued  Malarial  Fever.    Septic  variety. 

third  weeks  it  is  small  and  compressible,  and  in  severe  cases  ranges  from 
110  to  130  per  minute. 

The  appearance  of  the  tongue  varies  with  the  period  of  the  fever.  At 
first  it  is  swollen,  with  red  projecting  papillae,  and  has  a  light  white  coat- 
ing. As  the  typhoid  condition  becomes  more  marked  its  appearance 
changes ;  it  becomes  dry  and  brown,  and  frequently  the  brown  coating 
cracks  and  fissures  are  formed  in  the  mucous  membrane  underneath. 
Should  the  tongue  become  moist  and  begin  to  clean,  it  is  an  indication 
that  convalescence  is  being  established.  The  coating  is  removed  in  two 
ways,  either  gradually  from  the  edges  to  the  centre,  or  it  is  thrown  off  in 
flakes.  In  the  latter  case,  after  the  removal  of  the  coating,  the  tongue  as- 
sumes a  beefy  red  appearance,  and  after  a  short  time  may  again  become 
brown  and  dry.  Under  such  circumstances  there  will  be  a  renewal  of  the 
fever-symptoms.  After  the  fever  has  continued  a  few  days  the  surface  be- 
comes dry  and  harsh,  and  the  skin  assumes  a  dingy  hue,  which  is  quite  char- 
acteristic ;  sometimes  there  is  a  well-marked  jaundice.  The  urine  gradually 
diminishes  in  quantity  and  deepens  in  color  until  convalescence  com- 
mences, when  it  increases  in  quantity.     It  is  rarely  albuminous. 

Diarrhma  may  occur  at  any  period.  It  is  not  usually  excessive  until  the 
second  or  third  week.  There  is  nothing  characteristic  about  the  discharges. 
They  are  usually  of  an  exceedingly  fetid  odor,  watery  and  dark-colored  ;  in 
the  later  stages  of  the  disease  they  sometimes  contain  blood.  In  some  in- 
stances the  character  of  the  stools  is  termed  bilious  and  an  excessive  he- 
patic secretion  is  then  indicated  ;  at  other  times  they  are  of  dark  clay 
color,  showing  a  deficiency  of  the  biliary  secretion.  With  the  diarrhoea 
there  is  usually  more  or  less  abdominal  tenderness,  especially  in  the  right 


CONTINUED    MALARIAL   FEVER.  833 

iliac  region  ;  but  tympanitis  is  rarely  well-marked.  In  many  cases  there 
is  retraction  of  the  abdomen. 

As  already  stated,  headache  is  very  constant  in  the  early  period  of  the 
fever.  It  often  precedes  the  ushering-in  chill.  As  the  fever  progresses  it 
gives  place  to  a  delirium,  which  is  never  violent,  but  which  is  muttering 
in  character,  and  is  attended  by  restlessness  and  insomnia,  or  by  drowsi- 
ness, subsultus,  picking  at  the  bed-clothes,  and  great  nervous  prostration. 
If  delirium  is  not  present,  or  after  it  has  disappeared  during  convales- 
cence, there  is  great  lack  of  mental  vigor  and  a  tendency  to  apathy. 
The  other  nervous  phenomena,  which  are  usually  present  in  any  con- 
dition when  marked  typhoid  symptoms  exist,  are  not  prominent  in  this 
fever. 

The  subsequent  phenomena  which  may  attend  its  development  will  vary 
with  the  intensity  of  the  fever  and  the  resisting  power  of  the  patient. 
Epistaxis  is  not  uncommon  ;  bl-onchitis  is  a  frequent  complication.  In 
fatal  cases,  at  the  close  of  the  second  or  during  the  third  week,  symptoms 
of  extreme  prostration  come  on,  the  patient  gradually  passes  into  a  state  of 
stupor,  which  lapses  into  one  of  coma,  and  death  ensues.  In  cases  that  are 
to  recover,  usually  by  the  end  of  the  second  week  the  tongue  begins  to 
clean,  the  gastric  and  intestinal  symptoms,  with  the  exception  of  the  diar- 
rha3a,  begin  to  subside,  the  pulse  becomes  slower,  the  nervous  disturbances 
disappear,  the  appetite  returns,  and  the  patient  enters  on  a  convalescence 
which  is  usually  protracted.  Its  phenomena  may  be  modified  by  certain 
anti-hygienic  surroundings,  to  which  those  suffering  with  this  fever  may 
have  been  subjected  prior  to,  and  during,  its  development.  Thus,  when  it 
prevails  among  those  who  have  suffered  privations,  been  badly  fed,  badly 
clothed,  overcrowded  in  badly  ventilated  apartments,  or  surrounded  by  de- 
composing animal  and  vegetable  substances,  although  the  fever  is  attended 
by  the  same  general  phenomena,  there  are  certain  variations  which  ally 
it  to  relapsing  fever.  Prominent  among  these  are  neuralgic  and  arthritic 
pains  in  various  parts  of  the  body,  especially  in  the  back  and  limbs  ;  hem- 
orrhagic tendencies  marked  by  bleedings  from  the  gums  and  mucous  sur- 
faces ;  and  not  infrequently  large  ecchymoses  occur  in  various  parts  of  the 
body. 

In  this  class  of  cases  the  fever  is  of  a  low  type  from  the  commencement, 
with  quotidian  exacerbations  and  remissions.  Diarrhoea  usually  precedes 
the  development  of  the  febrile  symptoms.  Frequently  during  the  second 
week  a  muttering  delirium  comes  on,  accompanied  by  drowsiness  and  a 
tendency  to  stupor.  Despondency,  indisposition  to  make  any  exertion, 
and  a  state  of  utter  indifference  as  to  the  future  are  frequently  met  with 
during  the  entire  period  of  the  fever  ;  in  fact,  mental  and  bodily  prostra- 
tion is  more  marked  here  than  in  any  other  fever.  In  fatal  cases  death  may 
be  the  result  of  hemorrhage  from  the  mucous  surfaces,  or  from  exhaustion. 
In  cases  that  recover,  convalescence  comes  on  late,  and  is  slow  and  tedious. 
Diarrhoea  frequently  follows  the  subsidence  of  the  fever,  and  leads  to  a 
fatal  result. 

Differential  Diagnosis. — The  affections  with  which  continued  malarial 
53 


834  ACUTE    GEISTERAL   DISEASES. 

fever  is  likely  to  be  confounded,  are  typJioid,  remittent,  relapsing,  typhus, 
and  yellow  fever . 

The  septic  type,  in  many  of  its  phenomena,  so  closely  resembles  typhoid 
fever  that  frequently  it  is  difficult  to  make  a  differential  diagnosis.  The 
advent  of  continued  malarial  fever  is  usually  marked  by  a  distinct  chill, 
while  typhoid  comes  on  insidiously  and  is  attended  not  by  a  distinct  chill, 
but  by  a  chilly  sensation.  The  rise  of  temperature  in  continued  fever  is 
sudden  and  follows  no  typical  range,  while  in  typhoid  the  typical  range  of 
temperature  during  the  first  week  is  diagnostic  of  the  fever.  In  typhoid 
fever,  on  the  sixth  or  eighth  day,  rose-colored  spots  appear  ;  in  the  other, 
although  an  eruption  may  be  present  it  has  none  of  the  characteristics  of 
the  typhoid  eruption,  is  not  rose-colored,  does  not  disappear  on  pressure, 
and  remains  visible  throughout  the  whole  course  of  the  fever.  Besides  the 
absence  of  these  characteristic  symptoms  of  typhoid  fever,  there  is,  in  con- 
tinued malarial  fever,  a  distinct  periodicity  in  the  febrile  action,  a  certain 
icteroid  hue  of  the  skin,  hepatic  tenderness,  and  great  gastric  disturbance, 
conjoined  with  which  the  appearance  of  the  tongue,  the  character  of  the 
diarrhoea,  and  the  non-infectious  character  of  the  stools  will  serve  as  im- 
portant aids  in  the  differential  diagnosis  of  these  two  forms  of  fever.  If 
upon  microscopical  examination  of  the  blood,  free  pigment  is  found,  the 
■diagnosis  of  continued  malarial  fever  is  established. 

The  malarial  type  resembles  remittent  fever  in  its  ushering-in  symptoms. 
In  both  cases  there  is  a  chill  followed  by  fever,  attended  by  one  or  more 
distinct  exacerbations  and  remissions.  The  early  appearance  of  the  enteric 
symptoms,  attended  by  other  well-marked  typhoid  phenomena  by  the  end 
of  the  second  week,  establishes  the  diagnosis,  and  as  the  fever  progresses 
the  typhoid  condition  becomes  more  and  more  apparent.  Besides,  remit- 
tent fever  yields  more  promptly  to  quinine. 

Severe  cases  which  are  complicated  by  scorbutic  tendencies  marked  by 
petechiae  and  great  prostration  of  the  vital  powers  may  be  confounded  with 
iyphus  fever  ;  yet  the  severity  of  the  attack,  the  higher  range  of  tempera- 
ture, the  greater  frequency  of  the  pulse,  the  dusky  countenance,  the  ab- 
sence of  diarrhoea  and  all  other  abdominal  symptoms  in  typhus  fever,  ren- 
der it  easy  to  make  the  differential  diagnosis  between  the  two  types  of 
fever.  Besides,  typhus  fever  has  a  characteristic  eruption,  is  only  propa- 
gated by  contagion,  and,  if  it  prevails,  does  so  epidemically. 

Occasionally  yelloio  fever  has  been  confounded  with  continued  malarial 
fever.  The  range  of  temperature  is  lower  in  yellow  fever,  and  on  the  third 
or  fourth  day  it  falls  suddenly,  and  there  is  a  more  or  less  complete  remis- 
sion. The  circumorbital  pain,  the  appearance  of  the  eye,  the  pulse  rarely 
ranging  over  110,  the  peculiar  color  of  the  skin,  the  character  of  the  mat- 
ter vomited,  the  absence  of  diarrhoea,  and  the  shorter  duration  of  the  dis- 
ease, will  enable  one  to  make  the  diagnosis  of  yellow  fever.  The  urine  is 
rarely  albuminous  in  continued  fever  ;  nearly  always  so  in  yellow.  Again, 
yellow  fever  usually  prevails  epidemically,  and  is  confined  to  certain  locali- 
ties and  certain  seasons  of  the  year.  It  is  a  portable  disease,  and  the 
yellow  fever  poison  may  be  conveyed  from  an  infected  to  a  non-infected" 


CONTINUED   MALAEIAL   FEVER.  835 

district  by  means  of  clothing  or  merchandise,  while  the  poison  of  contin- 
ued fever  is  of  endemic  origin,  and  cannot  be  carried  beyond  the  infected 
district. ' 

Prognosis. — The  ratio  of  mortality  in  continued  malarial  fever  varies 
greatly  in  the  diiferent  regions  in  which  it  occurs,  and  as  the  malarial  or 
septic  element  predominates.  The  hygienic  surroundings  of  the  patient 
and  the  range  of  atmosphei'ic  temperature  will  also  very  greatly  influence 
the  prognosis.  Statistics  of  this  fever  in  different  localities  and  in  diiferent 
years  give  the  ratio  of  mortality  from  eight  to  ten  per  cent.  The  septic 
type  is  more  fatal  than  the  malarial.  Great  caution  should  be  exercised 
in  prognosticating  the  result  of  any  case,  for  the  mildest  cases  sometimes 
suddenly  assume  a  severe  type  and  terminate  fatally,  while  very  severe  and 
apparently  hopeless  cases  unexpectedly  improve,  and  recovery  takes  place. 

The  average  duration  of  those  cases  which  terminate  in  recovery  is  from 
three  to  four  weeks.  The  duration  varies  with  the  different  types  of  the 
fever:  in  the  malarial  variety  it  is  always  shorter  than  in  the  septic.  The 
period  of  convalescence  is  prolonged;  three  or  four  weeks  often  elapse 
before  the  patient  is  completely  restored  to  health.  A  fatal  relapse  may 
occur  at  any  period  during  convalescence.  In  those  cases  that  terminate 
fatally,  death  most  frequently  occurs  during  the  second  or  third  week ;  it 
may  occur  as  late  as  the  close  of  the  sixth  week. 

Its  most  frequent  complication  is  inflammation  of  the  respiratory  organs, 
the  development  of  which  is  marked  by  those  symptoms  which  usually 
attend  the  development  of  the  different  acute  pulmonary  affections.  In 
the  majority  of  instances  the  signs  of  bronchitis  are  not  present  until  the 
fever  is  well  established.  The  bronchitis  resists  treatment,  and  does  not 
disappear  until  convalescence  is  fully  established.  When  pneumonia  occurs 
it  is  catarrhal  in  character,  and  few  of  the  strongly  marked  rational  symp- 
toms of  ordinary  pneumonia  are  present.  The  physical  signs,  however, 
will  always  enable  one  to  determine  the  presence  of  pulmonary  complica- 
tions, and  any  great  irregularity  in  temperatui-e  during  the  course  of  the 
fever  should  be  an  indication  for  a  careful  physical  examination  of  the 
chest. 

It  is  sometimes  difficult  to  distinguish  between  the  cerebral  symptoms  of 
this  fever  and  those  symptoms  which  attend  meningeal  complications,  but 
the  meningeal  complications  are  of  so  very  rare  occurrence  that  it  is  safe 
to  assume  they  are  not  present  until  some  of  the  diagnostic  symptoms  of 
meningitis  occur.  Serious  abdominal  complications,  such  as  intestinal 
perforation,  peritonitis,  and  hemorrhage  are  rare,  but  when  they  do  occur 
their  advent  is  marked  by  such  urgent  symptoms  that  one  loses  sight  of  the 
ordinary  symptoms  of  the  fever.  It  is  hardly  necessary  to  refer  to  those 
modifications  in  the  clinical  history  of  this  fever  which  follow  the  develop- 
ment of  abscesses,  bed-sores,  gangrene,  etc.  The  occurrence  of  any  of 
these  complications  will  very  materially  influence  the  prognosis  in  any 
given  case.     Capillary  bronchitis  and  pneumonia  are  especially  dangerous 

1  The  points  of  difEerential  diagnosis  between  this  disease  and  relapsing  fever,  are  considered  under 
the  head  of  relapsing  fever. 


836  ACUTE   GEIfEEAL   DISEASES. 

when  they  develop  during  the  third  week  of  the  fever.  Anti-hygienic  sur- 
roundings, such  as  over-crowding  and  improper  food,  materially  affect  the 
prognosis.  If  continued  malarial  fever  prevail  among  those  who  are 
crowded  into  badly- ventilated  apartments,  who  from  filth  and  improper 
nutrition  have  septic  and  scorbutic  tendencies,  the  ratio  of  mortality  is 
much  greater  than  among  those  who  are  free  from  such  complicating  in- 
fluences. 

The  symptoms  which  may  be  regarded  as  indicating  an  unfavorable  ter- 
mination are  a  continued  high  temperature,  showing  little  or  no  tendency 
to  remission  ;  a  very  frequent,  feeble,  fluttering  joulse  ;  continued  hiccough ; 
profuse  diarrhoea,  the  discharges  at  times  being  involuntary  and  con- 
taining mucus,  pus,  and  blood ;  a  dry,  red,  cracked,  and  fissured  tongue ; 
great  drowsiness,  with  a  tendency  to  stupor  and  coma ;  and  the  appearance 
of  petechial  spots  on  the  surface  of  the  body,  attended  by  frequent  hemor- 
rhages from  the  lips,  gums,  and  tongue.  In  a  severe  case,  the  occurrence 
of  any  of  these  phenomena  renders  the  prognosis  more  unfavorable. 

The  character  of  the  prevailing  fever  will  also  greatly  influence  the  prog- 
nosis in  any  given  case.  If  the  type  of  the  prevailing  fever  is  mild,  or  if 
comparatively  few  deaths  have  occurred,  though  the  symptoms  in  a  given 
case  may  appear  unfavorable,  yet  recovery  is  probable.  If,  on  the  other 
hand,  the  type  is  severe,  and  many  deaths  have  occurred,  cases  apparently 
mild  will  suddenly  become  severe,  and  the  prognosis  becomes  unfavorable. 
As  already  stated,  the  hygienic  surroundings  and  the  previous  habits  of  the 
patient  very  greatly  influence  the  prognosis.  With  drunkards,  and  those  en- 
ervated by  vicious  habits,  a  mild  type  of  this  fever  will  probably  prove 
fatal. 

Treatment. — The  treatment  varies  with  its  type.  No  plan  can  be  pre- 
sented which  will  be  applicable  to  all  cases. 

The  first  question  which  meets  us  is  :  cannot  the  development  of  this  fe- 
ver be  prevented  ?  It  has  been  stated  that  its  development  was  principally 
due  to  three  causes — namely,  malarial  poison,  overcrowding,  and  improper 
diet.  In  a  large  proportion  of  instances  it  is  possible  to  do  away  with  the 
last  two  causes.  The  overcrowding  and  the  faulty  diet  may  be  prevented, 
and  thus  the  septic  poison  which  gives  to  this  fever  its  "  typhoid  "  type 
may  be  destroyed  or  its  development  prevented.  The  strict  observance  of 
hygienic  laws  in  the  localities  where  this  fever  prevails  has  in  some  instances 
entirely  changed  the  type  of  the  disease.  Even  after  the  fever  symptoms 
have  been  well  developed,  the  removal  of  patients  from  anti-hygienic  sur- 
roundings has  frequently  been  attended  by  the  most  satisfactory  results. 
When  isolated  cases  of  this  fever  are  met  with  in  localities  apparently  free 
from  such  sources  of  infection,  a  careful  search  should  be  instituted  in  or- 
der to  find  the  source  of  the  infection.  Defective  sewerage  and  faulty  drain- 
age have  been  found  to  be  fruitful  sources  of  infection. 

The  therapeutic  measures  which  may  be  employed  in  its  treatment  vary 
with  its  type  and  the  peculiarities  of  each  individual  case.  There  are  no 
specifics.  In  those  cases  in  which  the  malarial  element  predominates,  the 
administration  of  quinine  will  in  many  instances  arrest  its  progress  or 


CONTINUED    MALARIAL   FEVER.  837 

sliorten  its  duration  ;  but  in  those  cases  in  which  the  septic  element  pre- 
dominates, while  quinine  may  act  as  an  antipyretic,  it  has  little  power  to 
arrest  its  progress  or  to  shorten  its  duration,  but  it  will,  in  many  instances, 
render  the  course  of  the  fever  milder.  In  those  cases  in  which  the  malarial 
element  predominates,  which  are  ushered  in  by  distinct  chills,  followed  by 
one  or  two  distinct  remissions  and  exacerbations,  during  the  first  remission 
twenty  or  thirty  grains  of  quinine  should  be  administered,  in  houi'ly  doses 
of  ten  grains  each.  If  it  is  promptly  and  freely  administered,  it  seldom 
fails  to  produce  a  beneficial  effect ;  the  febrile  exacerbations  will  not  return, 
or  if  they  do  they  are  less  severe,  and  in  a  few  days  entirely  disappear.  In 
those  cases  which  begin  more  insidiously  and  are  developed  more  gradually, 
if  there  is  a  distinct  periodicity  to  the  febrile  phenomena,  without  distinct 
remission,  the  administration  of  quinine  may  cause  the  fever  to  run  a  milder 
course.  If  the  first  full  doses  of  quinine  fail  to  produce  any  effect  in  this 
class  of  cases,  its  administration  in  moderate  doses,  perhaps  ten  grains 
twice  a  day,  must  be  continued  for  several  days  before  it  will  markedly 
modify  the  severity  of  the  fever.  In  no  type  of  the  fever  does  the  quinine 
exert  any  specific  influence  except  over  the  malarial  element  ;  the  enteric 
phenomena  are  either  not  at  all,  or  only  indirectly,  modified  by  the  anti- 
pyretic power  of  the  drug.  Hence,  it  is  apparent  that  in  those  cases  in 
which  the  malarial  element  is  slight, -and  in  which  the  septic  element  is 
prominent,  while  quinine  fails  to  exercise  any  controlling  influence  over  the 
progress  of  the  fever,  it  will  mitigate  its  severity,  and  act  more  powerfully 
as  an  antipyretic  than  it  will  in  any  other  form  of  continued  fever.  War- 
burg's tincture  in  many  cases  will  have  a  controlling  jDower  over  the  fever 
when  quinine  fails. 

It  has  been  claimed  by  some  that  arsenic  has  a  specific  influence  over  the 
fever,  and  that  it  exercises  a  peculiar  and  most  beneficial  effect  upon  the  in- 
testinal lesions.  There  is  little  doubt  but  that  arsenic,  like  quinine,  acts 
beneficially  in  many  cases  of  the  malarial  type  of  this  fever  ;  but  unques- 
tionably this  beneficial  effect  is  due  to  its  acknowledged  power  over  malarial 
affections,  and  not  to  any  specific  influence  which  it  has  over  the  fever.  As 
an  antiperiodic  it  is  inferior  to  quinine.  Eucalyj)tus  does  not  act  as  bene- 
ficially in  continued  malarial  fever  as  in  the  simpler  forms  of  malarial 
fever. 

It  is  of  importance  to  remember  that  this  class  of  patients  do  not  bear 
well  the  prolonged  application  of  cold  to  the  surface,  either  by  means  of 
the  cold  bath  or  the  cold  pack,  and  that,  unless  the  antipyretic  power  of 
quinine  is  added  to  the  application  of  cold,  very  little  benefit  will  be  ob- 
tained from  the  use  of  the  latter.  The  danger  resulting  from  the  in- 
judicious use  of  cold  baths  is  greater  in  this  than  in  any  other  infectious 
disease. 

The  rules  for  the  administration  of  stimulants  are  the  same  as  those 
given  for  their  administration  in  typhoid  fever.  The  effects  of  the  first 
few  doses  should  be  carefully  watched.  They  should  never  be  given  in- 
discriminately, for  there  is  greater  danger  of  over-stimulating  in  this  than 
in  any  other  fever.     Their  use  is  indicated  whenever  signs  of  heart-failure 


838  ACUTE   GENERAL   DISEASES. 

are  present,  such  as  a  feeble  pulse  and  an  indistinct  first  sound  of  the  heart. 
No  fixed  rule  can  be  laid  down  as  regards  the  quantity  to  be  administered 
in  any  given  case  ;  it  will  vary  with  the  type  of  the  fever  and  the  previous 
habits  of  the  patient ;  it  should  always  be  administered  at  stated  intervals. 
The  period  of  the  fever  at  which  stimulants  should  be  commenced  will 
also  vary.  In  some  cases  stimulants  are  never  required,  while  in  other 
cases,  from  the  very  outset  of  the  fever,  they  are  demanded.  In  the 
majority  of  cases  their  use  is  not  indicated  before  the  end  of  the  second 
week.  It  must  be  borne  in  mind  that  alcohol  is  not  a  specific,  curative 
agent  in  this  fever,  but  that  the  object  of  its  administration  is  to  sustain 
the  heart  and  prevent  the  vital  powers  from  falling  below  the  point  at 
which  reparative  processes  are  possible.  The  use  of  stimulants  is  not 
necessarily  contraindicated  when  delirium  is  present.  Frequently  after 
their  administration  the  delirium  will  pass  away,  and  only  when  it  is  de- 
cidedly increased  by  their  use  should  they  be  abandoned. 

The  state  of  the  bowels,  skin  and  kidneys  demands  the  closest  attention. 
If,  early  in  the  disease,  the  bowels  are  constipated,  a  calomel  purge  com- 
bined with  ten  or  fifteen  grains  of  quinine  will  often  be  followed  by  marked 
benefit.  In  any  stage  of  fche  disease  brisk  purgation  should  be  avoided. 
If  diarrhoea  is  present,  it  should  not  be  interfered  with  unless  it  becomes 
exhausting  ;  then  it  should  be  checked  by  small  doses  of  opium  combined 
with  astringents.  Symptoms  referable  to  disturbance  of  the  nervous  system 
sometime  require  special  treatment.  If  there  is  extreme  restlessness,  mus- 
cular twitchings,  or  active  delirium,  opium  may  be  administered  in  full 
doses.  The  effect  of  the  first  dose  must  be  carefully  watched.  If  sleep 
soon  follows  its  administration,  and  the  delirium  gradually  subsides  with- 
out any  aggravation  of  the  other  symptoms,  its  use  may  be  continued  ;  if, 
instead  of  producing  sleep,  the  patient  becomes  more  wakeful,  and  the  de- 
lirium is  increased  and  more  active,  and  the  other  symptoms  are  greatly 
aggravated,  its  use  must  be  immediately  abandoned.  Under  these  circum- 
stances chloral  may  be  tried  with  great  care.'  Quain  advises  gr.  xv.-xx.  of 
bromide  of  potassium  under  similar  conditions. 

Some  claim  that  spirits  of  turpentine  in  the  treatment  of  this  form  of 
fever  has  almost  a  specific  power,  while  others  regard  it  useful  only  as  a 
stimulant.  My  own  experience  leads  me  to  employ  it  only  as  a  stimulant 
during  the  second  and  third  week  of  the  disease,  when  there  is  great  pros- 
tration and  marked  typhoid  symptoms.  It  may  be  given  as  an  emulsion  in 
doses  of  twenty  drops  every  two  hours.  The  diet  best  suited  to  patients 
with  this  fever  is  milk  administered  in  the  same  way  as  was  proposed  in 
the  case  of  typhoid  fever  patients.  Special  complications  occurring  during 
the  non-septic  variety  must  be  met  with  such  remedies  as  the  condition  of 
the  patient  and  the  peculiar  complications  may  require. 

J  Wood  recommends  Hoffman's  anodyne  and  spts.  seth.  nitrosi  for  restlessness ;  and  musk,  asafoetidaa 
camphor,  and  similar  drugs  for  the  hiccough. 


BERKICIOUS   MALARIAL   FEVER.  839 


PERmCIOUS   MALAEIAL   FEVEE. 


This  form  of  fever  has  received  other  names,  at  different  times  and  in 
different  localities.  It  has  been  called  congestive  fever,  ardent  fever,  tropical 
typhoid  fever,  and  pernicious  fever.  The  latter  name  seems  most  appro- 
priate, and  at  the  present  time  is  generally  adopted. 

It  is  true  that  in  the  majority  of  cases  there  is  more  or  less  congestion  of 
the  internal  organs,  and  sometimes  the  patient  is  overwhelmed  by  these  con- 
gestions, but  in  a  large  number  of  cases  no  such  congestions  exist,  and  under 
such  circumstances  the  designation  pernicious  is  to  be  preferred.  In  its 
severe  and  dangerous  form  it  may  be  remittent  or  intermittent  in  character, 
and  may  assume  any  of  the  types  of  periodical  fever,  but  the  quotidian  and 
tertian  types  are  the  most  common.  Sometimes  its  pernicious  character  is 
clearly  marked  at  the  onset  of  the  fever,  during  the  first  paroxysm  ;  at 
other  times  it  comes  on  insidiously,  and  its  pernicious  character  is  not 
suspected  until  after  the  occurrence  of  two  or  three  paroxysms. 

There  are  several  well-marked  and  distinct  varieties  of  pernicious  fever — 
the  most  common  and  most  important  of  which  are  the  comatose,  the  delir- 
ious, the  algid,  and  the  gastro-enteric.  It  is  the  locality  in  which  perni- 
cious fever  prevails  that  gives  the  fever  its  distinctive  peculiarity.  Perni- 
cious fever  not  infrequently  appears  as  an  epidemic  ;  sporadic  cases  are  met 
with  in  those  regions  where  simple  intermittent  and  remittent  fevers 
prevail. 

Morbid  Anatomy. — Its  anatomical  lesions  are  similar  in  kind  to  those  of 
intermittent  and  remittent  fevers,  but  they  differ  very  much  in  degree.  For 
instance,  the  pigmentation  is  more  abundant.  The  abundance  of  the  pig- 
ment, and  the  extent  of  the  pigmentation  will  vary  with  the  severity  of 
the  fever.  The  other  changes  in  the  different  organs  and  tissues  of  the  body 
are  very  similar  in  character  to  those  described  in  connection  with  inter- 
mittent and  remittent  fever.  The  post-mortem  appearances  in  pernicious 
fever  vary  with  the  intensity  of  the  malarial  infection  and  the  peculiar 
atmospheric  conditions  under  which  the  fever  is  developed.  In  some  in- 
stances there  will  be  evidences  of  intense  engorgement  of  the  blood-vessels  of 
the  brain,  and  the  entire  brain  substance  will  be  more  or  less  thoroughly 
pigmented.  In  others,  minute  blood-extravasations  will  be  found  scattered 
here  and  there  throughout  the  substance  of  organs.  Small  blood-extravasa- 
tions into  the  spinal  cord,  accompanied  by  more  or  less  pigmentation,  are 
very  apt  during  life  to  be  attended  by  tetanic  spasms.  In  persons  dying 
of  pernicious  fever  after  the  third  attack,  I  have  found  all  the  organs  of  the 
body  pigmented.  Sometimes  there  is  intense  engorgement  of  the  liver,  that 
is,  the  most  marked  post-mortem  changes  will  be  found  in  that  organ,  and 
the  amount  of  pigmentation  present  will  correspond  with  the  intensity  of 
the  congestion.  With  intense  engorgement  of  the  organ  there  are  usually 
blood-extravasations. 

Occasionally,  infarctions  occur  in  the  spleen,  and  around  each  there  will 
be  a  mass  of  pulpy  material.    The  spleen  is  more  invariably  found  softened 


840  ACUTE   GENEEAL  DISEASES. 

than  in  any  other  fever.  In  connection  with  this  softening,  which  is  very 
extensive  and  similar  to  that  found  in  typhoid  fever,  the  organ  rapidly  be- 
coming a  soft,  pulpy,  bloody  mass,  it  is  also  enlarged  even  beyond  what  it  is 
in  typhoid  fever  and  is  darker  in  color  than  normal.  It  is  unnecessary  to 
describe  in  detail  the  enlargement  of  the  capillary  vessels  which  occurs  as  a 
necessary  result  of  this  intense  engorgement.  Sometimes  the  kidneys  and 
the  lungs  are  the  seat  of  intense  hyperae.mia,  as  the  result  of  which  the 
functions  of  these  organs  are  more  or  less  extensively  interfered  with. 
Hemorrhagic  infarctions  in  the  lungs  are  not  infrequent.  A  low  form  of 
pneumonia  is  sometimes  present.     The  heart  is  pale  and  flabby. 

Etiology. — The  exciting  and  predisposing  causes  of  pernicious  fever  differ 
from  those  of  the  simpler  forms  of  malarial  fever  only  in  degree,  not  in 
kind,  but  a  higher  range  of  temperature  is  requisite  for  the  development  of 
pernicious  fever.  It  prevails  only  in  those  localities  where  the  average 
range  of  temperature,  for  a  time,  reaches  65°  F. 

Symptoms. — Pernicious  fever  may  commence  abruptly ;  generally  the  pre- 
monitory symptoms  which  mark  its  development  do  not  differ  from  those 
which  mark  the  development  of  intermittent  and  remittent  fever.  In  most 
varieties  the  attack  commences  with  a  chill,  which  is  usually  severe  and 
prolonged.  The  attack  may  commence  with  distinct  intermittent  parox- 
ysms of  the  quotidian  type,  but  rarely  more  than  two  of  these  intermittent 
paroxysms  will  occur  before  it  assumes  the  pernicious  type  ;  or  a  remittent 
fever  with  a  distinct  exacerbation  and  remission  may  go  on  for  four  or  five 
days  before  its  pernicious  character  will  be  developed.  The  milder  form 
either  gradually  passes  from  a  simple  intermittent  into  a  pernicious  fever 
by  a  progressive  increase  in  the  severity  of  the  paroxysm,  or  a  single  parox- 
ysm of  not  unusual  severity  is  suddenly,  followed  by  a  pernicious  one  ;  a 
fatal  result  rarely  occurs  until  the  third  paroxysm  is  passed.  Again,  a  dis- 
tinct chill  may  be  followed  by  a  condition  that  will  at  once  be  recognized  as 
one  of  the  varieties  of  pernicious  fever.  The  ushering-in  symptoms  will 
always  vary  with  the  type  of  disease  which  is  about  to  be  developed.  I  shall 
not  describe  the  phenomena  that  attend  all  these  different  varieties,  but 
only  those  most  commonly  met  with. 

As  the  varieties  in  type  of  this  fever  are  as  numerous  as  the  localities  in 
which  they  occur,  and  as  the  type  in  any  locality  may  change  with  every 
succeeding  year — that  is,  the  type  of  one  year  may  be  very  unlike  that  of 
the  preceding  or  following  year — it  is  very  difficult  even  to  classify  its  dif- 
ferent forms.  The  slight  variations  which  are  met  with  in  the  pathologi- 
cal lesions  of  the  different  varieties  are  still  more  difficult  of  description 
and  classification.  For  instance,  there  is  one  variety  which  is  character- 
ized by  a  tendency  to  coma,  called  the  comatose  variety  ;  another  is  charac- 
terized by  a  tendency  to  a  peculiar  form  of  delirium,  termed  the  delirious 
'Variety  ;  still  another  is  characterized  by  a  marble-like  coldness  of  the  sur- 
face, called  the  algid  variety  ;  again,  we  have  one  which  is  characterized 
by  vomiting  and  purging,  or  choleraic  symptoms,  termed  the  gastro-enteric 
iiariety ;  then  one  in  which  there  is  acute  jaundice,  termed  the  icteric 
■i^ariety ;  then  one  in  which  there  are  profuse  hemorrhages,  termed  the 


PERNICIOUS   MALARIAL   FEVER. 


841 


hemorrhagic  variety  ;  and  still  another  in  which  there  is  profuse  diaph- 
oresis, termed  the  cnlUquative  variety. 

Comatose  Variety. — A  patient  has  a  distinct  paroxysm  of  one  of  the  sim- 
pler forms  of  malarial  fever  (intermittent  or  remittent),  with  no  s^Decial 
phenomena  attending  it,  except  that  he  has  had  a  more  than  usually  severe 
headache  ;  with  this  there  has  been  perhaps  vertigo,  stammering  and  in- 
distinctness in  the  speech,  an  inability  to  talk  with  freedom,  and  a  more 
than  usual  tremulousness  during  the  hot  stage.  From  this  condition  he 
passes  as  usual  into  the  hot  stage  of  an  intermittent,  or  rapidly  into  an  ex- 
acerbation of  remittent,  then  into  a  state  of  stupor  and  unconsciousness, 
and  finally  lies  upon  his  back,  with  a  flushed  face,  congested  conjunctivae, 
dilated  pupils,  slow,  deep,  stertorous  respiration,  and  perhaps  a  very  slow 
pulse,  or,  if  slow  at  first,  it  may  soon  become  frequent.  The  axillary  tem- 
peratures range  from  105"  to  107°  F.  The 
patient  is  now  partially  unconscious  ;  he  is 
apparently  paralyzed  ;  the  urine  is  retained 
in  the  bladder,  and  the  bowels  move  invol- 
untarily. If  the  pulse  is  slow,  it  is  full 
and  hard.  The  respiration  becomes  more 
and  more  stertorous,  and  unconsciousness 
more  and  more  complete.  Usually  a  moist- 
ure makes  its  appearance  within  twelve 
hours  from  the  commencement  of  the  first 
paroxysm,  and  the  patient  awakes  to  con- 
sciousness perspiring  profusely.  The  head- 
ache and  giddiness  pass  off,  and  if  the  fever 
which  preceded  it  was  remittent,  there  may 
be  a  well-marked  remission  ;  if  it  was  an 
intermittent,  there  may  be  a  distinct  inter- 
mission. With  the  next  remittent  exacer- 
bation or  during  the  hot  stage  of  an  inter- 
mittent, the  pain  in  the  head,  giddiness, 
unconsciousness,  and  all  the  symptoms  al- 
ready described  will  return  with  greater  in- 
tensity than  before.  With  the  second  at- 
tack the  patient  may  pass  into  a  fatal  coma.   Temperature  Record^in^a  case  of  Pemi- 

In  this  variety  patients    sometimes  pass  {Comatose  variety.) 

into     a     condition     of     apparent    death, 

which  may  last  for  hours.  Some  are,  nevertheless,  perfectly  conscious,  see- 
ing and  hearing  everything  which  occurs  around  them,  although  unable  to 
move  or  utter  a  sound  ;  others  are  unconscious.  Even  though  the  strong- 
est counter-irritants  are  applied  to  the  surface,  there  is  no  sign  of  life, 
until,  at  the  beginning  of  the  sweating  stage,  the  patient  comes  to  con- 
sciousness. If  a  patient  sitrvives  the  second  paroxysm,  quite  probably  he 
will  die  during  the  third.  With  each  successive  paroxysm  the  prognosis 
becomes  more  and  more  unfavorable  ;  patients  sometimes  lie  in  a  comatose 
condition  for  days,  and  finally  die  apparently  from  cerebral  congestion. 


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Fig.  175. 


842  ACUTE    GENEEAL   DISEASES. 

Delirious  Variety. — In  this  variety,  the  patient,  after  passing  into  the 
hot  stage  of  an  intermittent  or  into  the  exacerbation  of  a  remittent,  becomes 
delirious.  Mild  delirium  is  not  uncommon  during  the  progress  of  an  inter- 
mittent or  a  remittent  fever,  but  the  delirium  now  referred  to  is  of  a  more 
active  character.  If  delirium  is  developed  during  the  exacerbation  of  a  re- 
mittent or  during  the  hot  stage  of  an  intermittent,  which  has  been  preceded 
by  severe  headache,  dizziness,  ringing  in  the  ears,  and  great  restlessness, 
one  may  be  quite  certain  that  he  has  to  deal  with  a  case  of  pernicious  fever, 
especially  if  it  is  prevailing  in  the  locality.  In  this  variety  of  pernicious 
fever  there  will  also  be  more  or  less  headache  during  the  interval,  and  per- 
haps other  peculiar  cerebral  phenomena.  The  delirium  which  appears  is 
always  violent  in  character  ;  perhaps  the  patient  will  require  restraint ;  he 
may  be  disposed  to  jump  out  of  the  window,  or  in  some  way  to  do  injury 
to  himself  or  those  around  him.  During  the  paroxysm  of  delirium  the 
face  becomes  flushed,  the  eyes  brilliant,  the  conjunctivae  injected,  the 
pupils  dilated,  and  the  patient  is  constantly  crying,  singing,  and  trying  to 
escape.  In  those  who  are  extremely  anaemic  the  countenance  assumes  a 
pale,  sunken  aspect.  The  pulse  is  full  and  hard,  and  the  carotids  beat 
violently,  the  temperature  often  reaches  107°  or  108°  F.  This  delirious 
state  may  continue  for  hours.  Suddenly  the  patient  passes  from  it  into  a 
condition  of  collapse,  or  gradually  sinks  into  a  coma  from  which  he  never 
wakens.  During  the  whole  period  the  axillary  temperature  rarely  falls  be- 
low 105°  F. 

In  favorable  cases  the  delirium  gradually  becomes  milder,  a  profuse  per- 
spiration comes  on,  and  the  patient  falls  into  a  prolonged  sleep,  from  which 
he  awakens  conscious,  though  weak  and  exhausted,  with  headache  and 
vertigo,  but  without  the  slightest  recollection  of  what  has  passed.  These 
attacks  of  delirium  may  be  repeated  three  or  four  times  before  a  fatal  ter- 
mination is  reached,  but  so  much  danger  attends  them,  that  a  second  attack 
should  never  be  allowed  to  occur  if  it  can  be  prevented. 

In  this  variety  of  pernicious  fever,  other  nervous  phenomena  may  accom- 
pany or  take  the  place  of  the  delirium,  such  as  epileptiform  convulsions, 
tetantic  spasms,  etc.  The  tetanic  spasms  sometimes  resemble  the  phe- 
nomena of  hydrophobia.  That  form  of  tetanus  which  occurs  in  various 
malarial  districts,  and  is  sometimes  called  sporadic  tetanus,  I  believe 
will  be  found  to  have  many  things  in  common  with  this  type  of  pernicious 
fever. 

Oastro-Enteric  Variety. — In  this  variety  the  patient,  after  he  has  passed 
into  the  hot  stage  of  an  intermittent,  or  the  exacerbation  of  a  remittent, 
is  seized  with  almost  incessant  vomiting  and  purging.  The  vomiting  and 
purging  are  peculiar,  altogether  unlike  that  w'hich  is  sometimes  present  in 
the  simpler  forms  of  malarial  fever.  There  is  blood-stained  material,  both 
in  the  matter  vomited  and  in  that  discharged  from  the  bowels.  In  some 
instances,  the  discharges  may  be  so  reddened  as  to  look  like  beef-brine  or 
the  washings  of  raw  meat;  sometimes  the  proportion  of  blood  is  so  great 
as  to  cause  the  discharges  to  have  the  appearance  of  clear  blood.  In  some 
endemics  the  discharges  assume  the  appearance  of  rice-water,  having  no 


PERNICIOUS    MALARIAL   FEVER. 


843 


odor,  and  similar  in  appearance  to  those  of  Asiatic  cholera.  The  patient 
has  no  abdominal  pain  or  tenderness,  but  has  a'sense  of  weight  and  burning 
in  the  stomach,  accompanied  with  cramps  in  the  calves  of  the  legs,  cold- 
ness and  blueness  of  the  surface,  with  a  small,  almost  imj^erceptible  pulse, 
sunken  eyes,  and  the  "facies"  of  cholera.  So  closely  do  these  patients 
resemble  in  appearance  those  of  Asiatic  cholera  that  this  disease  has  fre- 
quently been  mistaken  for  it.  During  the  attack  the  thirst  is  most  in- 
tense. The  respiration  is  peculiar  ;  it  consists  of  a  double  inspiration, 
followed  by  a  double  sighing  expiration.  The  restlessness  is  yery  great, 
the  patient  is  constantly  tossing  from  one  side  to  the  other  ;  sometimes,  an 
hour  or  two  before  death,  he  suddenly  springs  up  and  walks  across  the  room. 

The  usual  length  of  the  fatal  paroxysm  is  from  three  to  six  hours. 
Patients  die  in  a  state  of  collapse.  After  the  vomiting  and  diarrhoea  have 
assumed  the  characteristic  appearances  already  described,  very  few  patients 
recover.  As  death  approaches,  the  pulse  becomes  more  frequent,  feeble, 
irregular,  and  fluttering  in  character.  The  respiration  is  more  and  more 
prolonged  and  sighing,  the  skin  cold  and  shrivelled,  and  covered  with  a 
cold,  clammy  perspiration.  It  frequently  happens  when  all  these  symp- 
toms are  present  that  the  patient  cannot  be  convinced  that  he  is  seriously 
ill,  and  wishes  to  get  out  of  bed  and  go  out  of  doors. 

Algid  Variety. — This  variety  is  characterized  by  coldness  of  the  surface 
of  the  body,  while  the  rectal  temperature  may  range  from  104°  to  107°  F. 
The  attack  begins  with  a  chill  of  not  un- 
usual severity  or  duration,  but  soon  after 
the  patient  enters  into  the  hot  stage  of  the 
paroxysm,  or,  during  the  exacerbation  of  a 
remittent,  the  surface  of  the  body  begins 
to  grow  cold,  while  at  the  same  time  he 
complains  of  a  sensation  of  burning  and 
intense  thirst.  A  cold  perspiration  soon 
covers  the  surface.  The  pulse  becomes 
slower  and  slower,  falters,  and  disappears  at 
the  wrist.  Alternately  the  extremities  and 
face  become  cold  ;  only  the  abdomen  re- 
tains its  normal  temperature.  The  surface 
has  a  cold,  marble-like  feel,  and  the  tem- 
perature in  the  axilla  may  fall  to  88°  or 
84°  F.  In  the  comatose  and  delirious 
varieties  the  temperature  rises  higher  than 
normal,  and  may  reach  106°  or  107°  F,,  but 
in  this  variety  it  sometimes  falls  two  or 
three  degrees  below  the  normal.  The 
tongue  becomes  white,  moist,  and  cold;  the 
breath  is  cold,  and  the  voice  feeble  and  in- 
distinct. The  action  of  the  heart  is  feeble, 
often  perceptible  only  on  auscultation.  The 
mouth  is  clean,  and  the  patient  seems  to  himself  to  be  in  a  comfortable 


Day: 

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Fig.  176. 
Temperature   Record  in  a  case  of  Per- 
nicious Fever. 
{Algid  varietT/.) 


844  ACUTE    GENERAL   DISEASES. 

condition,  except  that  he  feels  exhausted  and  is  sensible  of  great  internal 
heat.  The  mind  is  clear.  The  expression  of  the  countenance  is  that  of 
death. 

This  variety  is  very  insidious  in  its  progress.  To  one  not  familiar  with 
it,  the  calm  which  follows  the  febrile  excitement  will  be  mistaken  for  relief, 
perhaps  attributed  to  some  plan  of  treatment  pursued,  or  to  some  remedial 
agent  which  has  been  employed.  If  a  patient  in  one  of  these  paroxysms  is 
to  pass  on  to  recovery,  the  pulse  gradually  returns  in  the  wrist,  and  the  sur- 
face regains  its  normal  feel  and  temperature.  As  the  warmth  returns  to  the 
surface,  the  patient  passes  on  to  convalescence  in  the  same  manner  as  pa- 
tients recover  from  a  comatose  or  delirious  paroxysm.  An  algid  pernicious 
paroxysm  is  rarely  preceded  by  a  distinct  intermission,  and  it  rarely  has  any 
appreciable  remission.  Once  established,  it  marches  steadily  on  to  a  fatal 
issue,  unless  arrested  by  treatment. 

There  is  another  variety  which  will  occasionally  be  met  with,  in  which  a 
profuse  perspiration,  called  a  "■  colliquative  sweat,"  comes  on  at  the  end  of 
the  fever  stage  and  continues  through  the  succeeding  intermission,  accom- 
panied by  great  prostration,  feeble  heart  action,  and  labored  respiration. 
Upon  the  second  or  third  return  of  this  sweat  the  patient  sinks  and  dies, 
apparently  from  exhaustion.  Again,  severe  hemorrhages  from  the  stomach, 
bowels,  or  kidneys  may  occur  during  the  sweating  stage  of  a  pernicious  par- 
oxysm and  endanger  the  life  of  the  patient  from  sudden  syncope. 

A  mild  form  of  hsematuria  sometimes  occurs  independent  of  a  pernicious 
paroxysm  in  chronic  malarial  poisoning. 

Icteric  Variety. — This  is  always  endemic,  confined  to  certain  localities, 
and  occurring  in  them  whenever  any  form  of  pernicious  fever  prevails.  It 
begins  with  a  violent,  long-continued  chill,  during  which  jaundice  shows 
itself.  The  jaundice  gradually  deepens,  and  extends  over  the  whole  body. 
Intense  nausea  accompanies  its  development,  with  a  copious  vomiting  of 
bile,  and  a  bilious  diarrhoea.  The  patient  suffers  with  a  most  intense  head- 
ache, pain  in  the  region  of  the  spleen  and  over  the  kidneys,  and  a  feeling  of 
numbness  in  the  limbs.  The  pulse  is  small,  frequent,  and  hard.  The  urine 
is  dark  colored.  As  the  hot  stage  comes  on,  the  pulse  becomes  fuller  and 
more  frequent,  the  respiration  is  labored,  the  skin  very  hot,  the  tempera- 
ture reaching  106°  or  107°  F.,  and  the  thirst  is  most  intense.  This  stage 
lasts  three  or  four  hours,  and  often  terminates  in  death.  If  the  patient 
passes  into  the  sweating  stage,  recovery  usually  takes  place.  During  the 
intermission  the  mind  is  clear,  but  the  jaundice  continues.  Unless  the 
disease  is  controlled  by  treatment,  each  succeeding  paroxysm  becomes 
more  and  more  severe. 

This  variety  is  incorrectly  called  pernicious  bilious  remittent  fever.  If 
the  attack  is  mild,  there  is  only  a  slight  staining  of  the  skin,  but  in  that 
form  in  which  there  is  an  apparent  arrest  of  the  functions  of  the  liver,  the 
patient  may  die  deeply  jaundiced  within  two  or  three  days  after  the  first 
discoloration  appears.  The  mild  form  of  so-called  bilious  remittent  fever, 
in  which  the  febrile  movement  is  constant,  is  very  different  from  the  form 
under  discussion,  and  is  better  classed  under  the  head  of  simple  remit- 


PERNICIOUS   MALAEIAL   FEVER.  845 

tent.  All  these  different  varieties  depend  on  the  same  blood-iooisoning, 
differing  in  its  manifestations  according  to  its  intensity  and  the  predispos- 
ing atmospheric  or  septic  conditions  which  may  exist  in  the  localities  where 
they  are  developed. 

Differential  Diagnosis. — The  diagnosis  of  pernicious  fever  is  sometimes 
very  difficult.  In  determining  whether  a  given  case  is,  or  is  not,  one  of 
pernicious  fever,  the  first  inquiry  will  be  in  regard  to  the  character  of  the 
prevailing  fever.  If  pernicious  fever  is  prevailing  in  the  locality,  a  diagno- 
sis will  easily  be  made  ;  if,  however,  the  first  case  in  the  locality  falls  under 
observation,  probably  great  difficulty  will  be  experienced  in  making  a  diag- 
nosis, and  this  difficulty,  to  a  certain  extent,  will  vary  with  the  type  of  the 
fever.  If,  for  example,  a  case  belongs  to  that  class  in  which  there  is  a 
tendency  to  coma,  delirium,  etc.,  it  may  be  confounded  with  some  form  of 
cerebral  disease.  This  form  of  pernicious  fever  has  been  mistaken  for  cere- 
bral apoplexy,  meningitis,  and  acute  urcemia. 

As  a  rule,  it  is  not  difficult  to  draw  the  line  between  apoplexy  and  perni- 
cious fever  of  the  comatose  or  delirious  variety.  The  constant  and  promi- 
nent symptom  of  apoplexy  is  hemiplegia,  which  is  of  rare  occurrence  in  per- 
nicious fever.  It  may  occur,  but  if  it  does,  it  is  developed  slowly.  Nei- 
ther coma  nor  hemiplegia  is  ever  reached  suddenly  in  pernicious  fever.  Eise 
in  temperature,  rapid  pulse,  and  all  the  phenomena  of  intense  febrile  ex- 
citement are  present  before  the  occurrence  of  either.  On  the  other  hand, 
in  apoplexy  the  hemiplegia  is  of  sudden  development,  attended  by  a  slow 
pulse,  irregular  contracted  pupils  ;  or,  perhaps,  one  j)upil  is  dilated  and 
the  other  contracted,  and  its  occurrence  is  preceded  by  a  sudden  loss  of  con- 
sciousness, and  not  attended  or  preceded  by  high  febrile  excitement. 

As  regards .  pernicious  fever  and  meningitis,  although  in  both  diseases 
the  patient  reaches  a  condition  of  coma,  yet  in  meningitis  days  elapse  be- 
fore the  coma  is  reached,  and  during  those  days  there  has  been  pain  in 
the  head,  photophobia,  and  delirium,  extending  over  a  considerable  period 
of  time  ;  whereas,  in  pernicious  fever  the  patient  reaches  his  condition  of 
coma  within  twelve  hours.  Besides,  in  pernicious  fever  there  will  be  a 
history,  not  only  of  the  prevailing  type  of  malarial  disease,  which  will  in- 
dicate its  character,  but  the  attack  of  coma  or  delirium  will  be  preceded 
by  a  distinct  malarial  paroxysm — perhaps  two  of  these  paroxysms  ;  then 
the  patient  will  pass  rapidly  into  a  state  of  coma.  In  meningitis  the  fever 
rarely  ranges  above  102°  or  103°,  the  face  is  pale,  the  abdomen  retracted, 
and  the  pulse  is  tense  and  wiry — all  markedly  contrasting  with  delirious 
pernicious  fever. 

The  gastro-enteric  and  cold  or  algid  varieties  of  pernicious  fever  closely 
resemble  cholera.  They  may  be  distinguished  from  it  by  the  character  of 
the  primary  discharges.  There  may  be  a  time  in  this  type  of  pernicious 
fever  when  the  discharges  will  very  closely  resemble  those  of  cholera ;  but 
they  will  always  have  been  preceded  by  one  or  two  bloody  discharges.  In 
cholera  there  is  albumen  in  the  urine,  the  occurrence  of  which  is  com- 
paratively rare  in  pernicious  fever.  In  cholera  there  are  the  peculiar  sur- 
roundings of  the  patient,  the  prevalence  of  cholera  in  the  locality,  etc. 


846  ACUTE    GE^JTERAL   DISEASES. 

When  the  endemic  is  at  its  height  it  is  almost  impossible  to  make  a  differ- 
ential diagnosis  between  the  two  diseases  from  the  clinical  history  of  the 
cases  ;  but,  when  we  take  the  early  history  of  the  endemic,  at  which  time 
the  cases  at  their  commencenient  were  marked  by  distinct  intermittent  or 
remittent  paroxysms,  the  true  character  of  the  disease  is  very  readily  de- 
termined. If  in  any  given  case  there  is  still  a  question  whether  it  is  or  is 
not  one  of  pernicious  fever,  it  may  be  determind  with  positiveness  by  a 
microscopical  examination  of  the  blood,  which  will  be  found  to  contain 
free  pigment. 

The  icteric  variety  of  pernicious  fever  which  often,  in  many  of  its  phe- 
nomena, so  closely  resembles  yellow  fever,  maybe  distinguished  from  it 
not  only  by  the  history  of  its  development,  but  by  the  fact  that  when  it 
prevails  as  an  endemic,  those  are  seized  with  the  fever  who  have  been  long- 
est under  the  influence  of  malarial  poison,  whereas  new-comers  are  not 
usually  attacked  ;  in  yellow  fever  districts  new-comers  are  almost  certain 
to  contract  the  disease.  The  symptoms  in  icteroid  pernicious  fever  tend 
to  become  typhoid  and  adynamic,  while  in  yellow  fever  the  symptoms  are 
active  and  there  is  little  tendency  to  a  typhoid  condition.  Then  the  jaun- 
dice of  yellow  fever  appears  late  in  the  disease,  while  the  jaundice  of  this 
form  of  pernicious  fever  comes  on  early,  even  before  the  chill  passes  away. 
Again,  bloody  urine  is  frequently  present  in  this  type  of  pernicious  fever, 
while  in  yellow  fever  hsematuria  rarely  occurs  without  the  accompanying 
evidences  of  nephritic  inflammation.  The  presence  of  free  pigment  in  the 
blood  will  aid  in  settling  the  question  of  diagnosis  in  difficult  cases. 

Prognosis. — In  all  varieties  of  pernicious  fever  the  prognosis  is  unfavor- 
able, unless  it  can  be  controlled  before  the  occurrence  of  the  second  parox- 
ysm. The  prognosis  will  depend  in  a  great  degree  upon  the  character  of 
the  prevailing  endemic  or  epidemic,  as  also  upon  the  stage  of  the  epidemic, 
for  the  ratio  of  mortality  is  always  greater  during  the  earlier  period  of  an 
epidemic  than  during  its  decline.  All  agree  that  the  prognosis  is  better  in 
every  variety  of  pernicious  fever  if  there  are  distinct  intermissions,  however 
short  may  be  their  duration.  If  the  paroxysm  does  not  last  more  than 
twelve  hours,  and  terminates  in  a  distinct  remission,  the  prognosis  is  far 
better  than  when  one  paroxysm  follows  another  without  any  distinct  re- 
mission. Unquestionably  the  most  favorable  cases  are  those  of  the  tertian 
type.  Those  varieties  in  which  the  cases  most  frequently  terminate  fatally 
are  the  gastro-enteric  and  the  algid  ;  those  in  which  recovery  is  most 
likely  to  occur  are  the  comatose  and  delirious. 

The  prognosis  is  also  much  influenced  by  the  age  and  condition  of  the 
patient  and  by  the  presence  or  absence  of  complications.  The  mortality 
is  greatest  among  the  very  young  and  very  old,  and  among  the  intemperate. 
Patients  with  pernicious  fever  may  die  suddenly  during  a  paroxysm,  or  the 
paroxysms  may  be  prolonged  and  run  into  each  other,  and  the  patient  may 
finally  pass  into  a  typhoid  or  collapsed  condition.  *  If  the  second  or  third 
paroxysm  is  not  attended  by  signs  of  intense  visceral  congestion,  if  it  de- 
clines with  profuse  warm  sweats,  if  it  has  been  preceded  by  distinct  inter- 
vals, if  the  urine  is  free,  and  the  appetite  early  returns,  a  speedy  recovery 


PERKiCIOUS    MALAEIAL   FEVEB.  847 

is  at  hand.  On  the  other  hand,  if  the  second  or  third  paroxysm  is  pro- 
tracted and  accompanied  by  great  anxiety  and  restlessness,  with  active  de- 
lirium and  a  tendency  to  coma,  with  coldness  of  the  surface  ;  if  there  is 
intense  pain  in  the  epigastrium,  with  tingling  of  the  surface,  and  scanty 
and  high-colored  urine;  if  there  is  profuse  vomiting  and  purging,  bleeding 
at  the  nose,  and  cold,  colliquative  sweats.;  if  the  pulse  becomes  small  and 
feeble,  or  the  radial  pulse  is  imperceptible,  the  danger  is  very  great,  and  a 
fatal  issue  is  almost  certain.  Sometimes  severe  and  fatal  dysentery  comes 
on  at  the  end  of  a  paroxysm  ;  at  other  times,  as  the  paroxysm  subsides, 
the  fever  assumes  a  typhoid  type,  and,  after  a  period  of  continued  fever 
ranging  from  ten  to  twelve  days,  it  terminates  fatally. 

Treatment. — The  expectant  plan  of  treatment  cannot  be  practised  in  the 
treatment  of  pernicious  fevers.  The  alarming  symptoms  crowd  upon  one 
another  with  great  rapidity,  and  it  is  only  by  prompt  and  vigorous  measures 
that  in  the  severe  forms  of  the  disease  the  patient  can  be  rescued  from  im- 
pending death.  The  issue  of  life  or  death  often  hangs  upon  a  single  hour. 
Some  have  proposed,  before  administering  the  only  specific  which  we 
possess  capable  of  controlling  this  disease,  to  produce  free  purgation  by  the 
administration  of  cathartics  ;  others  to  bleed  and  freely  vomit  the  patients. 
If  the  case  is  one  of  the  gastro-enteric  variety,  emetics  and  purgatives  are 
certainly  very  plainly  contraindicated.  It  is  now  a  well  established  fact 
that  in  no  variety  of  pernicious  fever  do  patients  bear  depletion.  In  India, 
where  the  most  severe  types  of  this  fever  prevail,  the  English  surgeons  are 
very  positive  in  their  testimony  upon  this  point.  All  forms  of  depletion 
have  been  abandoned  by  them.  Although  stimulating  enemata  and  friction 
to  the  surface  may  act  as  aids  in  the  management  of  the  algid  and  delirious 
varieties,  they  must  not  be  relied  upon  as  having  any  controlling  influence 
over  the  disease. 

Those  who  have  bad  the  most  extended  opportunities  for  testing  the  dif- 
ferent remedies  and  plans  of  treatment  which  have  been  employed  in  the 
management  of  this  fever  are  united  in  the  opinion  that  quinine  and  opium 
are  the  only  agents  which  can  be  relied  upon  for  controlling  its  different 
varieties.  In  fact,  the  hypodermic  use  of  these  drugs  has  inaugurated  a 
new  era  in  its  treatment,  for  in  a  large  proportion  of  the  severer  forms  it  is 
impossible  to  get  the  full  effect  of  either  of  these  remedies  by  the  ordinary 
methods  of  their  administration,  the  usual  avenues  for  their  introduction 
being  closed.' 

Whatever  solution  may  be  used,  administer  from  five  to  seven  grains  of 

»  The  solntion  of  quinine  commonly  employed  by  the  English  surgeons  for  this  purpose  is  made  by 
adding  one  hundred  and  fifty  grains  of  quinine  and  fifty  drops  of  dilute  hydrochloric  acid  to  four  ounces 
of  water,  and  then  evaporating  the  solution  to  two  ounces.  Of  this,  thirty  drops  may  be  administered  at 
CHch  injection.  Some  add  carbolic  acid  to  a  solution  of  quinine  in  dilute  sulphuric  acid  ;  the  carbolic 
acid  is  added  to  prevent  abscess  at  the  point  where  the  injection  is  introduced. 
The  formula  for  this  solution  is  as  follows  : 

Quiniffi  disulphatip gr-  !• 

Acidi  sulphuric,  dil t^'V. 

Acidi  carbolici tH,  ij- 

Aquse  destillat 5  i- 

M. 
Thirty  minims  is  the  quantity  usually  administered  at  each  hypodermic  injection. 


.  848  ACUTE    GEiq-BRAL   DISEASES. 

quinine  every  hour  until  the  paroxysm  has  passed  away,  then  continue  its 
use  in  the  three-grain  doses  every  four  hours.  With  the  first  hypodermic 
of  quinine  administer  one-fourth  of  a  grain  of  morphia.  The  morphine 
should  be  administered  with  each  dose  of  quinine  until  the  patient  is 
brought  fully  under  its  influence,  without  regard  to  the  stage  of  the 
paroxysm. " 

During  the  past  few  years  a  remedy  known  as  "  Warburg's  Tincture  " 
has  been  quite  extensively  employed  in  the  treatment  of  pernicious  and 
other  forms  of  malarial  fever.^  Each  half  ounce  of  this  tincture  contains 
seven  and  a  half  grains  of  quinine.  It  is  recommended  to  give  half  an 
ounce  of  this  tincture  at  the  onset  of  the  paroxysm  ;  if  this  does  not  con- 
trol it,  the  same  quantity  must  be  repeated  in  four  hours.  If  it  cannot  be 
retained  by  the  stomach,  it  may  be  administered  in  capsules,   §i  every 

1 1  have  recently  used  the  following : 

QuiniEB  sulphatis 3  i. 

Acidi  hydrobrom 3  ij. 

Aquae  destillat 3  vl. 

M. 
Thirty  minims  may  be  administered  at  each  injection. 

The  bimuriate  of  quinine  with  urea,  made  by  Messrs.  McKesson  and  Eobbins,  Phila.,  is  highly  recom. 
mended  for  hypodermic  injection,  as  it  is  very  soluble,  and  abscesses  seldom  or  never  follow  its  use. 
Formula  : 

Bimuriate  Quiiiia  and  Urea 3i, 

Aq.  Destillatae,  ad f  3  ij. 

M.  f.  soi. 
Two  minims  contain  one  grain  of  the  salt. 

»  Formula,  Warburg's  Tincture: 
Ead.  Rhei 
P.  Aloe  Soc. 

Ead.  Angelica  Officinalis,  35 sjy^ 

Ead.  Helenii 
Crocus  Hispan. 
Sem.  Foeniculi 

Cretse  Preparat.,  5a , sm 

Ead.  Gentian 
Ead.  Zedoar 
P.  Cubeb 
G.  Myrrhse 
G.  Camphor 

Boletus  Laricis,  55 z: 

Confect.  Damocratis* "" zjy 

Quiniae  Sulph i...  .".'!!!!.'!.'."!.".*!'.!!'.'.."!!.'.'!!.*     Slx'xxy. 

Sp.  Vini  Kect O  xx 

A  qu  83  P  u  r a3 !!!!!!!'./.*.*.'.!!    O  xi j 

Macerate,  in  a  water  bath,  twelve  hours,  express  and  filter. 

*  Confeotio  Damocratis : 

Cinnamon 

MjTih  fourteen  grams. 

White  Agaric,  Spikenard,  Ginger,  Spanish  Saferon,  Treacle,"  Mustard  Seed,  Frankln- e  even 

cense,  and  Chian  Turpentine,  each ^^„      „ 

Camel's  Hay,  Costus  Arabacus,  Zeodary,  Indian  Leaf,  Mace,  French  Lavender  Long 

Pepper,  Seeds  of  Harwort,  Juice  of  the  Rape  of  Clstus,  Strained  Storax,  Opponax 

Stramed  Galbanum,  Balsam  of  Gilead,  Oil  of  Nutmeg,  Russian  Castor,  each  eiaht       " 

Water  Germunder,  Balsam-Tree  Fruit,  Cubeb,  White  Pepper,  Seeds  of  Carrot  of       

Crete,  Foley  Mont,  Strained  Bdellium,  each.... gg^g^      « 

Gentian  Root,  Celtic  Hard,  Leaves  of  Dittany  of  Crete,  Red  Rose,  Seeds  of  Mace-' 

donium  Parsley,  Sweet  Fennel  Seed,  Seeds  of  Lesser  Cardamom,  Gum  Arabic 

Opium,  of  each „  „ 

Sweet  Flag,  Wild  Valerian,  Anise  Seed,  Sagapernum,  each.... .........'.'."". t^ree      " 

Spigrul,  St.  John's  Wort,  Juice  of  Acacia,  Catechu,  Dried  Bellies  of  Skunks,  each '.'.'. 'two  and  one-half      « 

Clarified  Honey. „.,»        „ 

The  roots,  etc.,  to  be  finely  powdered,  and  the  whole  mixed  thoroughljt. 


DEITGUE   FEVEE.  84f> 

twenty-four  hours.'  It  is  claimed  that  the  tincture  is  retained  by  the  stom- 
ach when  all  other  remedies  are  rejected.  Prof.  Maclean  says  that  he  has 
seen  the  most  hopeless  cases — those  manifesting  a  degree  of  severity  which 
seemed  to  preclude  the  jiossibility  of  recovery — commence  to  convalesce  as 
soon  as  the  patient  was  brought  under  the  influence  of  this  remedy.''  No 
special  rules  can  be  laid  down  in  regard  to  the  administration  of  stimulants 
in  pernicious  fever  ;  the  condition  of  the  patient  must  be  the  guide. 
They  are  only  of  service  as  means  to  aid  in  carrying  a  patient  over  a  dan- 
gerous period.  Their  continued  use  in  large  quantities  is  strongly  objected 
to  by  those  who  have  had  the  most  extensive  experience  in  the  management 
of  this  fever.  Do  not  wait  for  the  action  of  a  calomel  purge.  Do  not  resort 
to  any  depleting  measures.  However  mild  the  paroxysm,  no  time  should  be 
lost ;  bring  the  patient  as  rapidly  as  possible  under  the  influence  of  quinine 
and  opium,  or,  if  Warburg's  tincture  is  used,  administer  it  in  full  doses  as 
early  as  possible,  and  continue  its  administration  until  convalescence  is 
fully  establishedo 

DEJS^GUE   FEVEE. 

Dengue,^  hreah-hone,  or  dandy  fever  first  appeared  after  the  landing  of  a 
cargo  of  slaves  from  Africa,  hence  its  earliest  name  was  African  Fever.  It 
is  neither  an  intermittent,  a  remittent,  nor  a  pernicious  fever.  It  is  an 
acute  disease  which  appears  as  an  epidemic  in  hot  climates.  It  is  charac- 
terized by  a  febrile  excitement  remitting  in  its  character,  and  is  accom- 
panied by  more  or  less  intense  arthritic  pains,  attended  by  the  develop- 
ment of  a  papillary  eruption  resembling  that  of  measles. 

Morbid  Anatomy. — The  morbid  anatomy  of  this  variety  of  fever  does  not 
differ  essentially  from  that  of  the  severer  types  of  malarial  fever,  except  that 
a  cutaneous  eruption  commences  on  the  palms  of  the  hands  and  extends 
rapidly  over  the  entire  body.  In  most  cases,  arthritic  changes  of  a  rheu- 
matic character  are  present ;  usually  the  external  lymphatic  glands  are 
somewhat  enlarged.  This  disease  seems  to  be  an  exanthematous  malarial 
fever,  with  a  rheumatic  or  neuralgic  element. 

Etiology. — Dengue  or  break-bone  fever  prevails  epidemically  in  malarial 
districts  ;  it  may  occur  as  a  sporadic  disease.  Its  infection  has  been  carried 
in  clothing  from  one  seaport  to  another.*  Some  claim  that  the  disease  de- 
pends upon  a  specific  contagion ;  but  its  contagious  character  has  not  been 
established.     Its  prevalence  is  not  arrested  by  cold  weather.     The  intensity 

1  The  tincture  may  be  evaporated  nearly  to  dryness,  and  put  up  in  capsules  containing  from  one  to  two 
drams  each. 

2  Prof .  Maclean's  rules  for  its  administration  are  as  follows  :—"  One-half  ounce  (half  of  a  bottle)  is 
given  alone,  without  dilution,  after  the  bowels  have  been  evacuated  by  any  convenient  purgative,  all  fluids 
being  withheld  ;  in  three  hours  the  other  half  of  the  bottle  is  administered  in  the  same  way.  Soon  after- 
ward, particularly  in  hot  climates,  profuse,  but  seldom  exhausting,  perspiration  is  produced  ;  this  has  a 
strong  aromatic  odor,  which  I  have  often  detected  about  the  patient  and  his  room  on  the  following  day. 
With  this  there  is  a  rapid  decline  of  temperature,  immediate  abatement  of  frontal  headache— in  a  word, 
complete  defervescence,  and  it  seldom  happens  that  a  second  bottle  is  required.  If  so,  the  dose  may  be 
repeated  as  above.  In  very  arlynamic  cases,  if  the  sweating  threatens  to  prove  exhausting,  nourishment 
in  the  shape  of  beef-tea,  with  the  addition  of  Liebig's  extract  and  some  wine  or  brandy  of  good  quality, 
may  be  required." 

3  El  dengue  means  in  Spanish,  affectation,  a  dandified  manner. 

*  Dengue  seems  to  have  a  specific  poison  ;  and  the  disease  is  in  some  degree  infectious.    Some  regard  it 
as  more  highly  contagious  than  even  the  exanthematous  fevers. 
54 


850 


ACUTE    GE]!q"ERAL   DISEASES. 


of  the  malarial  poison  unquestionably  lias  some  influence  in  increasing  or 
lessening  the  severity  of  this  fever.  In  districts  slightly  malarial  its  type 
is  usually  mild  ;  but  in  districts  strongly  malarial  its  type  is  severe.  It  at- 
tacks all  classes  and  all  ages,  rich  and  poor,  black  and  white,  the  very 
young  and  the  very  old.  Occasionally  it  has  occurred  as  the  precursor  of 
yellow  fever.  In '1780  it  was  epidemic  in  Philadelphia.  In  1827  a  very 
extended  epidemic  of  this  fever  prevailed  in  the  West  Indies  ;  during  the 
prevalence  of  this  epidemic,  the  specific  poison  of  the  disease  was  trans- 
ported in  clothing  and  merchandise  to  many  neighboring  seaports.  In 
our  Southern  States,  in  1880,  it  prevailed  as  an  epidemic.  One  attack 
does  not  protect  against  a  second. 

Symptoms. — The  period  of  incubation  is  estimated  at  from  three  to  five 
days.  Its  initiatory  symptoms  are  sudden  and  well  pronounced,  and  its  de- 
velopment is  very  rapid.  In  the  majority  of  cases,  the  earliest  symptoms 
are  headache,  photophobia,  great  restlessness,  chilliness  alternating  with 
flashes  of  heat,  and  pain  in  the  back,  limbs  and  joints ;  the  small  joints. 

swell,  and  there  is  soreness  and  stiff- 
ness of  the  muscles.  The  skin  be- 
comes hot  and  dry,  and  in  some  in- 
stances the  temperature  reaches  107° 
or  108°  F.  The  pulse  is  rapid,  rang- 
ing from  120  to  140  beats  per  minute.. 
The  face  is  flushed  and  the  eyes  red 
and  watery.  Thomas  says  that  in 
children  it  often  begins  with  a  con- 
vulsion.* 

After  the  fever  has  continued  about 
twelve  hours,  the  pains  in  the  joints, 
and  back  become  intense,  and  shoot 
down  the  sciatic  nerve.  Nausea^ 
vomiting,  and  pain  in  the  epigastrium 
are  usually  prominent  symptoms. 
Early  in  the  fever  the  lymphatic 
glands  become  involved  ;  the  ingui- 
nal are  first  affected,  then  those  in 
the  axilla  and  neck ;  they  increase  very  rapidly  in  size,  and  become  ex- 
ceedingly tender.  The  testicles,  or  rather,  the  epididymes,  enlarge,  and 
the  swelling  continues  until  the  subsidence  of  the  other  symptoms.  The 
active  febrile  excitement  continues  from  twelve  hours  to  three  or  four  days, 
when  it  subsides,  leaving  the  patient  in  an  exceedingly  feeble  and  prostrate 
condition.  Sometimes  the  fever  abates  suddenly,  with  critical  symptoms, 
as  in  relapsing  fever,  such  as  profuse  sweats,  diarrhoea,  or  epistaxis.  Pro- 
fuse diarrhoea  may  usher  in  the  disease.  The  patient  after  being  in  a  pas- 
sive  condition  for  two  or  three  days,  passes  into  the  period  of  remission. 
The  pains  now  become  less,  the  glandular  swellings  diminish,  there  is  less 
febrile  excitement,  but  the  fever  does  not  entirely  subside. 

>  Dengue.    J.  G.  Thomas,  M.D.,  Savannah,  1881. 


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Fig.  177. 
Temperature  Record  in  a  severe  case  of  Dengue 
Fever. 


DENGUE   FEVEJt.  851 

After  two  or  three  days  a  second  fever  paroxysm  occurs.  About  the 
same  period  intervenes  between  the  first  and  second  paroxysm  as  between 
the  first  and  second  paroxysm  in  relapsing  fever.  The  second  paroxysm 
of  fever  is  more  intense  than  the  first,  the  pain  in  the  joints  is  more  severe^ 
and  finally,  when  the  fever  has  reached  its  maximum,  and  the  j^ain  is  most 
intense  (usually  on  the  fifth  or  sixth  day),  an  eruption  makes  its  appear- 
ance. It  first  appears  upon  the  palms  of  the  hands,  then  upon  the  neck  ; 
soon  it  extends  downward  and  is  seen  upon  the  chest,  and  finally  spreads 
over  the  entire  body.  Usually  it  is  papillary  in  character  and  very  closely 
resembles  the  eruption  of  scarlatina.  As  soon  as  the  eruption  is  developed, 
the  febrile  symptoms  subside  and  the  patient  goes  on  to  convalescence.  A 
second  and  terminal  rash  usually  appears  in  crops  after  defervescence.  It 
is  miliary,  or  may  resemble  herpes  or  urticaria.  Dengue  without  fever  is 
where  the  joint  and  febrile  symptoms  are  absent,  but  the  rash  (both  ini- 
tial and  secondary)  is  present.  This  is  common  in  children.  The  intense 
arthritic  pains  accompanying  the  papillary  eruption,  and  the  glandular 
swellings  are  the  characteristic  symptoms  of  this  type  of  fever.  As  the 
second  paroxysm  of  fever  subsides,  the  patient  is  left  with  stiffness  and 
soreness  of  the  joints,  which  sometimes  do  not  pass  away  for  weeks. 

Occasionally  the  disease  assumes  a  typhoid  type,  the  tongue  becomes 
coYered  with  a  dark  brown  coating,  the  gums  become  red  and  spongy,  the 
pulse  slow  and  feeble,  and  the  surface  is  covered  with  a  cold  sweat.  As 
soon  as  the  second  eruption  appears,  the  patient  is  generally  free  from 
fever,  and  passes  on  to  a  rapid  and  complete  convalescence.  During  its 
active  period  there  is  a  peculiar  tendency  to  syncope.  In  very  severe  cases 
the  pain  in  the  testicles  will  continue  after  the  subsidence  of  the  fever,  and 
a  serous  effusion  will  take  place  into  the  tunica  vaginalis.  The  joints  will 
remain  painful  and  flabby.  There  will  be  extreme  nervousness  and  anxi- 
ety. The  heart's  action  will  be  intermittent,  and  the  lymphatic  glands 
which  have  been  enlarged  form  indurated  tumors  which  very  rarely  sup- 
purate. 

The  duration  of  this  fever  varies  with  the  period  of  remission.  Its  aver- 
age duration  is  about  eight  days.  In  those  epidemics  where  there  is  an  ab- 
sence of  articular  pains,  the  mucous  membranes  of  the  mouth  and  throat 
are  involved.  In  some  epidemics  the  fever  has  occurred  five  or  six  times  in 
the  same  individual. 

The  course  of  the  disease  may  be  divided  into  periods.  First,  that  of 
febrile  exacerbation  lasting  two  or  three  days,  then  an  intermission  of 
two  or  three  days,  then  a  second  febrile  exacerbation  which  lasts  two  or 
three  days,  then  convalescence.  Its  average  duration  is  from  three  to  eight 
days. 

DiflFerential  Diagnosis. — This  fever  may  be  confounded  with  rheumatism, 
or  with  remittent  fever.  In  some  of  its  phenomena  it  closely  resembles 
relapsing  fever. 

It  may  be  distinguished  from  remittent  fever  by  the  persistency  of  the 
rheumatic  and  neuralgic  pains,  by  the  cutaneous  eruption,  and  by  the 
length  of  the  remission. 


852  ACUTE   GENEEAL   DISEASES. 

It  may  be  distingaished  from  rheumatism,  as  it  prevails  epidemically, 
and  a  period  of  febrile  excitement  precedes  the  arthritic  phenomena. 

It  may  be  distinguished  from  relapsiag  fever  by  the  eruption  and  by  the 
character  of  the  remissions. 

Prognosis. — The  prognosis  is  always  favorable,  although  the  symptoms 
whicli  attend  its  development  may  be  alarmingly  severe.  The  prognosis 
is  only  unfavorable  when  it  occurs  in  the  very  aged  or  in  feeble  infants.' 

Treatment. — This  fever  always  runs  a  definite  course,  and  its  treatment 
is  the  symptomatic  treatment  of  fever,  combined  witli  well-recognized 
anti-rheumatic  remedies.  It  is  claimed  that  emetics  and  free  purgation 
diminish  its  severity.  A  favorite  combination  is  ipecacuanha,  calomel,  and 
colchicum — which  is  to  be  administered  every  night  in  cathartic  doses. 
Calomel  should  never  be  administered  alone,  nor  in  combination  with  other 
drugs,  if  its  specific  effect  is  likely  to  be  produced.  The  administration 
of  colchicum  witli  spirits  of  nitre  and  nitrate  of  potash,  in  such  proportion 
that  profuse  diaphoresis  may  be  produced,  in  connection  with  effervescing 
draughts,  will  usually  afford  relief  from  the  pain  in  the  head  and  limbs. 
Should  the  arthritic  pains  persist,  opium  may  be  administered  in  sufficient 
quantity  to  afford  relief.  Salicylate  of  soda  is  of  great  benefit  where  ar- 
thritic pains  are  severe. 

During  the  remission  the  bowels  shoyld  be  kept  freely  opened  with  sa- 
lines, and  quinine  combined  with  an  alkali  should  be  given  at  stated  inter- 
vals. J^arcotics  may  be  given  in  small  doses  to  produce  sleep,  should  the 
patient  be  wakeful.  By  the  employment  of  these  measures  a  return  of 
fever  may  be  prevented  and  the  arthritic  pains  will  gradually  subside. 
If  this  plan  is  pursued,  should  the  fever  return,  it  will  be  mild  in  char- 
acter, attended  by  little  constitutional  disturbance.  The  weakness  and 
exhaustion  which  attend  convalescence  may  be  combated  by  the  free  use  of 
wine  or  malt  liquors. 

The  diet  should  be  most  nutritious.  JSTourishment  should  be  admin- 
istered at  stated  intervals,  during  the  night  as  well  as  during  the  day.  The 
lymphatic  enlargement,  especially  in  the  inguinal  region,  should  be  treated 
locally  with  iodine.  Citrate  of  iron  and  quinine  will  be  found  of  great 
service  during  convalescence.  If  a  single  joint  remains  swollen  and  tender 
for  a  considerable  period  after  the  subsidence  of  the  fever,  the  occasional 
application  of  a  blister  is  recommended. 

In  some  epidemics,  relapses  after  an  interval  of  two  or  three  weeks 
have  been  of  frequent  occurrence.  They  run  a  milder  course  than  the 
primary  fever.  The  relapses  more  closely  resemble  an  attack  of  articu- 
lar rheumatism  than  the  primary  fever.  Quinine  is  said  to  furnish  great 
protection  against  a  relapse. 

1  Among  sequels  Thomas  records  heart  affections,  but  does  not  say  what  these  are  ;  though  he  says  they 
are  not  the  same  as  in  rheumatism.  Peripheral  paralysis  of  the  forearm  may  occur.  Catarrh  of  the  fauces, 
trachea  or  oesophagus  is  mentioned  as  a  sequela. 


CHEONIC   MALARIAL   INFECTION".  853 


CHRONIC    MALARIAL   INFECTION. 


Malarial  cachexia,  or  chronic  malarial  infection,  may  be  a  sequela  of  any 
form  of  acute  malarial  disease.  It  may  be  developed  in  those  who  have 
never  suffered  from  any  form  of  malarial  fever,  but  who  have  resided  for 
some  time  in  a  malarial  district.  One  who  has  had  repeated  attacks  of 
intermittent  or  remittent  fever,  and  has  become  exceedingly  ansemic,  with 
an  enlarged  spleen  and  enlarged  liver,  may  be  regarded  as  in  a  condition  of 
chronic  malarial  cachexia.  Again,  a  person  who  has  never  had  a  distinct 
paroxysm  of  malarial  fever,  but  who  has  lived  for  some  time  in  a  malarial 
district,  becomes  anaemic  with  enlarged  spleen  and  liver,  and  presents  the 
phenomena  of  chronic  malarial  infection. 

Morbid  Anatomy. — The  morbid  anatomy  of  chronic  malarial  infection 
does  not  differ  from  that  of  the  severer  types  of  malarial  fever,  except  in 
the  more  advanced  stages  of  the  tissue-changes.  Thus  the  spleen  is  often 
ten  or  twelve  times  its  normal  size,  tough,  firm  and  resistant.  Its  surface 
is  uneven,  its  capsule  thickened  and  more  or  less  adherent  to  the  adja- 
cent organs.  Its  sii,bstance  is  rich  in  pigment  matter,  and  presents  the 
minute  changes,  either  of  simple  hyperj)lasia  or  amyloid  degeneration. 
Similar  tissue-changes  take  place  in  the  liver  and  kidneys.  In  some  in- 
stances the  muscular  tissue  of  the  heart  undergoes  fatty  or  amyloid  de- 
generative changes.  (Edema  of  the  subcutaneous  cellular  tissue,  and  an 
accumulation  of  fluid  in  the  serous  cavities,  are  common  attendants  of 
chronic  malarial  cachexia. 

Etiology. — It  may  be  the  result  of  prolonged  exposure  in  a  district  only 
slightly  malarial,  or  of  a  short  exposure  in  a  district  strongly  malarial. 

Symptoms. — Those  who  are  the  subjects  of  chronic  malarial  infection 
complain  of  vertigo,  ringing  in  the  ears,  loss  of  memory,  disturbances  of 
sight,  loss  of  appetite,  nausea,  dyspeptic  symptoms,  and  pain  and  oppres- 
sion in  the  epigastrium.  The  bowels  are  rarely  constipated  ;  diarrhoea  is 
often  present  in  the  morning.  The  sleep  is  disturbed  ;  it  may  be  profound, 
but  it  is  unrefreshing.  The  patient  awakes  in  the  morning  with  a  con- 
fused feeling  about  the  head  and  a  general  feeling  of  discomfort.  Some 
complain  of  pains  in  the  back  and  loins  and  along  the  sciatic  nerve  ;  others 
of  pain  and  tenderness  in  the  joints  and  stiffness  of  the  muscles  of  the  limbs 
and  back ;  they  become  easily  fatigued  on  exertion,  have  shortness  of 
breath  and  palpitation  of  the  heart. 

The  nervous  system  seems  to  suffer  most  severely.  One  of  the  most  com- 
mon nervous  manifestations  is  local  anaesthesia,  which  usually  shows  it- 
self upon  the  outer  surface  of  the  thighs.  Itching,  burning,  and  a  sense 
of  formication,  tingling,  or  numbness  are  very  common  symptoms.  Not 
infrequently  numbness  of  the  arms  and  fingers  and  tickling  and  burning 
of  the  feet  are  complained  of,  and  a  patient  will  fear  that  he  is  about  to 
have  an  attack  of  paralysis. 

Hemiplegia  sometimes  occurs.  I  remember  one  case  in  which  there 
was  complete  loss  of  power  of  the  right  arm  and  leg,  yet  no  facial  paraly- 


854  ACUTE   GEKEEAL  DISEASES. 

sis.  This  patient  had  never  had  a  paroxysm  of  malarial  fever,  and  for  that 
reason  the  possibility  of  malarial  infection  had  been  excluded.  Similar 
manifestations  of  chronic  malarial  infection  quite  frequently  occur  in  those 
who  have  never  had  a  distinct  malarial  paroxysm. 

Chronic  malarial  infection  may  be  unattended  by  any  nervous  manifesta- 
tions. This  form  shows  itself  in  catarrhal  inflammations  affecting  the 
mucous  membrane  of  the  stomach,  intestines  and  bronchial  tubes.  Pa- 
tients have  a  form  of  bronchitis  which  is  really  a  chronic  malarial  affection. 
A  gastro-enteritis,  in  which  there  is  marked  interference  with  digestion, 
may  be  developed.  If  this  is  treated  with  the  ordinary  remedies  for  dys- 
pepsia, no  good  result  is  accomplished,  while  a  few  doses  of  quinine  will 
relieve  the  patient  and  establish  the  diagnosis.  The  chronic  intestinal 
catarrh  which  results  from  chronic  malarial  infection  may  give  rise  to  a 
troublesome  diarrhoea  which  will  assume  all  the  characteristics  of  chronic 
diarrhoea.  As  already  stated,  anaemia  is  a  very  common  result,  and  pal- 
pitation of  the  heart  is  a  very  frequent  and  sometimes  distressing  accom- 
paniment of  such  ansemia.  It  often  gives  rise  to  temporary  attacks  of 
melancholia  and  hypochondriasis.  Persons  imagine  they  have  disease  of 
the  heart,  kidney,  or  spine,  etc. 

Another  nervous  manifestation  of  chronic  malarial  infection  is  neuralgia. 
Certain  nerve-trunks  or  their  roots  seem  to  be  directly  involved,  while  the 
nerve-centre  connected  with  the  affected  nerve-trunks  escapes.  The  first 
branch  of  the  fifth  nerve  is  most  liable  to  be  affected.  This  neuralgia  fol- 
lows a  periodic  course.  Persons  over  forty  are  most  liable  to  be  affected  by 
it.  Usually  the  nerve-trunks  first  affected  are  the  ones  involved  in  suc- 
cessive attacks  ;  thus  if  a  certain  intercostal  nerve  is  the  seat  of  the  primary 
neuralgic  paroxysm,  at  each  subsequent  attack  this  particular  nerve  will  be 
the  seat  of  the  neuralgia. 

In  some  instances  chronic  malarial  infection  manifests  itself  by  hemor- 
rhages from  the  mucous  surfaces,  such  as  epistaxis,  hsematemesis,  haema- 
turia,  etc.  The  most  troublesome  cases  of  menorrhagia  (occurring  inde- 
pendent of  a  mechanical  cause)  often  recover  after  the  administration  of 
large  doses  of  quinine,  when  all  the  remedies  ordinarily  employed  in  such 
cases  have  failed  to  produce  the  desired  result. 

DiflPerential  Diagnosis. — The  first  question  that  now  arises  is  :  How  can  we 
decide  whether  the  manifestations  are  malarial  or  non-malarial  ?  In  the 
majority  of  cases  there  will  be  some  enlargement  of  the  spleen.  There  is 
not  necessarily  any  rise  in  temperature.  The  manifestations  will  be  more 
or  less  paroxysmal.  If  the  patient  has  localized  anaesthesia  or  hyper- 
esthesia, it  will  be  found  to  be  more  severe  at  some  particular  hour  in  the 
morning  or  evening.  If  the  patient  has  lost  power  over  one  portion  of  the 
body,  he  will  find  that  the  loss  of  power  is  more  marked  at  a  certain  period 
of  the  day.  The  patient  may  not  observe  this  periodic  tendency,  and  it  is 
frequently  elicited  only  after  careful  examination  and  close  questioning 
by  the  physician.  In  the  severer  cases  of  chronic  malarial  infection, 
when  there  is  hemiplegia  or  some  structural  change  affecting  the  mu- 
cous membrane  of  the  stomach,  intestines,  bronchial  tubes,  etc.,  there  are 


CHRONIC    MALARIAL   INFECTION.  855 

also  evidences  of  pigmentation  of  the  tissues.  Free  pigment  is  frequently 
found  in  the  blood. 

The  diagnosis  of  chronic  malarial  infection,  to  a  certain  extent,  depends 
upon  the  circumstances  which  attend  its  development.  If  the  individual 
has  repeatedly  suffered  from  malarial  paroxysms,  or  if  he  has  resided  for 
some  time  in  a  malarial  district  without  having  had  a  distinct  malarial 
paroxysm,  and  although  the  peculiar  malarial  cachexia  which  is  so  charac- 
teristic of  malarial  poisoning  is  not  present,  yet  it  is  always  well  to  carefully 
consider  the  question  of  malarial  infection. 

While  the  manifestations  of  chronic  malarial  poisoning  are  legion — and 
in  many  instances  they  very  closely  simulate  the  phenomena  of  other  dis- 
eases— still,  with  a  history  of  possible  malarial  exposure,  and  after  exclud- 
ing all  other  conditions,  we  determine  that  the  patient  is  suffering  from 
some  form  of  blood  poisoning,  and  then  the  nature  of  the  poisoning  is 
readily  determined.  In  very  doubtful  cases  one  may  confirm  an  uncertain 
diagnosis  by  treatment. 

Prognosis. — The  prognosis  in  chronic  malarial  infection  depends  ujion 
the  severity  of  its  manifestations,  and  the  degree  of  enlargement  of  the 
spleen  and  liver.  When  the  symptoms  are  mild  and  the  spleen  is  but 
slightly  enlarged,  and  when  neither  ascites  nor  oedema  of  the  lower  ex- 
tremities is  present,  the  prognosis  is  generally  good.  If  the  patient  is  very 
anaemic,  the  spleen  very  greatly  enlarged,  and  the  area  of  hepatic  dulness 
very  much  increased,  the  prognosis  is  unfavorable.  When  distinct  tumors 
can  be  detected  in  the  spleen  and  liver,  they  indicate  an  exceedingly  grave 
form  of  malarial  infection  ;  if  the  tumors  are  large,  they  can  rarely  be  re- 
duced. If  the  individual  in  whom  these  tumors  are  found  removes  from 
a  malarial  district,  a  long  time  may  elapse  before  they  very  much  interfere 
with  his  health  and  comfort. 

The  possibility  of  a  patient  being  able  to  take  up  his  permanent  residence 
in  a  non-malarious  region  must  be  taken  into  consideration  before  a  prognosis 
is  given  in  any  case.  So  long  as  such  a  patient  is  under  malarial  influences, 
however  slight,  the  progress  of  the  disease  cannot  be  permanently  arrested; 
and  when  the  manifestations  of  the  graver  forms  of  malarial  infection  are 
present,  there  is  little  prospect  that  the  disease  can  be  temporarily  relieved 
"while  he  remains  in  a  malarial  district. 

Treatment. — The  first  and  most  important  thing  to  be  accomplished  in 
the  treatment  of  chronic  malarial  infection  is  the  removal  of  the  individual 
from  a  malarious  district  to  a  high,  warm,  mountainous  region.  It  is  of 
the  greatest  importance  that  all  exposure  to  wet  and  cold,  and  the  damp  air  of 
the  evenings  and  nights,  should  be  avoided;  the  sleeping  apartments  must  be 
dry  and  airy,  and  flannel  should  be  worn  next  to  the  skin.  So  long  as  the 
thermometer  shows  even  a  slight  febrile  movement,  quinine  must  be  given 
in  full  doses.  If  anaemia  is  present,  iron  must  be  combined  with  the  qui- 
nine, and  administered  immediately  before  or  after  taking  food.  In  those 
cases  in  which  the  spleen  and  liver  are  very  much  enlarged,  when  no  febrile 
excitement  is  present,  iodide  of  iron  comhinedwith  cod-liver  oil  will  be  found 
of  great  service. 


856  ACUTE    GENERAL   DISEASES. 

It  is  claimed  by  some  that  muriate  of  ammonia  has  a  very  beneficial  effect 
in  this  class  of  cases,  but  my  own  experience  does  not  lead  me  to  favor  it 
One-half  an  ounce  of  Warburg's  tincture  taken  daily  for  ten  days,  two  hours 
before  breakfast  in  the  morning,  is  often  efficacious  when  quinine  fails.  If 
the  bowels  are  constipated,  aloes  or  rhubarb  should  be  given  in  connection 
with  some  of  the  saline  mineral  waters. 

In  those  cases  in  which  the  measures  already  referred  to  fail  to  produce 
any  improvement  or  afford  any  permanent  relief,  arsenic  may  be  resorted 
to,  but  the  effects  of  the  drug  must  be  carefully  watched,  and  on  the  ap- 
pearance of  oedema  or  of  gastric  disturbance,  it  must  be  promptly  discon- 
tinued. It  must  be  borne  in  mind  that  the  use  of  all  these  therapeutic 
agents  is  not  sufficient;  proper  attention  must  be  paid  to  hygienic  measures. 

The  neuralgiae  which  are  such  frequent  manifestations  of  this  infection 
are  best  treated  by  combining  a  full  dose  of  opium  with  large  doses  of  qui- 
nine. If  paralysis  is  a  manifestation  of  the  malarial  poisoning,  strychnine, 
iron  and  quinine  may  be  combined  in  its  treatment,  in  connection  with 
cold  douches  and  friction  to  the  paralyzed  limbs.  A  most  nutritious  diet 
and  a  liberal  use  of  good  wine  are  indicated  in.  all  cases.  The  daily  use  of 
brandy  in  small  quantities  is  often  of  great  service. 

In  regard  to  the  use  of  quinine  in  this  class  of  cases,  I  am  convinced  that 
its  indiscriminate  use  does  harm.  After  fairly  testing  its  effects,  if  no  relief 
is  obtained,  it  should  be  discontinued  for  a  time,  or  at  least  until  the  bene- 
ficial effect  of  a  removal  from  a  malarial  district  is  tried,  or  until,  by  the 
use  of  mild  cathartics  and  daily  administration  of  cod-liver  oil  and  iron,  the 
patient  is  in  a  condition  to  be  benefited  by  it.  Quinine  seems  to  have  no 
effect  upon  many  who  suffer  from  the  severe  manifestations  of  this  infection, 
so  long  as  they  remain  in  a  malarial  district,  but  as  soon  as  they  remove  to 
a  non-malarial  district  it  acts  promptly.  It  is  of  the  greatest  importance 
that  one  should  be  familiar  with  the  condition  in  which  quinine  is  indicated 
in  the  treatment  of  this  class  of  affections.  Avoid  depressing  remedies  in 
all  forms  of  chronic  malarial  infection  :  drastic  cathartics,  exhausting 
diaphoretics,  and  other  depressing  remedies  must  not  be  used.  They  do 
great  harm  by  exhausting  the  already  enfeebled  vital  powers.  Especially 
is  this  true  in  regard  to  the  free  use  of  mercurials,  which  are  so  commonly 
resorted  to  in  this  affection.  Unquestionably,  an  occasional  cathartic 
dose  of  calomel  is  of  service,  but  the  administration  of  small  doses  repeated 
after  short  intervals  to  produce  its  constitutional  effects,  will  always  be  fol- 
lowed by  the  more  serious  manifestations  of  the  malarial  infection. 

The  exhausted  system  of  this  class  of  patients  needs  rest,  concentrated 
nutrition,  and  the  influence  of  a  change  of  climate. 


SECTION  Y. 

CHEONIO  GENEEAL  DISEASES. 

1.  Eheumatism.  11.  Haemophilia. 

2.  Gout.  12.  Scurvy. 

3.  Diabetes.  13.  Purpura. 

4.  AnaBmia.  14.  Myxoedema. 

5.  Chlorosis.  15.  Scrofula. 

6.  Progressive  Pernicious  AnsBmia.        16.  Eickets. 

7.  Leucocythsemia.  17.  Alcoholism. 

8.  Pseudo- Leukemia.  18.  Trichinosis. 

9.  Addison's  Disease.  19.  Syphilis. 
10.  Ammonaemia. 

EHEUMATISM. 

Eheumatism  is  a  term  still  vaguely  used  to  cover  all  inflammatory  and 
painful  affections  of  the  fibrous  tissues  about  the  joints  and  in  the  muscles 
which  depend  upon  some  constitutional  morbid  state.  There  are  five  dis- 
tinct varieties  : — 

1.  Acute  Articular  Eheumatism,  or  Eheumatic  FsTer. 

2.  Sub-acute  Articular  Eheumatism. 

3.  Chronic  Articular  Eheumatism. 

4.  Arthritis  Deformans. 

5.  Muscular  Eheumatism,  "Myalgia." 

ACUTE    AKTICULAE    EHEUMATISM. 

Acute  articular  rheumatism,  or  rheumatic  fever,  is  the  most  acute  man- 
ifestation of  the  morbid  constitutional  state. 

Morbid  Anatomy. — The  blood  when  drawn  from  the  vessels  coagulates 
rapidly,  the  fibrin  Avhich  can  be  derived  from  it  is  in  excess  of  the  normal ; 
sometimes  it  reaches  ten  per  cent.,  and  it  is  readily  separated  from  the  other 
constituents.  The  number  of  red  discs  is  diminished  and  the  serum  is  al- 
kaline. 

The  joints  are  the  chief  points  of  attack  ;  yet  in  many  cases  where  they 
have  been  greatly  enlarged  and  excruciatingly  painful  during  life,  no  change 
has  been  detected  after  death.  The  synovial  membrane  is  usually  injected  ; 
the  capillaries  are  dilated,  and  the  reddening  is  best  marked  where  the  mem- 
brane joins  the  cartilage.  The  cells  of  the  synovial  fringes  multiply  ;  the 
epithelial  cells  are  enlarged  and  often  surrounded  by  fat.  The  lymphatics 
of  the  synovial  adventitia  are  enlarged  ;  and  the  cartilage-cells  proliferate 
and  the  fundamental  substance  segments.    'Sometimes  the  articular  carti- 


858  CHEONIC    GEENRAL   DISEASES. 

lages  are  cedematous.  Smail  hemorrhages  may  occur  in,  or  a  thin  fibrinous 
exudation  may  cover,  the  synovial  membrane.  The  ends  of  the  bones  have 
been  found  abnormally  vascular  in  a  few  cases.  Inflammatory  oedema  of 
the  peri-articular  tissues  is  very  common."  The  fluid  in  the  joint-cavity 
may  be  normal,  or  it  may  be  increased  in  amount  and  slightly  turbid.  ]?loc- 
culi  of  lymph  are  sometimes  seen  floating  in  it ;  and  at  times  it  contains  an 
abnormal  number  of  cell  elements.  These  elements  often  undergo  fatty 
change,  and  may  resemble  Gluge's  corpuscles.  The  color  of  the  fluid  varies  ; 
its  reaction  is  alkaline.  Albumen  and  fibrin  are  found  in  abundance.  Urate 
of  soda  is  never  found.  If  the  temperature  has  been  high,  the  liver  and 
other  internal  organs  may  show  cloudy  swelling,  or  parenchymatous  de- 
generation. 

Etiology. — Acute  rheumatism  may  be  regarded  as  a  constitutional  dis- 
ease,— "  a  specific  inflammation  of  joint  structures  attended  with  fever." 
Some  claim  that  there  is  an  excess  of  sulphur  in  the  blood  of  rheumatic 
patients ;  others  regard  the  disease  as  due  to  a  change  in  the  normal  rela- 
tions of  the  salts.  Another  view  is  that  lactic  acid — the  normal  product  of 
disassimilation  of  fibrous-tissue — accumulates  in  the  blood  in  excess  on  ac- 
count of  a  change  in  the  blood  salts,  consequent  upon  some  change  in  the 
albumen.^  It  is  a  disease  of  temperate  climates,  occurring  mostly  between 
December  and  March. 

There  is  an  hereditary  tendency  in  about  thirty  per  cent,  of  cases.  It 
attacks  persons  between  fifteen  and  thirty  oftener  than  those  of  any  other 
age.  In  old  age  it  is  exceedingly  rare.'  It  is  most  frequently  met  with  in 
those  exposed  to  wet  and  cold,  as  cabmen,  laborers,  and  maid-servants.  It 
attacks  men  oftener  than  it  does  women.  Insufiiciency,  or  a  j)oor  quality 
of  food,  and  prolonged  residence  in  a  damp  atmosphere  or  dwelling  predis- 
pose to  it. 

Any  impairment  of  the  general  health  from  defective  nutrition  renders 
one  more  liable  to  a  rheumatic  attack.  Erysipelas,  dysentery,  scarlatina 
and  gonorrhoea  are  named  among  its  exciting  causes.  Pregnancy  is  said 
to  have  caused  rheumatic  arthritis,  and  prolonged  lactation  may  induce  it. 
Scrofula,  phthisis,  and  cancerous  affections  so  often  precede  rheumatism 
that  a  connection  between  them  cannot  be  denied.  The  exciting  causes  in 
one  predisposed  to  it  are  exposure  of  the  unprotected  surface  to  sudden 
changes  of  temperature,  to  wit  :  cold  and  suddenly  checking  perspira- 
tion. 

Symptoms. — In  many  instances  dyspeptic  symptoms  precede  a  rheumatic 
attack,  which  usually  comes  on  suddenly  at  night.  A  distinct  febrile 
movement  may  precede  the  articular  symptoms  for  twenty-four  or  forty- 
eight  hours.  Uneasiness  and  restlessness,  a  vague  feeling  of  malaise,  or 
slight  and  indefinite  pain  in  the  joints  that  are  to  be  affected,  may  also 

J  Garrod  states  that  the  only  change  found  in  some  cases  is  a  lax  state  of  the  ligaments  and  opacity  of 
the  cartilages. 

"Richardson's  experiments  consisted  in  injection  of  lactic  acid  into  the  peritoneal  cnvity  of  a  cat.  The 
next  day  peri-  and  endocarditis  were  developed.  Canstatt  regards  the  articular  aflfection  as  the  result  of  it 
disturbance  of  innervation,  consequent  upon  peripheral  irritation  set  up  by  a  chill. 

»  Diseases  of  Old  Age.— Charcot  and  Loomis.    N.  Y.,  188],  pp.  150,  151. 


ACUTE   ARTICULAR    RHEUMATISM. 


859 


precede  its  development.  In  all  cases  there  is  aching  pain  and  stiffness  in 
some  one  of  the  larger  joints,  which  rapidly  increase  in  severity,  accom- 
panied by  a  rise  in  temperature  proportional  to  the  rapidity  of  the  develop- 
ment of  the  articular  symptoms  and  the  number  of  joints  involved.  The 
temperature  commonly  ranges  from  102"  to  103°  F.  ;  but  it  occasionally 


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Fig.  178. 

Temperature  Record  in  a  mild  case  of  Acute 

Rheumatism. 


Fig.  179. 

Tsmperatnre  Record  from  the  eighth  day  in  a 

fatal  case  of  Acute  Rheumatism. 


rises  to  105°  F.,  and  109°  and  110°  F.  have  been  reached  before  death  in 
severe  cases.  There  are  distinctly  marked  exacerbations  and  remissions, 
the  minimum  temperature  being  nocturnal.  The  pulse  is  full,  bounding 
and  compressible,  as  a  rule  keeping  pace  with  the  temperature  ;  it  often 
reaches  120  per  minute  independent  of  the  fever,  seemingly  on  account  of 
the  severe  pain. 

The  joints  attacked  become  red,  swollen,  and  so  tender  that  the  weight  of 
the  bed-clothes  cannot  be  borne,  nor  can  the  patient  bear  the  shaking  of 
the  bed  by  the  footsteps  of  attendants.  Fluctuation  can  soon  be  made  out 
in  those  joints  whose  situation  permits  examination.  Muscular  cramps 
usually  accompany  the  joint  symptoms.  The  face  is  flushed  and  the  body 
is  bathed  in  a  copious,  sour  smelling,  and  acid  sweat,  especially  about  the 
affected  joints.  Sudamina  are  common.  The  saliva  is  said  to  become 
acid,  and  inflammatory  fluids  poured  out  into  serous  cavities  during  rheu- 
matic fever  have  been  found  distinctly  acid  in  reaction.  There  is  great 
anxiety  and  restlessness,  but  the  sufferer  dares  not  move,  so  agonizing  is 
the  pain  in  the  joint. 

The  urinary  secretion  is  diminished,  its  color  being  darker  than  normal. 
On  cooling  it  deposits  a  brick-dust  sediment  of  urates.  Its  specific  gravity 
varies  from  1.025  to  1.030.     Urea  and  coloring  matter  are  in  excess,  while 


860  CHEONIC    GENERAL   DISEASES. 

the  chlorides  are  diminished.  Sulphates  and  albumen  are  not  infrequently 
found.  Uric  acid  is  increased.'  The  tongue  is  covered  with  a  thick 
creamy  fur.  There  is  anorexia  and  great  thirst,  the  bowels  are  usually 
constipated  and  the  fgeces  are  dry. 

The  large  joints  are  usually  involved  first.  The  joint  involvement  is 
remarkably  symmetrical  :  thus  one  ankle  joint  swells,  and  as  soon  as  this 
subsides  its  fellow  is  immediately  attacked,  and  the  affection  travels  rapidly 
from  one  joint  to  another  in  a  symmetrical  course.  There  is  little  oedema, 
pitting  or  cuticular  desquamation  after  the  acute  symptoms  have  subsided, 
except  in  the  very  weak  and  feeble.  As  a  rule,  one  joint  remains  swollen, 
for  three  or  four  days,  while  others  are  being  successively  involved.  By 
the  seventh  or  eighth  day  half  a  dozen  articulations  may  be  involved.  The 
hip-,  finger-  and  toe-joints,  the  spinal  articulations,  and  the  symphysis 
pubis  are  ral-ely  involved.  Not  infrequently  sudamina,  herpes  urticaria, 
and  miliaria  accompany  the  articular  symptoms. 

There  is  usually  little  mental  distui-bance  ;  but  when  the  temperature 
reaches  105°  F.  there  is  often  great  restlessness,  insomnia,  and  a  mild  wan- 
dering delirium.  I  regard  this  delirium  (when  not  occurring  in  drunk- 
ards) as  indicative  of  extensive  blood  changes  and  a  sign  of  great  danger. 
One  of  the  characteristics  of  rheumatic  fever  is  the  intense  auaemia  devel- 
oped in  a  few  days  after  its  onset,  even  when  no  antiphlogistic  remedies 
have  been  employed.  Auscultation  of  the  heart  reveals  ''blowing  "  hsemic 
murmurs,  even  when  no  cardiac  complications  exist.  The  articular  symp- 
toms often  subside  suddenly,  and  cardiac  or  cerebral  symptoms  as  suddenly 
make  their  appearance.  Cerebral  symptoms  are  always  attended  by  high 
temperature.  The  cerebral  and  cardiac  phenomena  are  not  due  to  a  metas- 
tasis in  the  strict  sense  of  the  term,  nor  yet  are  they  complications.  There 
is  some  bond  of  connection  between  these  cerebral  and  heart  lesions  and 
the  joint  affections, — the  exact  nature  of  the  connection  is  not  known.  The 
fibrous  tissue  of  the  heart  is  as  liable  to  be  involved  as  the  joints  ;  and  in 
many  young  subjects  the  heart  involvement  precedes  that  of  the  joints. 

Differential  Diagnosis.— ^The  connection  between  gout  and  rheumatism  is 
considered  under  the  head  of  gout. 

Pycemia  may  be  mistaken  for  rheumatic  fever  ;  but  the  recurring  chills, 
sickly,  siveet  breath,  slow  development,  jaundiced  skin,  previous  history, 
and  finally  the  presence  of  infarctions,  multiple  abscesses  and  thrombi  are 
sufficient  to  distinguish  pygemia  from  rheumatic  fever.  Suppurative  syno- 
vitis may  occur  in  pyaemia,  but  not  in  acute  rheumatism. 

JVow-rheumatic  arthritis  is  to  be  distinguished  by  its  persistence  in  one 
joint,  by  the  absence  of  the  characteristic  sweats,  by  the  graver  local  and 
more  trivial  constitutional  symptoms,  and  by  the  absence  of  cardiac  com- 
plications. 

Prognosis. — Apart  from  the  complications,  acute  polyarticular  rheumatism 
is  7iot  a  fatal  disease  ;  three  per  cent,  is  its  average  death  rate.  The  disease 
lasts  from  three  to  four  days  in  one  joint ;  the  whole  duration  of  the  fever 
and  attendant  arthritis  is  from  three  weeks  to  thirty  days.     The  rule  is  that 

'  Parkes  and  Garrod,  respectively,  found  thirteen  and  eleven  and  one-half  grains  in  a  quart  of  urine. 


ACUTE   ARTICULAR    RHEUMATISM.  8G1 

no  crippling  of  the  joints  follows  the  acute  attack.  If  the  course  of  the  dis- 
ease is  prolonged,  complications  are  usually  present ;  in  many  cases  its  course 
is  erratic  in  that  just  as  convalescence  is  apparently  established  all  the  acute 
symptoms  reappear.  It  runs  no  cyclical  course, — there  is  no  definite  limit 
to  its  duration  ;  patients  may  recover  in  two  or  three  days  or  a  week,  or  it 
may  persist  for  a  month  or  longer ;  generally  the  milder  the  attack  the 
shorter  its  duration.  I  have  seen  six  or  seven  weeks  elapse  before  the  joints 
have  returned  to  their  normal  state  ;  in  such  cases  all  the  joints  become 
involved  in  succession  and  the  articular  phenomena  are  persistent.  The 
more  robust  the  individual  the  sooner  is  convalescence  established.  Some- 
times the  fever  subsides  and  the  joint  affections  persist. 

.  The  frequent  occurrence  of  endo-  and  pericarditis  leaves  little  doubt  as  to 
their  intimate  connection  with  the  rheumatism.  The  younger  the  subject 
the  more  liable  are  the  cardiac  affections  to  occur.  Statistics  are  most  di- 
verse on  this  point ;  some  say  five,  others  seventy-five  per  cent,  of  all  cases 
of  rheumatic  fever  are  accompanied  by  cardiac  inflammations.  Endarteri- 
tis, pleurisy,  pneumonia,  cerebral  and  spinal  meningitis,  laryngitis,  bron- 
chitis and  peritonitis  are  its  principal  complications.  A  strange  sequel  of 
rheumatic  fever  is  chorea. 

Another,  graver,  sequel  is  ulcerative  endocarditis.  Instead  of  comiDlete 
recovery  acute  rheumatism  may  become  subacute  or  chronic.  Muscular 
rheumatism  frequently  follows  an  attack  of  acute  articular  rheumatism. 
The  worst  legacy  acute  rheumatism  leaves  is  a  crippled  valvular  apparatus 
in  the  heart.  ^ 

Treatment. — The  hygienic  surroundings  of  rheumatic  patients  should  be 
yery  carefully  attended  to.  The  temperature  of  the  apartment  should  range 
from  68°  to  70°  F. ;  all  draughts  should  be  avoided,  and  the  patient  should 
be  clothed  in  flannel  and  covered  with  flannel  sheets.  The  diet  should  be 
milk  and  seltzer- water.  If  this  is  not  well  borne,  concentrated  food,  other 
than  animal,  can  be  given.  Animal  food  and  alcoholic  stimulants  are  con- 
traindicated  during  the  active  period,  of  the  disease.  As  soon  as  the  fever 
declines,  nutritious  and  easily  digested  animal  fOod  may  be  freely  given. 

Only  a  few  of  the  many  external  applications  which  have  been  made  to 
the  affected  joints  will  be  referred  to.  Cold  by  the  means  of  ice-bags  to 
the  joints  has  been  strongly  recommended.  Friction,  with  chloroform  or 
opium  in  glycerine  combined  with  alkalies  and  the  tincture  of  aconite  is  a 
favorite  plan  with  some.  ''Hot-packs"  by  means  of  flannel  compresses 
wrung  out  in  water  as  hot  as  the  patient  can  bear,  or  bathing  the  joints  in 
warm  laudanum  and  then  covering  them  with  oiled  silk  is  always  grateful 
to  the  patient.  Wunderlich  and  Niemeyer  advocate,  respectively,  ethyl 
chloride  and  ether  to  be  rubbed  over  the  affected  joints.  The  "  blister 
plan,"  which  consists  in  surrounding  all  the  affected  joints  with  fly  blisters, 
temporarily  relieves  the  pain,  but  the  rheumatic  attack  is  not  shortened, 
nor  do  they  afford  any  permanent  benefit.     My  experience  leads  me  to  the 

'  Two  casesof  acute  rheumatism  wore  recently  (July  31st,  ]882)  reported  by  Mayer  in  "Henoch's  Klinilc," 
where  peculiar  and  piKnificunt  complications  were  observed.  The  patients  were  children  ;  and  both  had 
little.  tnm/>rs  develop  about  the  joints  (malleoli,  elbo\v,  etc.),  that  on  section,  after  death,  proved  to  be  con- 
nective-tissue neoplasms  which  had  a  tendency  to  necrobiosis  or  to  osseous-like  change. 


862  CHRONIC    GENERAL    DISEASES. 

opinion  that  if  the  affected  joints  are  protected  from  changes  of  tempera- 
ture by  cotton  batting  and  oiled  silk,  all  is  accomplished  that  can  be  by 
local  applications. 

Internal  Medication. — Innumerable  remedies  have  been  brought  to  the 
notice  of  the  profession  as  specifics  in  the  treatment  of  rheumatism,  yet  it 
is  still  the  most  unmanageable  of  all  diseases.  Garrod  is  of  the  opinion 
that  colored  water  is  about  as  potent  as  anything.  He  claims  that  rheu- 
matic fever  is  a  "  self-limiting  disease,"  sometimes  running  a  long,  some- 
times a  short  course.  Bleeding,  mercury,  and  antimony  and  mercury  are 
no  longer  employed.  Some  advocate  the  use  of  iodide  of  potassium  ;  some 
colchicum,  some  veratria,  some  guaiacum,  and  some  quinine.  Garrod's 
"  quino-alkaline  "  plan,  which  combines  quinine  with  the  alkaline  treat- 
ment, is  a  favorite  method  with  many.  It  is  claimed  that  the  so-called 
alkaline  treatment  shortens  its  duration  and  diminishes  the  frequency  of 
cardiac  complications.  It  consists  in  the  administration  of  the  soda  salts 
in  from  3v  to  3x  daily  until  the  urine  becomes  alkaline. 

My  experience  inclines  me  to  the  opinion  that  while  alkalies  in  the  early 
stages  relieve  the  pain  in  the  Joints,  they  do  not  shorten  the  duration  of 
acute  rheumatism,  and  if  long  continued  they  do  positive  harm.'  The 
tincture  of  the  chloride  of  iron,  in  one-half  drachm  doses,  is  especially  ser- 
viceable as  soon  as  the  temperature  reaches  100°  F.  Within  the  past  few 
years  salicin,  salicylate  of  soda,  and  salicylic  acid  have  been  very  exten- 
sively employed.  It  is  claimed  that  immediate  relief  follows  the  adminis- 
tration of  the  salicylates — that  the  temperature  falls,  that  the  pain  and 
swelling  of  the  joints  subside,  and  that  the  duration  of  severe  attacks  has 
been  limited  to  thirty-six  or  forty-eight  hours.  But  it  causes  great  depres- 
sion of  the  heart,  increases  the  liability  to  cardiac  complications,  causes 
irritability  of  the  stomach,  and  places  the  patient  in  a  weak  and  debilitated 
state  ;  for  the  past  year  I  have  seldom  employed  it,  for  my  experience 
shosvs  that  while  in  some  cases  it  may  relieve  the  urgent  symptoms  of  the 
disease  in  two  or  three  days,  relapses  are  almost  certain  to  follow,  and  the 
duration  of  the  disease  is  not  shortened,  and  I  have  seen  very  serious  toxic 
effects  follow  its  use.  Benzoic  acid  and  benzoate  of  soda  are  claimed  by 
some  to  act  more  efficiently  than  salicylic  acid  and  to  be  less  harmful.  I 
have  not  seen  any  good  results  follow  their  use. 

My  plan  of  treatment  in  a  severe  articular  rheumatism,  after  regulating 
the  hygienic  surroundings  and  the  diet  as  already  indicated,  is  to  render 
the  urine  neutral  by  the  free  administration  of  the  carbonate  of  potash  or 
soda,  and  to  administer  regularly  every  six  hours,  sufficient  morphia  hypo- 
dermically  to  relieve  pain  and  to  keep  the  patient  comfortable.  If  this 
plan  is  judiciously  followed  until  the  acute  rheumatic  symptoms  subside, 
and  the  patient  then  placed  on  iron  and  cod-liver  oil,  I  am  confident  it 
will  recommend  itself  to  every  unprejudiced  observer.  The  treatment  of 
the  various  complications  is  considered  under  their  appropriate  heads. 

1  Gull,  Sutton,  and  Lebert  found  marked  diminution  in  the  duration  of  rheumatism  from  steady 
administration  of  lemon  juice. 


OHEOSriC    ARTICULAR   EHEUMATI8M.  863 


SUB-ACUTE    RHEUMATISM. 

Sub-acute  rheumatism  is  usually  a  sequela  of  acute,  or  occurs  in  one  who 
has  at  some  time  had  an  acute  attack  ;  it  is  attended  by  slight  if  any  fever  ; 
the  pain  in  the  joints  is  not  severe,  except  on  motion  ;  and  the  swelling  and 
redness  are  not  excessive,  and  are  limited  to  one  or  two  joints,  usually  the 
large  ones.  There  is  no  tendency  to  disorganization  or  permanent  crip- 
pling of  the  affected  joints ;  and  although  it  may  last  six  or  seven  weeks, 
or  three  or  four  months,  the  joints  usually  return  to  their  normal  condi- 
tion. The  blood  changes  are  the  same  as  in  acute.  The  articular  symjD- 
toms  are  less  metastatic  than  in  acute  ;  angemia  is  always  well-marked,  and 
cardiac  complications  are  not  infrequent.'  The  treatment  is  a  milk  diet, 
iron  and  cod-liver  oil,  and  a  warm  climate,  and  heat  to  the  affected  joints. 
The  so-called  anti-stimulants  have  failed  in  my  hands  to  relieve  or  cure. 

CHRONIC    ARTICULAR    RHEUMATISM. 

Chronic  articular  rheumatism  usually  involves  only  a  few  joints  ;  it  oc- 
curs most  frequently  in  those  who  have  had  rheumatic  fever  in  early  life. 
Although  it  may  be  of  long  duration  it  rarely  induces  extensive  changes  in 
the  joints. 

Morbid  Anatomy. — The  parts  affected  are  the  iibrous  tissue  around  the 
joints,  the  fibrous  envelopes  of  the  nerves,  the  aponeurotic  sheatlis  of  the 
muscles,  the  fasciae,  and  the  periosteum.  The  synovial  membrane  is  thick- 
ened, the  fringe-like  processes  are  hypertrophied  and  very  vascular,  and 
the  synovial  fluid  becomes  turbid  and  cloudy.  The  ligaments  are  thick- 
ened, the  cartilages  relaxed,  shaggy,  and  sometimes  in  a  state  of  fatty  de- 
generation. The  more  protracted  the  disease  the  greater  the  thickening  of 
the  peri-articular  structures,  and  the  thicker  and  scantier  will  be  the  fluid 
in  the  joint.  The  fibrous  tissue  developed  about  the  joints  causes  more  or 
less  stiffness  and  loss  of  motion,  but  not  ankylosis. 

Etiology. — It  is  a  disease  of  adult  and  advanced  life,  occurring  oftenest 
in  those  whose  hygienic  surroundings  are  bad,  and  who  are  exposed  to  wet, 
cold,  or  sudden  changes  of  temperature.  A  residence  in  dark  and  damp 
dwellings  predisposes  to  it.  Previous  attacks  of  acute  articular  rheuma- 
tism develop  a  tendency  to  chronic  rheumatism.  It  is  often  hereditary,  and 
then  there  may  be  no  appreciable  exciting  cause  to  its  development.  Both 
sexes  are  equally  liable. 

Symptoms. — There  is  aching  and  constant  pain  in  some  one  or  more  of 
the  larger  joints,  usually  the  knee  or  ankle,  but  sometimes  those  of  the 
upper  extremities.  The  affected  joints  are  tender  and  slightly  swollen,  and 
their  movements  are  constrained.  No  fever  is  present.  The  aching  and 
deep-seated  pains  are  often  worse  at  night.  When  it  is  the  result  of  expos- 
ure, heat  will-  give  a  grateful  sense  of  relief ;  when  a  rheumatic  diathesis 
exists,  the  heat'  of  the  warm  bed-clothes  increases  the  pain,  and  relief  is 

I  Barwell,  who  calls  this  disease  "  Sub-acute  Eheumatic  Synovitis,"  says  it  may  lead  to  hydrops  articuli. 
—Diseases  of  the  Joints,  1881,  p.  138,  et  neq. 


8b4  CHRONIC    GENERAL   DISEASES. 

often  obtained  by  exposure  of  the  joint  to  dry  cold.  Old  people  with  rheu- 
matic Joints  are  great  "weather  prophets,"  often  being  able  to  foretell  the 
coming  of  a  storm.  After  rest,  motion  gives  great  pain,  but  use  renders 
the  joint  temporarily  more  supple  and  less  painful.  The  pains  undergo 
exacerbations  and  remissions,  and  the  disease  may  continue  for  years  with- 
out causing  much  deformity  or  great  crippling  of  the  joints.  The  muscles 
near  the  joint  usually  undergo  more  or  less  atrophy,  and  as  a  result  the  af- 
fected joints  appear  larger  than  they  really  are. 

Palpation  may  reveal  fluctuation  in  the  joint,  and  auscultation  gives  a 
rough,  grating  crepitus  during  motion. 

Differential  Diagnosis. — Chronic  articular  rheumatism  may  be  distin- 
guished from  arthritis  deformans  by  the  absence  of  deformity  of  the  af- 
fected joints,  the  history  of  previous  acute  rheumatic  attacks,  the  large 
joints  being  mainly  involved,  the  partial  or  complete  recovery  during  warm 
weather,  and  its  return  on  exposure  to  wet  and  cold  ;  arthritis  deformans 
is  a  steadily  progressive  disease,  one  joint  after  another  being  involved  and 
never  recovered  from. 

Prognosis.— There  is  little  chance  of  complete  recovery  after  middle  life  ; 
it  is  only  possible  in  those  cases  treated  at  the  onset  under  favorable 
hygienic  conditions.  In  long-standing  cases,  wasting  of  the  muscles  may 
lead  to  great  crippling  of  the  joint.  Muscular  rheumatism  is  a  frequent 
accompaniment  of  articular.  Chronic  rheumatism  never  affects  the  dura- 
tion of  life,  except  as  it  may  deprive  the  patient  of  exercise  and  sleep,  and 
thus  interfere  with  nutrition. 

Treatment. — This  form  of  rheumatism  is  benefited  mostly  by  local  treat- 
ment, such  as  blisters,  iodine,  belladonna,  aconite,  opium,  and  chloroform 
liniments,  veratrum  ointment,  etc.,  etc.  Most  rheumatic  patients  have 
their  favorite  prescriptions  for  local  use,  which  they  claim  afford  them 
almost  instant  relief.  If  there  is  but  little  pain  in  the  joints,  ammonia 
and  turpentine  liniments  are  of  service.  Thick  flannels  should  always  be 
worn  about  the  joints.  Some  advocate,  for  both  pain  and  stiffness,  spong- 
ing the  joints  with  hot  water.  The  Galvanic  or  Faradic  current  will  tem- 
porarily reduce  the  swelling  and  pain,  and  sometimes  improves  the  mobility 
of  the  joint.  Local  or  general  baths  form  an  essential  part  in  the  treat- 
ment of  this  form  of  rheumatism.  Hot  air,  or  vapor  baths  are  not  so 
efficacious  as  hot  water.  Many  of  the  hot  saline  springs  for  bathing  have 
acquired  a  great  reputation  in  the  treatment  of  this  form  of  rheumatism, 
cures  being  effected  in  cases  that  had  resisted  all  other  methods  of  treat- 
ment.' Massage  and  rubbing  are  always  beneficial  ;  and  undoubtedly 
much  of  the  good  that  is  claimed  for  certain  liniments  is  due  to  the  rub- 
bing and  manipulation  of  the  joints  during  their  application. 

Internally,  tonics  should  be  employed,  such  as  iron,  quinine,  strychnine, 
etc.  Cod-liver  oil  is  the  most  useful  of  all  internal  remedies,  and  should 
be  administered  continually.  All  the  means  for  improving  the  general 
health  of  the  patient  should  be  carefully  considered,  and  if  possible  he 

1  Those  which  I  have  found  most  efficacious  in  this  country  are  the  Hot  Springs  of  Arkansas,  the  Vir- 
ginia Hot  Springs,  and  the  Richfield  Springs  in  New  York  State. 


ARTHEITIS   DEFORMANS.  865 

should  reside  in  a  dry,  warm  climate.  Colchicum,  arsenic,  iodide  of  po- 
tassium, and  guaiacum  have  gained  reputation  in  its  treatment,  as  have 
also  the  turpentine  and  cajeput  oils  combined  with  sulphur ;  but  I  have 
been  unable  to  find  sufficient  proofs  of  their  beneficial  effects  to  strongly 
recommend  their  use.  Recently,  Rawson  advises  guarana,  and  Heller 
liquor  ammonii.* 

The  diet  must  be  highly  nutritious  and  absolutely  non-stimulating ;  I 
am  convinced  that  errors  in  diet  and  ''fits  of  indigestion"  prolong,  and 
are  powerful  to  develop  this  disease.  Exercise  is  important,  and  if  pos- 
sible a  sea  voyage  in  a  warm  climate  should  be  taken. 

ARTHRITIS    DEFORMAlSrS. 

{Bheumatoid  Arthritis.) 

Arthritis  deformans  is  a  chronic  inflammation  of  the  synovial  capsule, 
the  ligaments  and  tissues  of  the  joint,  unattended  by  suppuration  and  with 
little  fluid  accumulation  in  the  articular  cavity. 

Morbid  Anatomy, — The  synovial  membrane  and  articular  cartilages  are 
first  involved.  The  fringes  of  the  former  are  increased  in  number,  and 
are  very  vascular  :  they  are  called  "the  destructive  vegetations"  of  the 
synovial  membrane.  The  central  portion  of  the  articular  cartilages  be- 
comes roughened  or  villous,  gets  gradually  worn  down,  and  finally  disap- 
pears, and  the  bones  thus  laid  bare  undergo  eburnation.  The  ivory-like 
surfaces  are  striated,  the  strise  running  in  the  direction  of  the  articular 
movements.^  While  the  central  portion  of  the  cartilage  is  disappearing, 
its  margin  forms  nodular  irregular  outgrowths.  The  synovial  fringes  take 
part  in  the  hypertrophic  processes,  and  form  pyriform  excrescences,  which, 
after  a  time,  become  converted  into  fibrous  tissue.  These  outgrowths  in 
some  cases  blend  with  the  osseous  structure  of  the  epiphysis,  and  in  others 
become  detached  and  are  free.  Lateral  expansion  of  the  joint  surfaces 
with  enlargement  of  the  ends  of  the  bones  takes  place  and  leads  to  de- 
formity, dislocation,  and  immobility.  All  the  joints  may,  in  course,  be 
involved,  especially  those  of  the  hands  and  feet.  The  thickened  ligaments 
sometimes  undergo  partial  cartilaginous,  osseous,  or  fatty  degeneration. 

The  tendons  are  sometimes  thinned  and  ossified.  The  fluid  in  the  joint 
cavity  is  thick,  turbid  and  yellow,  and  alkaline  in  reaction.  There  are  no 
blood  changes  ;  no  urates  are  found  in  the  joints.  The  adjacent  muscles 
undergo  atrophy. 

Etiology. — This  disease  is  regarded  by  some  as  a  peculiar  form  of  chronic 
rheumatism,  while  others  regard  it  as  an  essentially  different  disease.  It 
may  occur  at  any  age ;  but  the  tendency  to  it  increases  with  advancing 
years.  Women  are  more  liable  to  it  than  men.  The  smaller  joints  are 
most  often  involved  in  women  ;  the  larger  in  men.  It  is  very  rare  in  dry, 
hot  climates.      Damp  dwellings,  poor  food,  and  mental    depression  are 

'  Wien.  Med.  Presse,  Dec,  1875. 

*  Charcot  calls  ebumatiou  a  "  sclerosis  of  bone,  accompanied  by  vascularization  of  the  deep  parts." 
55 


866 


CHEONIC   GENERAL   DISEASES. 


powerful   predisposing  causes.     Thin  people  suffer  oftener  than  the  cor- 
pulent.    It  is  met  with  of tenest  in  the  poorer  classes. ' 

Symptoms. — The  symptoms  of  arthritis  deformans  are  all  referable  to 
the  changes  which  occur  in  the  joints.  It  may  come  on  insidiously,  neu- 
ralgic pains  sometimes  preceding  stiffness  and  deformity.  As  the  soft 
parts  atrophy,  the  joints  stand  out  distorted  and  rigid  from  the  flabby  mus- 
cular surroundings.  There  are  usually  severe  inflammatory  symptoms, 
the  joints  are  only  slightly  tender  to  pressure,  but  motion  always  gives 
pain.  Months  and  years  may  elapse  before  the  articular  changes  are 
completed  ;  but  once  started,  they  are  progressive,  until  the  joint  is  anky- 
losed  or  deformed.^  The  immobility  of  the  joints  depends  upon  the 
osteophytes  or  fibro-cartilaginous  transformation  of  the  synovial  mem- 
brane or  fibrous  union  of  the  surfaces  of  the  bared  bone. 

In  some  cases  the  disease  begins  with  all  the  signs  of  rheumatic  fever, 

with  inflammatory  symptoms  of  a  mild 
type.  No  cardiac  signs  are  present, 
and  no  excess  of  uric  acid  can  be 
found  in  the  Uood.  The  acute  symp- 
toms gradually  subside,  leaving  the 
joint  irreparably  crippled.  The  small 
joints  are  usually  first  involved.  The 
metacarpo-phalangeal  articulations  of 
the  index  and  middle  fingers  are 
usually  first  attacked.  In  forty-five 
cases,  the  smaller  joints  of  the  hands 
and  feet  alone  were  involved  in  twenty- 
five  ;  the  great  toe  in  four  ;  the  hands 
and  feet  with  a  large  joint  in  seven  ; 
the  large  joint  first,  then  the  fingers  in 
nine.  After  a  time  large  joints,  the 
temporo-maxillary  articulation,  or  the 
articular  "processes  of  the  vertebrae, 
especially  the  cervical,  become  involved. 
The  hip,  shoulder,  elbow,  knee,  and 
hands  are  its  favorite  sites.  In  many 
joints  abnormal  mobility  is  developed, 
i.  e.,  the  hip  may  slip  up  and  down  in 
its  socket.  Subluxations  are  common, 
in  the  fingers  especially. 

Early  in  the  disease  a  friction  crepi- 
tus is  heard  as  the  articular  surfaces 
are  rubbed   upon   each  other,  which  becomes  coarser  as   the  disease  ad- 
vances.    There  are  painful  spasms  of  the  muscles  in  the  affected  limb, 
more  marked  at  night  and  just  before  a  storm.     When  the  disease  is  local- 

1  Charcot  advocates  a  nervous  origin,  especially  when  it  begins  in  the  smaller  joints.  Barwell  regards 
it  as  due  to  colitis,  originating  in  "  some  constitutional  cachexia,"  which,  in  some  of  its  tendencies,  re- 
eembles  the  rlieumatic  diathesis. 

^  Kemak  believes  that  the  painful  swellings  on  either  side  of  the  Joint  are  "  neurotic  nodes," 


Fig.  180. 
Deformity  from  Articular  Rheumatism. 


ARTHRITIS   DEFORMAiTS.  8G7 

ized  in  the  hip  joint,  it  has  been  called  "morbus  coxge  senilis."  In  such 
cases  the  limb  is  shortened  and  the  patient  limps.  The  greatest  variety  of 
deformity  takes  place  in  the  hands  of  those  who  have  been  long  the  sub- 
jects of  this  disease.  The  constitutional  disturbance  is  never  commensur- 
ate with  the  local  signs.  The  skin  becomes  dry  and  harsh  ;  there  is  great 
acidity  of  the  stomach,  cold  extremities  and  a  condition  of  extreme  anse- 
mia.* 

Differential  Diagnosis. — Arthritis  deformans  may  be  mistaken  for  chronic 
articular  rheumatism  without  deformity,  and  chronic  gout. 

Gout  is  hereditary,  and  occurs  more  in  males.  Arthritis  deformans  is 
rarely  hereditary,  and  occurs  oftenest  in  females.  Attacks  of  gout  are 
periodic,  and  the  small  joints  are  found  involved.  Arthritis  is  progressive, 
and  the  large  joints  are  generally  first  attacked.  Kidney  complications  are 
common  in  gout  and  rare  in  arthritis.  Chalk-stones  develop  in  the  joints  in 
gout  and  are  never  present  in  arthritis.  Uric  acid  is  always  in  excess  in 
gout,  and  never  in  arthritis  ;  deformities  and  ankyloses  are  less  marked  and 
extensive  in  gout  than  in  arthritis. 

Prognosis. — Arthritis  deformans  never  destroys  life,  and  is  never  recovered 
from  ;  patients  with  this  disease  may  attain  very  old  age.  The  greater 
the  number  of  joints  involved  the  more  deplorable  will  become  the  condi- 
tion of  the  patient.  There  is  rarely  complete  ankylosis.  When  false  joints 
form  there  is  a  possibility  that  such  patients  may  walk  or  move  about  with 
comfort.'^ 

Treatment. — Treatment  of  this  disease  is  very  unsatisfactory ;  for  the 
most  part  we  must  trust  to  local  measures  for  relief,  and  to  such  constitu- 
tional measures  as  shall  improve  the  general  health.  Quinine,  iron,  cod- 
liver  oil,  arsenic  and  strychnia  are  indicated.  The  diet  should  be  nutri- 
tious and  easily  digestible.  Alcoholic  stimulants,  if  they  improve  nutrition, 
are  of  service.  Change  of  climate  and  habits  of  life  is  often  followed  by 
an  arrest  in  its  progress.  Flannels  should  always  be  worn  next  the  skin. 
Mineral  waters  and  warm  salme  baths,  either  artificial  or  natural,  often 
temporarily  arrest  its  progress  and  relieve  the  pain  in  the  joints.  The 
preparations  of  indi^ie  and  the  acute  rheumatism  and  gout  remedies  have 
seemed  to  me  to  do  more  harm  than  good.  Local  frictions  with  iodine, 
mercury,  and  iodoform  sometimes  relieve.  If  the  pain  is  so  severe  as  to  pre- 
vent sleep,  it  must  be  relieved  by  anodynes.  Great  care  must  be  exercised 
in  their  use  that  the  patient  does  not  become  addicted  to  them.  The  con- 
stant or  Faradic  current  may  be  cautiously  tried ;  in  many  cases  it  is  of 
great  benefit.'  The  parts  should  be  moved  as  much  as  possible  if  the 
joints  are  not  painful.  In  the  so-called  acute  attacks  rest  is  necessary ; 
and  then  leeches  and  blisters  to  the  joints  are  indicated. 

'The  orly  vrlnary  change  is  diminution  in  the  amount  of  phosphoric  acid  by  nearly  fifty  per  cent.— 
{Drachnuinn.) 

2  Charcot  describes  numerous  cases  complicated  by  asthma,  megrim,  cystitis,  and  such  skin  diseases  as 
eczema,  Tiummnlar  psoriasis,  lichen,  and  arthritic  prurigo  ;  but  these  complications  are  the  result  of  the 
long  confinement  and  inability  to  excercise,  rather  than  necessary  sequelae. 

*  Bemak  and  AUhaua. 


868  CHRONIC   GENERAL   DISEASES. 

MTJSCULAE    RHEUMATISM. 

{Myalgia.) 

Muscular  rheumatism  is  a  rheumatic  affection  of  the  voluntary  muscles, 
the  fasciae,  periosteum,  and  other  fibrous  structures,  accompanied  by  pain 
and  tenderness,  but  by  no  other  evidences  of  inflammation.  It  has  been 
named  according  to  its  seat,  torticollis  (wry-neck),  cephalalgia,  pleurodynia, 
lumbago,  etc.,  etc' 

Morbid  Anatomy. — The  negative  results  of  autopsies  lead  to  the  conclu- 
sion that  there  are  no  constant  anatomical  lesions,  except  those  due  to 
transient  hypersemia,  or  to  scanty  serous  exudations  into  the  mugcles.  In 
a  few  cases  there  is  evidence  of  inflammation  of  the  fibrous  sheath  of  the 
muscles  and  of  muscle-degeneration.  Thickenings  and  adhesions  of  the 
neurilemma  of  the  nerves  supplying  muscles  that  have  long  been  subject 
to  chronic  rheumatism  have  been  found. 

Etiology. — Muscular  rheumatism  is  not  uncommon  in  the  children  of 
the  gouty  or  rheumatic.  It  is  often  intimately  associated  with  articular 
rheumatism,  which  sometimes  precedes,  sometimes  follows  it.  Exposures 
to  cold  and  damp  draughts  are  often  the  exciting  causes  of  an  attack,  es- 
pecially after  the  muscles  have  been  over-fatigued.  Sudden  straining  of 
a  muscle  may  induce  it.  It  often  seems  to  have  a  malarial  origin.  It  may 
come  on  suddenly  in  a  rheumatic  or  gouty  subject  without  any  appreciable 
exciting  cause. 

Symptoms. — An  attack  usually  comes  on  suddenly  with  severe,  deep-seated 
pain  in  the  group  of  muscles  affected.  The  pain  is  of  a  stretching  or  tearing 
character,  increased  by  movement  or  pressure  ;  it  is  always  more  severe  at 
night,  and  remits  or  disappears  during  the  day.  It  may  be  migrating  or 
remain  fixed  in  certain  muscles  or  fasciae.  It  is  usually  acute  when  the 
muscle  is  in  action,  and  dull  when  the  parts  are  at  rest.  Certain  positions 
mitigate  the  pain.  In  many  instances  it  will  wholly  disappear  in  a  few  mo- 
ments, and  the  sufferer,  who  perhaps  has  been  for  hours  enduring  excrucia- 
ting cramp-like  pain,  feels  a  sudden  sense  of  relief.  Such  attacks  are  fol- 
lowed by  lassitude. 

Lumbago,  pleurodynia,  and  wry-nech  are  the  most  common  forms. 

Lumbago,  or  rheumatism  of  the  muscles  on  either  side  of  the  lumbar 
spine,  usually  is  the  result  of  straining  the  lumbar  muscles,  or  sitting  on 
the  damp  ground,  or  is  excited  by  a  current  of  air  across  the  back.  The 
patient  is  unable  to  bend  backward  or  forward  ;  if  the  pain  comes  on  while 
he  is  in  a  sitting  posture,  he  is  compelled  to  walk  with  the  body  bent  at 
the  hips.  Lumbago  comes  on  very  suddenly,  and  the  pains  are  more  in- 
tense than  in  any  other  form. 

Intercostal  rheumatism,  ox  pleurodynia,  is  attended  by  many  of  the  symp- 
toms of  acute  pleurisy.     There  is  pain  in  the  side,  which  is  increased  by 

1  These  different  varieties  are  grouped  by  some  in  the  list  of  the  symptoms  of  chronic  rheumatism; 
others  regard  them  as  neuralgias. 


MUSCULAE   RHEUMATISM.  869 

every  respiratory  movement ;  the  sufferer  leans  to  the  affected  side.    Cough- 
ing, sneezing  and  defecation  render  the  pain  more  intense. 

In  wry-nech  the  muscles  on  one  side  of  the  nape  of  the  neck  are  involved. 
The  patient  holds  his  head  toward  the  muscles  that  are  affected,  so  as  to 
relax  them,  and,  in  attempting  to  turn  his  liead,  turns  his  whole  body  like 
a  pivot. 

If  the  frontal,  occipital,  or  temporal  muscles  are  involved,  it  is  termed 
rheumatic  cephalalgia. 

If  the  abdominal  muscles  are  involved,  it  is  termed  abdominal  rheumO' 
tism.  In  all  cases  there  is  ^am  and  rigidity  of  the  muscles  or  groups  of 
muscles  involved,  accompanied  by  a  fixed  position.  There  is  no  fever  or 
constitutional  symptoms. 

Differential  Diagnosis. — Lumbago  may  be  mistaken  for  renal  colic. 

In  renal  colic  there  is  no  tenderness  on  either  side  of  the  lumbar  spine, 
which  is  always  present  in  lumbago.  The  position  of  the  patient  is  not 
fixed  as  in  lumbago.  In  renal  colic  the  pain  radiates  along  the  ureter,  to 
the  end  of  the  penis,  and  is  often  accompanied  by  retraction  of  the  testicle 
on  the  .^^ected  side.  The  urine  is  diminished  during,  and  copious  and 
bloody  after,  the  attack. 

An  examination  per  vaginam  will  decide  between  uterine  disease  and 
lumbago. 

Lumbago  may  be  distinguished  from  disease  of  the  spine  by  the  fact  that 
in  the  latter  affection  pressure  on  the  ends  of  the  spines  will  produce  pain, 
while  lateral  pressure  gives  negative  results  ;  in  rheumatism  of  the  muscles 
the  reverse  is  the  case. 

Pleurodynia  may  be  mistaken  for  pleurisy  and  intercostal  neuralgia. 
Pleurisy  is  accompanied  by  fever,  increased  pulse-rate,  cough  and — on 
physical  examination — by  physical  signs  of  pleurisy.  None  of  these  condi- 
tions are  present  in  pleurodynia.  In  intercostal  neuralgia  there  are  three 
(diagnostic)  points  of  tenderness  :  at  the  exit  of  the  nerve  from  the  spine ; 
at  its  termination  near  the  sternum;  and  midway  between  these  points,  while 
there  is  no  tenderness  over  the  muscles.  In  pleurodynia  these  points  of 
tenderness  are  absent,  and  the  intercostal  muscles  are  tender. 

Abdominal  rheumatism  may  be  mistaken  for  peritonitis  ;  but  in  perito- 
nitis there  will  be  fever,  increased  pulse-rate,  and  well-marked  constitu- 
tional symptoms  which  are  absent  in  abdominal  rheumatism.  In  the  lat- 
ter, deep,  firm  pressure  affords  relief. 

Trichinosis  is  accompanied  by  symptoms  that  resemble  those  of  muscular 
rheumatism  ;  but  the  history  of  the  case,  the  oedema  of  the  feet,  and  a 
microscopical  examination  of  a  portion  of  the  muscle,  will  decide  the  diag- 
nosis. 

Prognosis. — No  danger  attends  this  form  of  rheumatism.  An  acute  at- 
tack may  last  a  few  hours  or  days.  If  it  become  chronic,  the  muscular 
pains  may  last  for  months.  Wry-neck  is  the  mildest  and  lumbago  the  se- 
verest variety.     One  attack  generally  favors  the  occurrence  of  a  second. 

Treatment. — In  the  young,  if  there  is  an  hereditary  tendency  to  rheuma- 
tism, cod-liver  oil  acts  as  a  prophylactic.     At  the  commencement  of  an  at- 


870  •  CHEONIC    GENERAL   DISEASES. 

tack  a  hot-air  or  Turkish  bath  will  be  of  service.  Guaiacum,  sulphur  and 
arsenic  are  the  favorite  drugs  in  chronic  cases.  Quinine  is  almost  a  specific 
in  the  malarial  form.  In  vigorous  persons  subject  to  muscular  rheumatism 
the  surface  should  be  warmly  covered  with  flannel,  and  the  individual  should 
accustom  himself  to  a  morning  rub-down  with  a  dry,  coarse  towel  after 
a  cold  sponging.     The  bromides  are  useful  in  some  cases. 

In  lumbago  hot  anodyne  fomentations  and  anodyne  liniments  will  often 
give  relief  if  vigorously  applied.  Hypodermics  of  morphia  may  be  given 
for  temporary  relief.  These  patients  should  remain  quiet  in  the  position 
that  gives  them  most  relief. 

In  intercostal  neuralgia,  cupping,  blisters,  and  hot  poultices  will  often 
relieve.  But  in  severe  cases  hypodermics  of  morphia  must  be  resorted 
to. 

In  wry-neck,  the  cervical  region  should  be  swathed  in  warm  flannel. 
Gentle  traction  likewise  aids  in  this.  The  constant  and  Faradic  currents 
may  be  passed  alternately  through  the  affected  muscle.  Showering  with 
water  as  hot  as  can  be  borne  is  very  efficacious  in  some  cases.  Acupunc- 
ture affords  relief  in  many  instances.  Veratria  and  aconite  are  often  used 
in  ointments.  Manipulation  by  a  skilled  ''rubber"  is  one  of  the  most 
efficient  means  of  local  treatment.  If  angemia  is  present  chalybeate  waters 
and  tonics  are  indicated. 

GOUT. 

Gout  is  a  constitutional  disease  of  mal-nutritiou,  characterized  by  an 
excess  of  uric  acid  in  the  blood  and  the  deposit  of  urates  in  the  cartilages 
and  fibrous  structures  of  Joints  and  throughout  the  bodv.  The  constitu- 
tional condition  is  generally  described  as  the  "gouty  diathesis,'- ^lith^mia  • 

and  the  term  gout  is  applied  only  to  the  phenomena,,  which  may  be  either 
acute  or  chronic,  attendant  upon  the  elimination  of  the  urates  and  their 
deposition  in  the  joints. ' 

Morbid  Anatomy.— The  primary  changes,  so  far  as  we  are  able  to  appre- 
ciate them,  are  in  the  blood  and  consist  in  an  excess  of  uric  acid.'  In  just 
what  way  the  nutritive  processes  are  at  fault,  and  whether  the  urates  found 
in  the  blood  are  there  as  the  result  of  an  excess  or  a  deficiency  of  activity, 
are  points  as  yet  undetermined.  In  acute  gout  this  excess  occurs  only  just 
previous  to,  and  during  the  paroxysm,  when  the  proportion  of  urates  may 
reach  1-20,000  or  even  1-6,000,  and  the  corpuscular  elements  are  un- 
changed, but  in  chronic  gout  it  is  permanent  though  in  much  smaller  ra- 
tio, and  is  accompanied  by  anaemia.  Traces  of  oxalic  acid  are  occasionally 
found  in  the  blood,  and  there  is  always  decrease  of  alkalinity  and  increase 
of  the  fibrin-factors. 

Although  the  blood  change  is  the  essential  one,  the  articular  are  the 
more  manifest  and  characteristic,  and  consist  in  the  deposit  of  the  urates  in 

» It  has  received  the  names  of  podagra,  chiragra,  gonagra  and  arthritis  according  as  it  affects  the  foot, 
hand,  knee,  or  several  joints. 

2  The  precise  combination  in  which  uric  acid  occurs  in  the  blood  is  undetermined.  It  is  probably 
*ither  as  the  acid  or  neutral  urate  of  soda. 


GOUT. 


871 


the  Joints  with  the  attendant  inflammatory  and  ulcerative  processes.  The 
primary  deposit  occurs  in  the  cartilage  capsule  and  cells  at  the  point  of 
least  vitality  and  most  remote  from  vascular  supply,  and  gradually  in  sub- 
sequent attacks  invades  the  cartilage,  periosteum,  synovial  fringes,  and 
fibrous  tissues  of  and  about  the  joint, 
where  it  is  found  between  the  connec- 
tive-tissue fibres.  This  deposit  con- 
sists principally  of  the  urate  of  soda 
in  the  form  of  minute  needle-shaped 
crystals,  but  to  the  unaided  eye  ap- 
pears amorphous  ;  chloride  of  sodium, 
urates  of  lime,  magnesia  or  ammonia, 
hippuric  acid  and  phosphate  or  car- 
bonate of  lime  are  present  in  small 
proportion.  In  the  earlier  stages  the 
articular  surfaces  are  slightly  granular 
in  appearance,  with  a  thin  amorphous 
incrustation.  But  as  the  acute  attacks 
are  repeated,  or  in  the  later  stages  of 
chronic  gout,  the  incrustation  in- 
creases, the  surfaces  are  decidedly 
roughened  ;  gradually  erosions  occur 
from  epithelial  degeneration  and  attri- 
tion, and  all  the  adjacent  structures 
are  infiltrated  and  covered  with  a  thick 
deposit  of  urates.  The  articular 
changes  may  go  on  to  entire  destruc- 
tion of  the  cartilages  and  articular  surfaces,  while  the  extra-articular  de- 
posits form  large  concretions  or  topM.  These  may  induce  ulcerative  and 
suppurative  processes  until  they  finally  protrude  through  the  skin,  are  dis- 
charged from  abscesses,  or  produce  fibrous  and  osseous  ankylosis.  The 
veins  about  the  joint  become  dilated,  varicosed,  and  filled  with  thrombi 
which  may  at  any  time  cause  embolism.  All  these  changes  are  gradual  in 
their  development,  but  each  attack  of  gout,  even  the  first,  leaves  its  per- 
manent mark  in  the  affected  joint.  Aside  from  the  acute  attack,  inflam- 
matory processes  of  a  low  grade  are  eventually  engendered  by  the  irritation 
of  the  deposits,  and  molecular  changes  enter  as  an  element  in  the  destruc- 
tive processes,  or  the  inflammation  may  result  in  the  production  of  ecchon- 
drosis. 

The  small  joints  of  the  body  are  most  frequently  affected,  and  of  these 
the  metatarso-phalangeal  articulation  of  the  great  toe  is  so  unquestionably 
first  as  to  render  it  the  classical  seat  of  acute  gout.  In  order  of  frequency 
after  this  are  the  joints  of  the  fingers,  knee,  elbow,  hip,  and  shoulder. 
Other  joints  are  but  rarely  affected.  But  all  the  cartilages  and  fibrous 
tissues  throughout  the  bodv  as  well  as  those  of  the  joints  may  be  the  seat 
of  gouty  manifestations.  Tophi  are  frequently  found  in  the  cartilages  of 
tne  ear,  nose,  or  eyelids,  and  are  then  of  the  highest  clinical  significance. 


Fig.   181. 
Section  of  a  Gouty  Cartilage. 

A.  Articular  smface. 

B.  Nominal  Caitilage. 

C  Crystals  of  urate  of  soda  in  the  stroma. 
D.  Dense  deposit  of  urates,  x  300. 


873 


CHROKIC    GE]S"EEAL   DISEASES. 


They  may  be  present  also  in  the  larynx,  sclerotic,  tendons  of  the  hands, 
and  even  on  the  spinal  dura  or  outer  coat  of  the  arterial  sheaths. 

The  most  important  visceral  lesions  are  found  in  the  kidney,  and  consist 
in  a  similar  deposit  of  urates  and  subsequent  cirrhotic  changes.  The 
primary  deposits  here  are  probably  in  the  tubules  and  their  epithelium, 
and  the  interstitial  deposits   and    fibrous    changes    are  secondary.     The 

kidney  presents  a  granular  appearance, 
and  on  section  the  fine  strise  of  urates 
may  be  seen  throughout  the  tubular 
structures.  More  abundant  deposits 
may  aggregate  in  the  pelvis  as  calculi 
and  incite  pyelitis.  The  heart  is  event- 
ually hypertrophied  and  may  present 
signs  of  fatty  degeneration,  while  the 
arteries  present  varying  stages  of  athe- 
roma from  the  primary  fibroid  changes 
to  distinct  calcareous  deposits.  Fibroid 
and  cirrhotic  changes  also  occur  in  the 
liver  and  stomach,  and  finally  uric  acid 
is  present  in  both  the  normal  and  patho- 
logical fluids  found  in  the  body. 

Etiology. — The  exact  nature  of  those 
changes  which  result  in  the  gouty 
diathesis  is  still  undetermined,  but  cer- 
tain etiological  relations  are  quite  clearly 
established.  Gout  is  pre-eminently  a 
disease  of  middle  life,  and  although  it  can  be  developed  in  any  constitution, 
heredity  can  be  traced  in  fully  sixty  per  cent,  of  cases,  and  almost  in- 
variably so  when  it  is  present  in  children  or  early  adult  life. 

Clinical  experience  proves  that  the  direct  exciting  cause  is  the  product 
of  the  following  factors  in  varying  proportions.  —  First.  An  excess  of  nitro- 
genized  material  in  the  system  from  over-eating  and  the  use  of  alcohol. 
Excess  as  applied  to  eating  is  a  relative  term,  and  in  certain  constitutions 
an  amount  of  food,  which  in  others  would  be  very  moderate,  may  so  exceed 
the  demands  of  the  system  as  to  be  the  cause  of  gout.  Of  alcoholic 
beverages  the  sweet  wines  and  malt  liquors  are  considered  more  gouty  than 
spirits. 

Second.  Deficient  or  suddenly  arrested  oxidation.  Lack  of  exercise  and 
its  consequent  abundant  supply  of  oxygen  are  the  most  frequent  causes 
of  such  deficiency  of  oxidation,  but  it  is  also  probable  that  the  con- 
stitutional and  hereditary  tendency  exerts  a  powerful  influence  over  the 
assimilative  function,  and  that  impaired  nervous  energy  may  be  the  ulti- 
mate cause  of  defective  oxidation. 

Third.  Failure  in  the  excretive  power  of  the  kidney.  Such  failure  may 
result  either  from  deficiency  of  the  eliminative  power  of  the  renal  epithe- 
lium or  mechanically  from  obstruction  of  the  tubules  by  deposits  of  urates, 
and  is  the  prime  factor  in  producing  the  acute  gouty  attack.     In  a  system 


Fig.  182. 


Vertical  Section  of  a  Malpighian  Pyramid  in 
Gouty  Nephritis. 

Thestrice,  consisting  of  urates,  folloio  the  general 
course  of  the  tubules.  Much  of  the  deposit  has 
been  ivashed  out  of  the  siJecimeii  in  hardening. 

X  30. 


GOUT.  873 

already  laden  with  urates,  a  few  glasses  of  wine,  a  fit  of  dyspepsia,  ex- 
posure, severe  mental  effort,  or  a  fit  of  anger  may  be  sufficient  to  bring  on 
an  attack  of  gout. 

Symptoms. — Gout  may  be  either  acute  or  chronic,  and  appear  as  *' regu- 
lar" in  the  joints,  or  as  irregular,  misplaced,  retrocedent  or  anomalous 
gout  in  the  non-articular  structures  and  the  internal  organs. 

In  most  cases  of  acute  gout  premonitory  symptoms  precede  the  first 
paroxsym  ;  there  will  be  a  history  of  occasional  pains  in  one  or  both  great  toe- 
joints,  a  feeling  of  malaise  with  sleeplessness,  constipation,  dyspepsia,  and 
perhaps  pain  in  the  side,  a  dry,  hot  skin,  scaly  eruptions  and  scanty  urine. 
Sometimes  an  attack  is  preceded  by  a  peculiar  sense  of  well-being,  even  ex- 
citation ;  at  others  by  great  anxiety,  irritability,  and  depression  of  spirits. 
Asthmatic  symptoms  often  precede  the  outbreak  of  an  attack.  Usually 
between  midnight  and  four  or  five  in  the  morning  the  individual  wakes 
with  a  burning,  throbbing  pain  in  the  ball  of  the  great  toe,  which  the 
slightest  pressure  greatly  intensifies. 

The  affected  joint  becomes  red,  swollen,  hot  and  shining ;  the  veins  are 
distended,  and  it  resembles  a  joint  about  to  suppurate.  There  is  some  fe- 
brile movement  which  varies  in  intensity  with  the  number  of  joints  affected. 
The  temperature  may  in  a  severe  attack  reach  105°  P.  The  pulse  is  full 
and  bounding  but  compressible.  As  the  fever  comes  on  the  pain  in  the  af- 
fected joint  is  so  great  that  the  patient  cannot  move  it;  he  becomes  restless, 
tossing  for  hours,  until  finally,  in  a  profuse  perspiration,  he  falls  asleep.  In 
a  few  hours  he  awakes  refreshed  and  comparatively  free  from  pain  ;  but  the 
affected  joint  is  swollen,  tense,  and  vividly  red.  He  continues  comfortable 
during  the  day,. but  about  the  same  hour  the  next  night  there  is  a  recurrence 
of  the  local  pain  and  the  fever,  which  is  followed  by  another  remission  the 
following  morning. 

These  nocturnal  exacerbations  and  morning  remissions  continue  with 
about  the  same  severity  for  two  or  three  days,  then  the  maximum  of  pain 
is  reached.  At  the  end  of  a  week  they  have  gradually  subsided  ;  the  af- 
fected joint  remains  tender  and  swollen  for  a  week  or  two  longer.  This 
swelling  is  due  to  oedema,  and  pits  on  pressure,  and  as  it  disappears  des- 
quamation occurs.  Following  the  attack,  there  is  a  feeling  of  well  being 
which  has  led  to  the  popular  belief  that  an  attack  of  gout  is  beneficial. 

There  is  usually  marked  digestive  derangement  during  an  attack,  with 
anorexia,  a  thickly  furred  tongue,  and  constipation.  The  urine  is  scanty, 
high  colored,  and  contains  less  uric  acid  than  normal,  dejiositing  on  cool- 
ing a  copious  sediment.  The  bladder  is  irritable,  and  there  is  a  scald- 
ing sensation  on  urination.  Intense  cramps  in  the  muscles  adjacent  to 
the  affected  joint  may  occur.  Occasionally  during  the  first  attack  both 
great  toe  joints  are  involved  ;  and  instead  of  disappearing  at  the  end  of  a 
week,  successive  outbreaks  occur  in  the  other  joints. 

An  individual  may  have  only  a  single  attack  ;  but  usually  a  second  su- 
pervenes within  a  year.  Gradually  the  attacks  approach  each  other,  and 
are  more  prolonged  though  less  severe,  until  a  condition  of  chronic  gout  is 
reached.     In  the  second  and  third  attacks  the  joint  formerly  involved,  or 


874 


CHEONIC    GENERAL   DISEASES. 


its  fellow  of  the  opposite  side,  presents  the  same  phenomena  as  in  the 
primary  attack. 

Although  all  gout  is  strictly  speaking  chronic,  by  chronic  gout  is 
understood  those  gouty  manifestations  which  are  developed  as  the  parox- 
ysms coalesce,  and  the  patient  is  scarcely  ever  free  from  some  gouty  mani- 
festation. Tophi  form  around  the 
affected  parts,  and  the  joints  be- 
come so  distorted  or  crippled  that 
walking  becomes  difficult.  Grad- 
ually the  health  deteriorates,  and 
feebleness  and  a  gouty  cachexia  be- 
come marked  and  visceral  derange- 
ments become  prominent.  When 
chronic  gout  follows  acute,  the  ar- 
ticular phenomena  are  always  prom- 
inent. But  when,  as  not  infre- 
quently happens,  gout  is  chronic 
from  the  onset,  tophi  form  early 
without  acute  inflammatory  symp- 
toms, and  the  visceral  affections  are 
prominent.  In  chronic  gout  the 
urine  is  greater  in  amount,  lighter 
in  color,  of  lower  specific  gravity, 
and  contains  less  uric  acid  than  nor- 
mal. In  a  few  cases  casts  and  al- 
bumen make  their  appearance. 
Misplaced  gout — gout  that  has  re- 
troceded  from  a  joint  to  an  inter- 
nal organ,  also  called  visceral,  masked,  internal  and  metastatic  gout — 
may  attack  any  organ  and  result  in  a  long  series  of  functional  disturb- 
ances. 

The  sequel*  and  complications  of  gout  are  numerous.  Those  referable 
to  the  nervous  system  are  vertigo,  neuralgia,  headache,  stupor,  convulsions, 
delirium,  apoplexy  and  lunacy.  *  Those  referable  to  the  vascular  system  are 
arterial  degeneration,  angina  pectoris,  cardiac  palpitation,  and  valvular  dis- 
ease. Those  referable  to  the  lungs  are  asthma,  which  alternates  very 
often  with  the  articular  phenomena  of  gout,  and  bronchitis,  which  some 
regard  as  the  commonest  manifestation  of  gout,  after  arthritis.  Eefer- 
able  to  the  digestive  tract  is  a  long  list  of  gastro-intestinal  catarrhs,  cir- 
rhoses  of  the  liver,  jaundice,  and  cirrhotic  kidney. 

Differential  Diag^nosis. — Grout  is  generally  easy  of  diagnosis.  It  may, 
however,  be  mistaken  for  rheumatism. 

Gout  attacks  the  small  and  rheumatism  the  large  joints.  A  rheumatic 
attack  is  of  longer  duration  than  a  gouty  paroxysm,  and  has  no  perio- 
dicity. In  gout  the  fever  is  slight,  102°  to  103°  F.,  and  is  in  inverse  ratio 
to  the  number  and  size  of  the  joints  involved  ;  in  rheumatism  there  is  usu- 

i  These  are  regarded  by  some  observers  as  evidences  of  cerebral  gout. — Garrod,  Todd,  Trousseau. 


Fig.  183. 
Deformity  from  Gout. 


GOUT.  875 

ally  a  higher  range  of  temperature.  Cutaneous  affections  are  common  m 
gout  and  rare  in  rheumatism.  The  heart  is  frequently  involved  in  acute 
rheumatism,  and  rarely  in  gout.  The  gouty  attack  coming  on  at  night  m 
the  great  toe  joint  is  in  marked  contrast  to  the  onset  of  rheumatic  fever. 
Acute  articular  rheumatism  is  a  disease  of  early  adult  life,  while  gout  is 
rare  before  thirty-five.  In  gout  there  is  a  history  of  high  living,  or  an 
hereditary  predisposition  ;  m  rheumatism  there  will  be  a  history  of  expos- 
ure or  exhaustion.  In  gout  there  is  an  excess  of  uric  acid  in  the  blood  ; 
this  is  never  the  case  in  rheumatism.  When  we  are  enabled  by  the  mi- 
croscope to  see  uric  acid  crystals  derived  from  serum  of  a  patient  with  an 
arthritis,  the  diagnosis  of  gout  is  established.  Tophi  never  form  in  rheu- 
matism, but  are  always  present  late  in  gout. 

The  joint  affection  oi  pyoemia  may  be  mistaken  for  gout ;  but  the  his- 
tory, in  connection  with  the  constitutional  signs  of  pyaemia,  will  remove  all 
doubt. 

Prognosis. — Gout  rarely  kills,  but  complete  recovery  from  it  is  also  rare. 
Death  is  generally  the  result  of  visceral  complications  or  of  the  cachexia 
induced  by  blood  changes.  The  prognosis  is  less  favorable  in  hereditary 
gout,  and  in  those  who  persist  in  high  living  and  the  use  of  alcoholic  bev- 
erages, and  when  the  larger  articulations  are  affected.  The  appearance  of 
albumen  in  the  urine,  and  total  absence  of  uric  acid  from  the  secretions 
are  grave  symptoms.  The  prognosis  is  exceedingly  unfavorable  when  there 
is  great  crippling  of  the  joints  accompanied  by  an  extensive  cachectic  con- 
dition. Concerning  the  doctrine  of  antagonisms,  it  has  been  proved  that 
gout  does  not  exclude  cancerous  or  phthisical  developments. 

Treatment. — The  treatment  of  gout  will  be  considered  under  four  heads  : 
(1)  General  hygiene ;  (2)  Dietetics  ;  (3)  External,  and  (4)  Internal  treat- 
ment. 

I.  Gouty  subjects  should  take  systematic  exercise  in  the  open  air,  espe- 
cially horseback-riding.  A  country  residence  is  to  be  preferred  to  the  city  ; 
and  a  warm,  dry  climate  at  a  moderately  high  elevation  is  preferable  to  a 
severely  cold  one.  They  should  always  be  clad  warmly  in  flannel,  and 
should  avoid  sudden  and  violent  physical  exertion,  severe  mental  strain,  and 
all  unnecessary  exposure  to  vicissitudes  of  temperature.  They  should  retire 
and  rise  early,  sleeping  in  a  large,  well-ventilated  apartment  without  drafts. 

II.  Dietetics. — Simple,  nutritive  food  should  be  taken  at  stated  intervals 
and  in  small  quantities.  Starving  will  not  cure  gout.  As  vegetables  may 
be  taken  more  freely  than  animal  food,  all  pastry,  eggs,  tea  and  coffee, 
and  alcohol  should  be  avoided,  and  great  care  should  be  taken  not  to  over- 
load the  stomach.  Game  and  highly  seasoned  food,  cheese,  dried  meats, 
tomatoes  and  strawberries  are  to  be  avoided.  Vegetables  that  contain  the 
least  starch,  such  as  cabbage  and  the  salads,  are  to  be  preferred.  The  prin- 
cipal articles  of  diet  should  be  beef,  mutton,  and  chicken,  bread,  milk,  and 
fruits.  Alkaline  mineral  waters,  seltzer,  vichy,  lithia,  etc.,  may  be  taken 
with  and  after  meals.  When  stimulants  must  be  given  on  account  of  the 
enfeebled  digestion,  light  wines,  whiskey  or  gin  will  be  found  least  objec- 
tionable. 


876  CHEOKIC   GENEEAL   DISEASES. 

III.  External  Treatment. — The  affected  limbs  should  be  kept  raised  above 
the  leyel  of  the  body  during  an  acute  attack,  and  wrapped  in  flannel  or 
cotton  batting.  Cold  applications  and  leeches  to  the  afliected  joints  do 
harm.  When  the  pain  is  intense  opium  may  be  applied  to  the  joint,  or 
morphine  may  be  injected  near  it.  Tepid  alkaline  washes  and  horse-chest- 
nut oil  are  strongly  advocated  by  many/  Vapor  and  Turkish  baths  are 
often  of  the  greatest  service  and  should  be  taken  weekly  during  the  inter- 
vals between  the  paroxysms. 

IV.  Internal  Treatment. — Colchicum  and  the  alkalies  are  our  chief 
remedies  during  the  paroxysm.  For  thirteen  centuries  colchicum  has 
been  used  in  this  disease ;  it  relieves  the  symptoms,  but  how  we  do  not 
know.  Its  efficacy  has  been  attributed  at  various  times  to  the  elimination 
of  uric  acid,  its  sedative  action  on  the  circulation,  its  purgative  and  nar- 
cotic powers.  My  rule  is  to  give  one  of  the  following  pills'  every  three 
hours  until  the  specific  purgative  action  of  the  colchicum  is  obtained  ;  or 
five  drops  of  the  fluid  acet.  ext.  of  colchicum  in  alkaline  water  may  be 
given  every  two  hours.  The  maximum  dose  of  the  latter  should  be  given 
at  the  end  of  the  attack  ;  small  doses  only  are  admissible  at  the  commence- 
ment. When  marked  cerebral,  circulatory,  or  gastro-enteric  phenomena 
occur,  colchicum  is  to  be  discontinued.  Carbonate  of  potash,  Kochelle 
salts,  and  the  urate  or  citrate  of  lithia,  are  important  adjuvants  to  the 
colchicum  treatment.'  Chloral,  opium,  and  hyoscyamus  may  be  given  dur- 
ing the  acute  attack,  to  relieve  the  pain  and  restlessness  of  the  patient. 
Common  ash  leaves,  cinchona  and  gentian,  the  sulphate  of  quinine,  and 
the  iodide  of  potassium  with  tr.  guaiac.  ammo,  have  been  extensively  used 
in  the  treatment  of  gout,  not  only  during  the  paroxysm  but  during  the 
interval.  The  benefit  derived  by  gouty  patients  at  the  different  springs 
which  are  so  highly  recommended  seem  to  me  to  be  due  to  the  change  of 
air  and  scene  and  to  the  dietetic  restrictions  more  than  to  the  bathing.  A 
restricted  diet,  exercise  in  the  open  air,  and  a  Turkish  bath  once  or  twice 
a  week  have  succeeded  with  me  as  well  as  a  residence  at  some  spring. 

In  chronic  gout,  tonics  (iron,  arsenic,  etc.)  are  usually  demanded.  The 
inhalation  of  oxygen  has  been  advocated  as  a  remedy  for  the  impoverished 
blood  condition.  Chemically  active  remedies — ammonia  phosphate  and 
benzoic  acid — have  not  proved  as  useful  clinically  as  theoretically.  It 
should  be  remarked  that  the  excessive  use  of  mineral  waters  is  contra- 
indicated  in  those  who  are  advanced  in  years,  in  individuals  whose  kid- 
neys no  longer  have  the  power  of  elimination,  and  in  those  with  whom 
alkalies  disagree  on  account  of  some  peculiar  idiosjTicrasy. 

1  Charcot  spenks  highly  of  atropine  and  blisters  as  topical  remedies. 

3  ^  Pulv.  ipecac gr.  i. 

Ext.  colchi.  acet gr.  i. 

H)'drarg.  protochlor.  (calomel) gr.  i. 

Ext,   aloes   fl gr.  i. 

Ext.  nuc.  vomic gr-  H- 

3  Strieker  caused  the  tophi  to  disappear  by  giving  1%  grains  of  lithia  carbonate  and  S}^  grains  of  soda 
bicarbonate  in  16  ounces  of  carbonic  acid  water  a  day. — Virchow's  Archiv.,  vol.  xsxv. 


DIABETES    MELLITUS.  877 


DIABETES   MELLITUS. 


The  term  diabetes  mellitus  is  applied  to  a  constitutional  disorder  arising 
from  malassimilation,  in  which  the  first  appreciable  change  is  the  presence 
of  sugar  in  the  blood.  When  the  proportion  of  saccharine  matter  reaches 
three  parts  in  one  thousand,  it  appears  in  the  urine,  producing  the  symp- 
tom which  has  given  the  name  to  the  disease.'  It  has  at  various  times 
been  regarded  as  a  disease  of  the  kidney,  alimentary  canal,  liver,  and 
nervous  system,  but  its  exact  pathogeny  has  never  been  determined. 

Physiological  experiments  and  clinical  facts,  however,  tend  to  show  that 
the  abnormal  condition  may  be  the  result  of  either  of  these  pathological 
processes  or  of  their  united  action  : 

First. — Excessive  activity  in  the  glycogenic  function  of  the  liver  or  in 
the  primary  assimilative  processes  may  so  overload  the  blood  with  sugar  as 
to  cause  it  to  appear  in  the  urine.  Whether  this  hyperactivity  is  the  re- 
sult of  active  hypergemia  simply,  or  arises  from  disturbed  nervous  supply 
is  uncertain.  The  occasional  appearance  of  diabetes  following  the  use  of 
stimulants,  and  its  very  general  occurrence  as  a  result  of  irritation  of  the 
vaso-motor  areas  in  the  floor  of  the  fourth  ventricle,  would  seem  to  indicate 
that  hypersemia,  either  from  local  or  central  irritation,  is  an  important 
factor,  but  what  nervous  influence  is  primarily  at  fault  in  producing  this 
mysteriously  perverted  functional  activity  is  undetermined. 

Second. — The  secondary  assimilation  may  fail  to  dispose  of  the  sugar  pro- 
duced, and  the  kidneys  are  again  called  upon  to  eliminate  it  from  the 
blood.  Until  physiology  can  speak  with  more  definiteness  than  to  say  that 
sugar  is  disposed  of  in  the  system  ''either  by  oxidation  or,  as  seems  more 
probable,  in  other  ways,"  ^  it  is  useless  to  speculate  as  to  what  organ  or 
functions  are  at  fault  in  this  form  of  diabetes. 

Morbid  Anatomy. — The  only  characteristic  lesion  is  the  presence  of  sugar 
in  the  blood  in  varying  proportions,  up  to  nine  or  ten  parts  in  a  thousand, 
and  secondarily  in  all  the  organs,  secretions  and  excretions.  It  is  most 
abundant  in  the  urine.  Glycogen,  acetone  and  kreatin  are  generally  pres- 
ent in  the  organs  and  fluids,  and  the  blood  contains  more  fat  than  nor- 
mally. The  parenchymatous  changes  in  the  viscera  are  principally  degen- 
erative, the  result  of  the  blood  change.  The  liver  is  usually  hyper^mic, 
with  possibly  some  fatty  degeneration.  The  lungs  are  nearly  always  tuber- 
culous, with  points  of  catarrhal  pneumonia,  or  possibly  of  gangrene,  at- 
tended by  pleurisy.  The  heart  is  soft  and  flabby,  and,  like  the  other  mus- 
cles, pale  and  dry.  The  spleen  is  hyper^emic,  hypertrophied  and  firm. 
Aside  from  hypersemia,  the  kidneys  often  present  the  usual  changes  of 
chronic  parenchymatous  nephritis  (large  white  kidney),  possibly  the  result 
of  the  excessive  work  thrown  upon  them.  Softening,  cirrhosis,  and  tumors 
may  be  present  in  the  brain,  and  when  they  involve  the  fourth  ventricle 
become  of  interest  from  an  etiological  standpoint.     Emaciation  becomes 

'  Synonyms  :   Glycosuria,  Glucosuria,  Mellituria,  Glycohaemia. 
2  Foster'8  Phys.,  25  Am.  Ed.,  1881,  p.  537. 


878  CHRONIC   GEISTERAL  DISEASES. 

marked  early,  and  in  protracted  cases  becomes  extreme.  The  skin,  which 
is  harsh  and  dry,  is  generally  the  seat  of  furuncles,  carbuncles,  bed-sores, 
and  gangrene. 

Etiology. — Diabetes  is  a  disease  of  early  adult  life,  and  is  met  with  more 
frequently  in  males  than  in  females.  In  some  cases  it  appears  to  be  heredi- 
tary. It  is  a  well-established  fact  that  mechanical  irritation  of  a  certain 
area  of  the  medulla,  an  area  corresponding  very  closely  with  the  vaso-motor 
area  in  the  fourth  ventricle,  invariably  produces  glycosuria,  and  clinical 
facts  prove  with  a  great  degree  of  certainty  that  diabetes  is  frequently  the 
result  of  lesions  producing  similar  irritation.  Such  irritation  may  result 
from  general  shock  or  concussion,  cerebral  hemorrhage,  softening,  cirrho- 
sis, abscess  or  tumors,  also  from  excessive  mental  labor,  shock,  grief,  and, 
possibly,  from  the  excessive  use  of  cerebral  stimulants.  Blows  upon  the 
epigastrium  are  included  in  its  list  of  causes.  Pregnancy,  impaired  diges- 
tion, and  immoderate  use  of  sugar,  new  wine,  and  alcohol  have  also  been 
named  as  causes. 

Symptoms. — Although  diabetes  may  be  acute  and  result  fatally  within 
two  or  three  weeks  from  the  time  the  increased  flow  of  urine  is  first  noticed, 
it  usually  comes  on  insidiously.  The  patient  notices  that  for  some  time  he 
has  been  passing  more  urine  than  usual,  and  has  been  unusually  thirsty. 
While  his  appetite  has  been  good,  and  he  has  taken  more  food  than  he  is 
accustomed  to,  he  is  losing  flesh  and  strength  ;  and  there  is  an  abnormal 
dryness  of  the  mouth,  throat  and  skin,  with  intolerable  itching,  followed 
by  desquamation.  His  sleep  is  disturbed  by  a  frequent  desire  to  empty  the 
bladder. 

As  the  disease  advances  he  becomes  listless  and  debilitated,  and  there  is 
decrease  or  abolition  of  sexual  desire  ;  in  women  the  menses  are  often  sup- 
pressed. The  tongue  is  red  or  coated,  and  nearly  always  thicker  than  nor- 
mal ;  the  gums  are  pale,  retracted,  and  bleed  easily,  and  the  teeth  become 
carious.  There  are  nausea,  vomiting,  and  well-marked  dyspeptic  symp- 
toms, with  constipation,  and  most  patients  complain  of  a  constant  sink- 
ing feeling  at  the  epigastrium.  In  many  instances  the  breath  has  a 
heavy,  sweet  odor,  and  the  taste  is  perverted.  Attacks  of  profuse  diarrhoea, 
lasting  for  a  day,  occur  in  advanced  cases,  and  may  precede  an  unexpected 
fatal  issue.  Headache,  often  amounting  to  intense  hemicrania,  is  common. 
There  is  derangement  of  the  special  senses,  especially  of  sight  (soft  cataract 
and  amblyopia)  ;  dulness  of  mind,  irritability  and  restlessness,  melancholia 
and  hypochondria.  The  temperature,  pulse-rate,  and  respirations  are  be- 
low the  normal. 

In  some  cases  the  classical  course  of  the  disease  will  be  varied  from  ;  there 
will  be  little  thirst  or  loss  of  appetite  and  no  emaciation;  the  patient  may 
even  gain  in  flesh.*  In  diabetes  from  " over-production  "  the  quantity  of 
urine  passed  is  greater  than  in  the  other  form,  the  skin  affections  are  more 
severe  and  frequent,  the  patient  does  not  emaciate,  but  loss  of  sexual  desire 

1  Frank  describes  a  "  diabetes  decipiens."  in  which  the  amount  of  urine  passed  is  not  above  the  normal, 
while  a  large  amount  of  sugar  is  present.  Quincke  relates  some  very  interesting  cases  of  diabetes  where 
delirium,  stupor  and  coma  have  appeared  before  de&th.— Berlin.  Klin.  Woch.  No.  1, 1880. 


DIABETES   MELLITUS.  879 

comes  earlier.  In  the  variety  clue  to  defective  assimilation,  the  emaciation, 
anaemia,  loss  of  strength  and  flesh,  and  palpitation,  vertigo,  and  dyspncea 
are  early  and  marked  signs,  while  the  nervous  phenomena  are  not  jiromi- 
nent. 

The  Urine. — Very  rarely  the  amount  of  urine  passed  is  but  little  increased; 
generally,  however,  it  very  rapidly  rises  to  twenty,  thirty,  fifty  or  more  pints 
in  twenty-four  hours.  The  calls  to  urinate  become  very  frequent  both  by 
day  and  night,  and  the  genitals  are  inflamed  and  excoriated.  The  urine  is 
acid,  of  a  light  straw  color,  with  possibly  a  faint  green  tint,  clear,  without 
sediment,  and  of  a  slightly  aromatic  odor  and  a  sweet  taste.  The  specific 
gravity  varies  from  1.030  to  1.070  with  an  average  of  1.040,  and  the  propor- 
tion of  sugar  from  a  trace  to  5-0  to  100  or  more  parts  in  a  thousand.  In 
rare  cases,  a  low  specific  gravity  of  1.008  or  1.010  is  recorded,  but  a  specific 
gravity  of  1.030,  when  the  quantity  of  urine  passed  is  normal  or  increased, 
should  always  lead  to  an  examination  for  sugar.  Urea  is  always  present  in 
increased  amount,  and  uric  and  hippuric  acid,  kreatinin,  sulphuric  and 
phosphoric  acids,  acetone,  alcohol,  and  albumen  are  frequently  found.  In 
certain  cases  where  the  patient  continues  to  fail,  although  the  quantity  of 
sugar  lessens,  inosite  appears  in  the  urine,  and  continues  to  increase  as  the 
sugar  lessens.  It  may  amount  to  two  or  three  hundred  grains  in  twenty- 
four  hours. 

In  those  cases  where  sugar  and  the  starchy  element  of  the  food  are  the 
sole  sources  of  the  diabetic  sugar,  diet  may  reduce  the  quantity  and  specific 
gravity  of  the  urine  to  the  normal  and  remove  all  traces  of  sugar  from  the 
urine  and  blood.  In  other  and  more  advanced  cases  animal  food  is  also 
converted  into  sugar,  and  in  such  conditions  dieting  can  only  modify  the 
urinary  symptoms.  In  a  third  class  of  cases  the  tissues  of  the  body  also 
contribute  to  its  formation,  and  the  quantity  of  sugar  eliminated  is  but  little, 
if  at  all,  affected  even  by  starvation.'  Urea  is  excreted  in  abnormally  large 
quantities  by  diabetic  patients  ;  some  claim  that  there  is  increased  decompo- 
sition of  albumen  into  urea  and  sugar.     Albumen  does  not  necessarily  indi- 

1  The  following  are  the  best  tests  to  determine  the  presence  of  sugar  in  the  urine  : — 

Trommer's  Test. — To  the  suspected  liquid  add  a  few  drops  of  a  slightly  alkaline  solution  of  tartrate  of 
copper.    Boil.    Sugar  precipitates  copper  as  a  yellowish  red  oxide. 

Fe.hling's  Test  is  founded  on  the  fact  that  glucose  has  the  property  of  precipitating  the  red  cupreous 
oxide  from  an  alkaline  solution  of  sulphate  of  copper. 

Dissolve  36.64  grammes  cupric  sulphate  in  200  c.c.  distilled  water. ;  dissolve  80  grm.  sodium  hydrate 
in  600  c.  c.  water,  and  add  173  grm.  Rochelle  salts.  Mix  the  two  solutions  and  add  water  to  make  one 
litre.  Keep  in  small,  carefully  sealed  bottles.  The  copper  in  one  c.  c.  is  entirely  precipitated  by  5  milli- 
grammes of  grape  sugar. 

Pour  5  c.  c.  of  the  above  test-solution  into  a  test  tube  and  heat  to  boiling  ;  add  the  suspected  urine, 
guttatim :  If  grape  sugar  is  present  the  blue  changes  to  green  and  the  red  oxide  of  copper  is  precipitated. 
When  the  blue  is  discharged  the  copper  is  precipitated. — Draper. 

Wnr)'en''s_  Test.— In  a  test  tube  containing  three  drams  of  urine  add  two  drops  of  a  solution  of  sul- 
phate of  copper  and  one-half  as  much  liq.  potass,  as  the  amount  of  urine  ;  boil,  and  if  the  urine  con- 
tains unrjar..  the  red  sub-oxide  of  copper  will  be  thrown  down. 

Maumsne's  Test  consisrs  in  heating  saccharine  urine  in  the  presence  of  bichloride  of  tin,  which 
canaes  it  to  throw  down  a  black-brown  "caramel  "  looking  deposit. 

yfoorf^n  y'fcf/ consists  in  boiling  liquor  potassie  with  the  suspected  urine;  if  sugar  is  present  a  bistre 
brown  appears. 

The  Fenrtentatirm  Test  consists  in  putting  German  yeast  in  a  test  tube  filled  with  the  urine,  and  standing 
It  inverted,  in  a  warm  place  :  alcohol  and  carbonic  acid  ai-e  formed  and  the  bubbles  of  the  latter,  tested 
With  lime  water,  give  evidence  of  its  character.    Non-saccharine  urine  does  not  ferment. 

Tcn-uloi  form  during  the  fermentation  as  a  scum,  and,  microscopically,  are  easily  recognizable. 


880  CHRONIC    GENERAL   DISEASES. 

cate  that  there  are  grave  kidney  changes  in  diabetic  subjects.  The  amount 
of  urine  passed  in  twenty-four  hours  varies  from  fifty  to  one  hundred  pints. 
The  large  amount  of  urine  secreted  distends  the  bladder ;  and  the  large 
amount  passed,  and  its  saccharinity,  cause  a  constant  itching,  burning  and 
uneasy  sensation  at  the  prepuce,  along  the  urethra,  and  at  the  neck  of  the 
bladder  ;  in  females,  it  may  cause  redness,  irritation,  excoriation,  or  an 
eczematous  condition  of  the  vulva.  Incontinence  of  urine  is  especially  fre- 
quent in  diabetic  children. 

Differential  Diagnosis.— Diabetes  mellitus  may  be  mistaken  iov  glycosuria, 
for  the  atrophic  form  of  Briglifs  kidney,  and  for  diabetes  insipidus  or 
polyuria. 

Diabetes  occurs  at  all  ages,  and  often  from  undiscoverable  causes  ;  simple 
glycosuria  is  very  common  in  tJie  aged,  in  the  insane,  in  fits  of  ague, 
after  sudden  excitement,  blows  on  the  head,  the  taking  of  chloral,  etc.  In 
diabetes  mellitus  the  amount  of  sugar  seldom  varies  much  from  day  to 
day;  while  in  non-diabetic  glycosuria  it  varies  greatly.'  Polyuria,  poly- 
phagia, and  polydipsia  are  marked  symptoms  in  diabetic  glycosuria.  The 
symptoms  referable  to  the  nervous  system  and  skin  are  prominent  in  dia- 
betes mellitus  ;  they  are  absent  in  simple  glycosuria.  Volumetric  analysis 
by  Eehling's  method  is  easy  in  diabetes  mellitus  ;  while  in  simple  gly- 
cosuria it  gives  obscure  results,  owing  to  the  presence  of  kreatinin. 

Diabetes  mellitus  is  at  once  distinguished  from  Briglifs  disease  or  dia- 
ietes  insipidus  by  the  presence  of  sugar  in  the  urine,  a  condition  which 
does  not  occur  in  either  of  the  other  diseases. 

Prognosis. — Although  diabetes  is  a  progressive  disease,  it  has  no  regular 
course,  and  the  prognosis  depends  very  largely  upon  the  form  which  the 
disease  assumes.  In  that  class  of  cases  where  diet  reduces  the  amount  of 
sugar,  or  possibly  at  first  removes  it  entirely  from  the  urine,  the  fatal  ter- 
mination may  be  long  delayed,  but  those  cases  which  appear  to  depend 
upon  faulty  assimilation  are  more  rapidly  fatal.  Between  these  extremes 
the  disease  may  last  from  a  few  weeks  to  ten  or  twelve  years.  Pulmonary 
tuberculosis  (twenty-five  to  thirty  per  cent.)  and  uraemia  (ten  to  twenty 
per  cent.)  are  the  most  frequent  causes  of  death.  Asthenic  inflammation 
with  suppuration  is  frequent  in  all  the  tissues,  and  boils  in  successive  crops, 
and  carbuncles,  are  frequent  complications  which  influence  the  prognosis. 
Pulmonary  gangrene  may  occur  with  an  odorless  breath.  Cataract,  am- 
blyopia, retinitis,  and  retinal  hemorrhage  are  often  present  even  in  cases 
not  attended  by  albuminuria. 

The  prognosis  is  more  unfavorable  the  younger  the  subject,  the  less 
amenable  to  treatment  the  case  proves  to  be,  and  the  severer  the  gastro- 
intestinal symptoms.  It  is  always  bad  in  those  who  emaciate  rapidly. 
Death  may  occur  from  marasmus,  gangrene,  dysentery,  ansemia,  or  not 
Infrequently  in  diabetic  coma. 

Treatment. — In  spite  of  the  fact  that  there  are  no  "  speciflcs  "  for  dia- 
betes, the  greater  number  of  cases  can  for  a  time  be  brought  under  control; 
and  to  this  end  dieting  is  of  first  importance. 

1  Gerin  Rozes. 


DIABETES   MELLITUS.  881 

All  saccharine  form  of  food,  or  any  article  that  can  be  converted  into 
sugar,  should  be  withheld.  Hence,  starchy  foods,  bread,  arrow-root,  tapi- 
oca, sago— such  vegetables  as  potatoes,  parsnips,  turnips,  carrots,  beans, 
and  peas  are  to  be  absolutely  avoided  or  partaken  of  sparingly.  Salads, 
greens,  acid  fruits,  all  kinds  of  flesh  and  fowl,  eggs,  cheese  and  butter' 
unsweetened  tea  and  coffee  can  be  taken.  Alcohol  in  any  form  is  harmful, 
but  should  exhaustion  demand  stimulation  a  light  sherry  or  claret  may  be 
permitted.'  Koumyss  is  sometimes  given  as  a  substitute  for  mild  stimu- 
lants. To  allay  the  intense  thirst  acidulated  drinks,  cracked  ice,  or  alka- 
line waters  may  be  used  in  as  moderate  quantities  as  possible  ;  while  water 
increases  the  amount  of  sugar  passed,  it  is  not  certain  that  it  increases  the 
amount  formed,  and  the  patient  should  use  water  in  moderation  rather 
than  attempt  distressing  self-denial.  A  meat  diet  is  therefore  to  be  en- 
joined. 

In  the  above  bill  of  fare  the  patient  will  not  find  much  that  is  unpleasant 
or  distasteful,  except  deprivation  of  bread.  Gluten  breads,  bran  cakes,  and 
biscuits  and  buns  made  from  almond  flour  have  been  devised  as  substitutes 
Some  patients  cannot  eat  bread  thus  made,  and  in  such  cases,  if  bread 
must  be  taken,  it  should  be  well  toasted.  Moderate  exercise  must  always 
be  advised,  and  the  skin  should  be  kept  thoroughly  active  by  means  of 
baths  ;  in  the  feeble,  warm  baths,  and  in  the  more  robust,  sea  or  cold  baths. 
But  as  pulmonary  complications  are  so  common,  the  body  must  always 
be  warmly  clothed.  The  success  of  dietetic  measures  depends  upon  the 
patients  rigidly  following  them. 

The  drugs  which  exert  a  most  beneficial  influence  are  the  extract  of 
opium,  morphia,  and  codeia.  They  must  be  used  sparingly,  and  usually 
only  when  the  meat  diet  is  given  up  for  a  time.  Small  doses  should  alwaj^s 
be  administered  at  first.  When  arthritic  muscular  and  neuralgic  pains 
are  severe,  narcotics  are  especially  beneficial.  Cures  are  reported  by  high 
and  trustworthy  authorities  from  their  use. 

On  theoretic  grounds,  lactic  acid  has  been  proposed  as  a  substitute  for 
sugar.  Ithas  been  given  until  arthritic  (rheumatic)  symptoms  have  appeared.^ 
Alkalies,  bicarbonates,  acetates,  and  citrates  are  highly  recommended. 
And  since  they  are  always  most  beneficial  in  the  form  of  natural  thermal 
mineral  waters  at  the  springs,  half  their  benefit  may  be  ascribed  to  change 
of  air,  mode  of  life,  and  the  surroundings  that  attend  a  visit  to  watering 
places.  Carbolic  acid  and  creosote  have  been  used  as  antiseptics,  and 
salicylic  acid  has  been  proposed  as  an  anti-fermentative  ;  sulphide  of  calcium 
is  of  benefit  where  there  is  much  suppuration  {e.  g.,  boils,  carbuncles,  etc.). 
Ergot  and  jaborandi  have  apparently  been  beneficial  in  some  cases  ;  the 
constant  galvanic  current  has  been  productive  of  good  results.  The 
anaemia  which  attends  it  demands   iron,  cod-liver  oil,  strychnia,  quinine 

1  Donkin  recommends  the  continuous  administration  of  sl^immed  milk,  three  or  four  quarts  a  day ; 
whfin  the  patients  are  able  to  pursue  this  plan  it  is  followed  by  pood  results. 

2  Two  Neopolitan  professors,  Primavera  and  Caucani,  claim  that  a  meat  diet  with  g  ij-iv  of  lactic  acid 
and  1  88.  of  alcohol  in  12  oz.  of  water  at  a  meal,  will  furnish  no  materials  for  the  formation  of  sugar, 
yet  will  be  a  substitute  for  the  saccharine  and  farinaceous  elements  of  the  food. 

56 


882  CHEOKIC    GENERAL   DISEASES. 

and  a  change  of  air  and  scene.     Surgical  operations  should  on  no  account 
be  undertaken  on  diabetic   patients. 

DIABETES    IlSrSIPIDUS. 

Diabetes  insipidus,  or  polyuria,  is  characterized  by  extreme  thirst  and 
the  secretion  of  a  large  quantity  of  colorless  urine,  of  low  specific  gravity, 
free  from  sugar  and  albumen.  It  is  also  called  hyperuresis  or  polydipsia, 
the  latter  term  having  reference  solely  to  the  intense  thirst  which  attends 
it. 

Morbid  Anatomy. — Polyuria  has  been  produced  both  by  mechanical  and 
pathological  lesions  of  the  brain  just  above  the  floor  of  the  fourth  ventricle. 
Disease  of  the  pineal  gland,  and  cerebral  disease  extending  into  the  medulla 
have  also  been  found  associated  with  it.* 

Etiology.— Diabetes  insipidus  may  occur  at  any  age  and  in  either  sex. 
Some  consider  its  immediate  cause  to  be  a  dilatation  of  the  capillary  vessels 
of  the  kidney,  which  has  its  origin  in  a  disturbance  of  the  sympathetic 
ganglia.  Blows  on  the  head,  injuries  to  the  medulla  or  region  of  the  fourth 
ventricle,  injuries  to  the  spinal  cord,  violent  emotions,  have  all  apparently 
caused  its  development.  Drinking  large  quantities  of  ice-water  when 
overheated,  and  exposure  to  cold  and  wet  are  among  its  supposed  causes. 
Diabetes  insipidus  temporarily  disappears  during  the  course  of  acute  febrile 
disease. 

Symptoms. — This  affection  may  come  on  insidiously  or  suddenly.  Its 
chief  symptom  is  the  passage  of  a  large  quantity  of  limpid  urine  ;  the  quan- 
tity varies  from  thirty  to  sixty  pints  j!?er  diem.  Its  specific  gravity  ranges 
from  1.003  to  1.008 ;  it  is  remarkably  clear,  faintly  acid,  and  of  a  greenish 
opalescent  hue.  Urea,  uric  acid  and  kreatin  are  secreted  in  larger  quanti- 
ties than  normal.  It  contains  no  sugar  or  other  abnormal  ingredients. 
Intense  thirst  accompanies  this  increased  flow  of  urine  ;  so  great  is  it  that 
patients  who  have  had  all  fluid  withheld  from  them  have  drunk  with  avidity 
their  own  urine.  The  quantity  of  urine  equals  the  amount  of  fluid  taken. 
The  skin  becomes  harsh  and  dry  ;  and  the  temperature  becomes  subnormal. 
'The  appetite,  gastric  and  intestinal  symptoms  are  all  very  variable.  A 
strong  corroborative  proof  of  its  nervous  origin  is  the  occasional  increased 
salivation  that  is  clearly  due  to  nerve  influence.^  The  other  symptoms 
which  attend  this  disease  are  variable.  In  some  cases  the  patients  are  well 
in  all  other  respects  :  in  others  there  is  vomiting,  rapid  emaciation,  and  the 
general  signs  of  acute  phthisis. 

Differential  Diagnosis. — A  careful  examination  of  the  urine  for  one  month 
will  distinguish  this  condition  from  all  other  diseased  conditions  which  are 
attended  by  the  secretion  of  abnormally  large  quantities  of  urine. 

Prognosis. — Recovery  from  diabetes  insipidus  is  rare,  although  it  may  last 
many  years  without  any  disturbance  of  the  general  health.  Pleurisy  and 
acute  rheumatism  occurring  during  its  course  have  been  followed  by  com- 

1  Dickenson  found  decjenerative  changes  in  the  solai-  plexus.    The  blood  is  said  to  contain  an  abnormally 
large  amount  of  solid  constituents. 
^  See  discussion  of  "submaxillary  gland  and  chorda  tympani  nei've"  in  Foster's  Physiology. 


ANEMIA.  883 

plete  recovery.'     In  most  instances  death  is  caused  by  intercurrent  dis- 
ease. 

Treatment. — When  a  cause  can  be  reached,  it  should  be  removed.  At  all 
times  the  body  should  be  warmly  clothed,  and  the  skin  kept  active.  The 
food  should  be  highly  nutritious  and  easily  digestible.  Great  attention  must 
be  paid  to  the  surroundings  and  general  hygiene  of  the  patient.  Narcotics 
have  been  advocated,  but  they  are  not  so  efficacious  as  in  diabetes  mellitus.^ 
Nitrate  of  potash,  iron,  alum,  lime-water,  tannic  and  gallic  acid,  creosote, 
bromide  of  potassium,  acetate  of  lead,  jaboralidi  and  belladonna  have  all 
been  recommended,  either  for  narcotic,  astringent  or  vaso-motorial  action  ; 
the  chief  idea  in  all  being  to  constringe  the  renal  capillaries.  The  constant 
galvanic  current  passed  between  the  loins  and  epigastrium  is  advocated,  and 
deserves  more  extensive  trial.  ° 

ANEMIA. 

Simple  anaemia  is  a  condition  in  which  the  number  of  the  red  corpuscles 
is  markedly  diminished  ;  when  local  it  is  called  ischsemia.  If  the  llood- 
mass  is  diminished  it  is  called  oligcBmia.  Spanc&mia  and  Jiydrcemia  are 
synonyms  of  ansemia. 

Morbid  Anatomy. — The  density  of  the  blood  is  diminished.  There  is 
diminution  in  the  number  and  size,  and  change  in  the  form  and  color  of  the 
red  blood  discs  ;  one  hundred  corpuscles  may  occupy  no  more  space  than  is 
normally  taken  by  seventy-five,  and  the  number  may  fall  below  one-half 
the  normal.  Besides  quantitative  there  are  qualitative  changes  in  the 
blood ;  the  amount  of  haemoglobin  in  the  red  discs  may  be  diminished 
twenty-five  per  cent.  When  corpuscular  abnormalities  are  due  to  imper- 
fect development  and  formation,  the  condition  is  called  ancematosis ; — 
but  when  they  have  been  perfect  and  have  subsequently  degenerated,  the 
name  JicBmoplithisis  is  applied. 

The  heart  in  one  who  has  died  in  a  state  of  extreme  anaemia  is  flabby 
and  pale  ;  the  blood  is  of  a  lighter  color  than  normal  and  more  fluid  ;  if 
coagula  exist  they  are  pale  and  crumbly.  There  may  be  a  diminution 
in  the  fibrinogen  and  fibrinoplastin.  There  is  usually  a  small  amount  of 
fluid  in  the  serous  cavities.  Ecchymoses  are  common  ;  and  minute  hemor- 
rhages may  be  found  at  various  points. 

Etiology. — Simple  anaemia  may  be  caused  by  anything  that  decreases  the 
number  of  red  corpuscles  or  that  interferes  with  their  production. 

Acute  anaemia  is  the  result  of  sudden  and  excessive  loss  of  blood ;  fe- 
brile anaemia  is  acute. 

Chronic  anaemia  may  be  the  result  of  numerous  small  bleedings,  or  of 
exhausting  discharges  other  than  blood,  which  attend  many  forms  of 
chronic  diseases.  It  is  a  constant  accompaniment  of  many  forms  of  chronic 
visceral  diseases,  of  which  Bright's  disease  is  the  best  example.  Chronic 
blood  poisons  cause  what  is  called  toxic  ansemia.     Interference  with  nutri- 

1  Dickenson  and  Dcsgranges. 

*  Rayer  and  Trousseau  strongly  advocate  valerian  ;  and  Sidney  Ringer  regards  ergot  and  ergotin  as  effi- 
cacious. 
»  Lay  cock  ;  The  London  Lancet,  vol.  ii.,  No.  7,  1875. 


884  CHROinc  general  diseases. 

tion,  from  insufficient  or  improper  quality  of  food,  an ti -hygienic  sur- 
roundings, etc.,  are  prolific  causes  of  simple  angemia.  Women  are  more 
liable  to  anaemia  than  men  ;  and  the  condition  is  much  more  frequent  at 
the  two  extremes  of  life,  than  during  the  period  between  twenty  and  sixty. 
A  tendency  to  an  anaemic  condition  is  not  infrequently  congenital.  Struct- 
ural changes  in  the  cytogenic  tissues,  and  disease  of  the  lymphatics,  induce 
anaemia.  Malignant  growths  and  chronic  tuberculosis  are  attended  by  con- 
ditions of  extreme  anaemia. 

Symptoms. — The  symptoms  of  acute  anasmia — such  as  results  from  pro- 
fuse hemorrhages — are  extreme  pallor,  pinched  features,  and  cold  sweats ;  the 
pulse  is  feeble,  rapid,  is  quickly  accelerated  by  slight  mental  excitement  or 
physical  exertion  ;  a  blowing  cardiac  murmur  and  even  a  '^ bruit  de  diable" 
is  present  in  severe  cases.  A  condition  of  syncope  is  of  frequent  occur- 
rence. Vomiting,  delirium,  tinnitus  aurium,  and  other  nervous  phenomena 
are  common.     The  thirst  is  intense,  and  the  urinary  secretion  is  scanty. 

In  chronic  ancemia  there  is  a  pale,  waxy,  or  sallow  hue  of  the  skin,  and 
a  pale,  bloodless  condition  of  the  mucous  surfaces.  The  skin  becomes  oede- 
matous  and  the  muscles  flabby.  The  hands  and  feet  are  always  cold.  A 
cachectic  or  marasmic  condition  is  developed  ;  the  skin  becomes  harsh,  and 
often  desquamates  in  patches.  As  a  result  of  long-continued  anaemia  a 
hemorrhagic  diathesis  may  be  established.  The  urine  is  pale,  contains 
less  urea  and  less  pigment  than  normal.  Dropsies  are  liable  to  occur  when 
anaemia  has  persisted  for  a  long  time.  The  temperature  is  frequently  sub- 
normal. Extreme  exhaustion  and  muscular  feebleness  are  among  its  ear- 
liest and  most  prominent  signs.  Anaemic  patients  are  irritable,  excitable, 
usually  hyperaesthetic  and  suffer  from  neuralgias.  Anaemic  females  com- 
plain of  a  pain  in  the  left  side  and  a  burning  sensation  on  the  top  of  the 
head.  They  are  often  hysterical.  Temporary  aphasia  may  result  from 
anaemia.  Anorexia  and  atonic  dyspepsia  result  from  deficiency  either  in 
quantity  or  quality  of  the  gastric  juice.  A  morbid,  craving  appetite  some- 
times exists. 

The  constant  and  important  signs  of  anaemia  are  haemic  murmurs,  which 
may  be  cardiac,  arterial,  or  venous.  The  cardiac  murmurs  are  systolic 
in  rhythm,  blowing  or  bellows-like  in  character,  and  have  their  point  of 
maximum  intensity  at  the  base  of  the  heart.  Arterial  murmurs  are  heard 
over  the  large  arteries,  and  they  may  be  accompanied  by  a  thrill  percepti- 
ble in  the  radial  vessels.  Over  the  Jugulars,  particularly  the  right,  there 
is  heard  a  continuous  venous  hum.  A  deep  inspiration  intensifies,  while 
coughing  diminishes  the  intensity  of  the  venous  hum.  It  is  also  dimin- 
ished by  the  horizontal  posture.  It  may  sometimes  be  felt  as  a  thrill  on  pal- 
pation. The  heart's  impulse  is  always  feeble ;  the  heart  sounds  are  muf- 
fled, and  the  radial  pulse  is  compressible  and  small.  Severe  attacks  of 
cardiac  palpitation  are  common. 

Differential  Diagnosis. — Acute  ansemia  from  either  internal  or  external 
hemorrhage  is  not  likely  to  be  confounded  with  any  other  condition.  The 
diagnosis  of  chronic  anaemia  is  readily  made  from  the  history  and  general 
appearance  of  the  patient,  and  by  the  presence  of  haemic  anaemic  murmurs. 


CHLOROSIS.  885 

Prognosis. — The  prognosis  in  anaemia  is  determined  by  the  conditions  un- 
der which  it  occurs.  The  earlier  its  cause  is  discovered,  and  the  more  readily 
removed,  the  better  the  prognosis.  Its  duration  varies  from  days  to  years  ; 
some  individuals,  especially  women,  are  ana3mic  during  their  entire  lives. 
When  it  is  associated  with,  or  dependent  upou,  organic  disease,  the  prog- 
nosis is  unfavorable.  Death,  in  acute,  cases,  results  from  annulling  the 
function  of  the  medulla,  or  cardiac  j^aralysis;  in  chronic  cases,  inanition  and 
exhaustion,  or  some  complication,  induce  the  fatal  issue.  Death  may 
occur  in  syncope,  convulsions  and  coma. 

Treatment. — The  treatment  of  anaemia  is  always  restorative,  and  must  be 
especially  directed  to  improving  the  blood-making  power.  Acute  anaemia, 
the  result  of  profuse  hemorrhage  from  wounds,  accidents,  during  labor, 
etc.,  must  be  treated  surgically  rather  than  medicinally.  The  preventive 
treatment  of  chronic  anaemia  when  it  depends  upon  exhausting  discharges, 
prolonged  lactation,  and  anti-hygienic  conditions,  is  the  removal  of  its 
causes.  The  diet  should  be  most  nutritious,  embracing  a  large  proportion 
of  nitrogenous  elements.  If  the  digestive  organs  are  feeble,  food  must  be 
taken  in  small  quantities  and  at  short  intervals.  Alcohol  is  food  to  anaemic 
patients.  Burgundy,  Madeira,  and  rich  wines  are  to  be  preferred  ;  but  in 
anaemic  females  the  malt  liquors  are  often  more  beneficial.  Daily  exercise 
in  the  open  air  and  exposure  to  the  direct  rays  of  the  sun  are  essential,  and 
should  be  taken  regularly  without  producing  excessive  fatigue.  The  clothing 
should  be  carefully  regulated  ;  in  winter  warm  flannels  should  always  be 
worn,  and  in  the  spring  and  fall  great  care  should  be  exercised  not  to  allow 
the  surface  to  become  chilled. 

Iron  is  the  one  drug  that  best  combats  anaemia.  There  are  many  prep- 
arations,, but  the  chloride,  Vallet's  mass,  Blaud's  pills,  and,  in  children, 
reduced  iron  or  the  citrate  are  the  forms  that  have  given  me  the  best  re- 
sults ;  it  should  be  given  after  meals.  The  combination  of  iron  with  quinia, 
strychnia  and  phosphorus  or  arsenic  is  efficacious  in  many  cases  when  iron 
alone  fails  to  improve.  Emulsions  of  cod-liver  oil  are  valuable  adjuvants 
when  they  can  be  borne  by  the  stomach.  It  should  not  be  given  after  it 
produces  headache  or  dyspeptic  symptoms.'  Eecently  I  have  found  malt 
extracts  combined  with  iron,  pepsin  and  pancreatic  preparations  efficacious 
when  there  is  deficiency  of  stomach  digestion.  The  operation  for  trans- 
fusion of  blood  or  milk  in  extensive  anaemia  has  never  proved  successful  in 
my  experience,  although  there  is  good  authority  for  resorting  to  it.  If  the 
bowels  have  a  tendency  to  constipation,  aloes  should  be  given  with  vegetable 
tonics.  Travel  and  a  change  of  climate,  often  act  beneficially  when  all 
other  means  have  failed. 

CHLOEOSIS. 

Chlorosis  is  a  special  form  of  anaemia,  which  occurs  almost  exclusively  in 
young  females  about  the  age  of  puberty,  without  any  assignable  cause. 

1  Goodhart,  Fothergill,  and  others  mniiitain  that  anasmia  predisposes  to  cardiac  dilatation,  and  hence 
propose  that  digitalis  should  be  combined  with  iron. 


886  CHKONIC   GENERAL  DISEASES. 

Morbid  Anatomy. — The  body  is  well  nourished,  the  organs  are  abnormally 
pale,  the  serous  cavities  contain  fluid,  and  there  is  more  or  less  oedema  of 
the  lower  extremities,  the  red  blood  corpuscles  are  diminished  in  number, 
and  the  hsemoglobin  is  less  in  amount  than  normal.  The  amount  of  albu- 
men in  the  blood-serum  is  often  increased  and  the  mass  of  the  blood  is 
increased. 

Virchow  states  that  a  constant  and  characteristic  lesion  of  chlorosis  is 
imperfect  development  of  the  vascular  system.  The  aorta  and  arteries  are- 
generally  smaller  in  chlorosis  than  normal,  and  thin  walled  ;  the  aorta, 
throughout  its  entire  extent,  may  only  reach  the  normal  size  of  the  caro- 
tids. Fatty  degeneration  of  the  tunica  intima  is  very  common,  and  this: 
coat  may  exhibit  spots  of  superficial  erosion.  The  intima  exhibits  fatty 
change  in  little  spots  or  streaks,  not  in  large  connected  masses.  The  mid- 
dle coat  is  seldom  involved.  The  heart  cavities  are  usually  somewhat 
dilated,  and  hypertrophy  of  their  walls  is  not  infrequent.  Spots  of  extrava- 
sation and  ecchymoses  may  be  found  on  the  mucous  surfaces  and  in  the 
serous  cavities.     The  ovaries  and  uterus  are  usually  abnormally  small. 

Etiology. — Chlorosis  is  regarded  by  some  as  a  neurosis,  the  blood  changes 
being  secondary  to  the  neurosis.  The  unaltered  state  of  the  cytogenic  or- 
gans—spleen, lymph  glands,  and  osseous  marrow — shows  that  it  is  not, 
strictly  speaking,  a  disease  of  the  hsematopoetic  system. '  There  is  always 
more  or  less  anaemia,  and  there  is  nearly  always  some  functional  derange- 
ment of  the  sexual  organs.  All  of  these  causes,  however,  are  not  sufficient. 
to  account  for  its  development  in  the  majority  of  cases.  In  very  many  in- 
stances its  cause  cannot  be  reached.  It  is  met  with  most  frequently  in 
young  girls.^  There  is  a  form  called  amenorrhoeal,  and  another  menor- 
rhagic  chlorosis.    Self-pollution  is  claimed  as  an  exciting  cause  of  chlorosis. 

Symptoms. — With  or  without  derangement  of  the  menstrual  function, 
chlorosis  comes  on  insidiously  in  precisely  the  same  manner  as  simple 
ansemia,  with  which,  in  its  early  stage  it  is  so  readily  confounded.  As  it 
develops,  the  mental  condition  changes,  the  individual  becoming  morose  or 
despondent.  The  countenance  assumes  a  peculiar  waxy,  yellow,  or  yellow- 
green  pallor.  The  face  is  puffy,  the  eyes  are  surrounded  by  deep,  blackish 
circles,  the  sclerotic  is  pearly,  and  the  mucous  membranes  are  pale  al- 
most to  the  verge  of  bloodlessness.  The  puffy  look  of  the  face  is  soon 
shared  by  the  rest  of  the  body  ;  but  it  is  not  oedematous.  ^  Sometimes  the 
cheek  will  retain  a  slight  degree  of  color  ;  and  on  excitement,  mental  or 
physical,  the  face  is  suffused. 

In  some  cases  the  onset  is  sudden,  and  the  above-named  signs  appear  soon, 
after  some  menstrual  derangement.  In  all  cases  lassitude,  muscular  weak- 
ness, dyspnoea,  and  fits  of  cardiac  palpitation  are  common.  Muscular  pains 
follow  violent  physical  exercise.     The  appetite  is  capricious ;  the  patient 

1  Virchow  regards  the  predisposition  to  it  as  dependent  upon  congenital  abnormalities  of  the  heart  or 
aorta.    Immermann  regards  chlorosis  as  due  (in  part)  to  functional  derangement  of  the  cytogenic  organs. 

2  Niemeyer  says  that  "  obstinate  chlorosis  attacks  all  youns  girls,  without  exception,  in  whom  the- 
menses  have  appeared  in  the  twelfth  or  thirteenth  year,  and  before  the  development  of  the  breast  and. 
pubes." 

'  Immermann  states  that  a  tendency  to  obesity  exists  in  chlorosis. 


CHLOROSIS.  887 

will  crave  the  most  indigestible  substances,  and  will  eat  with  avidity  chalk, 
slate  pencils,  ashes,  dirt,  or  strongly  acid  and  spiced  food.  Sometimes 
there  is  anorexia,  sometimes  Miliinia.  Cardialgia  is  a  common  symptom  ; 
it  is  accompanied  by  a  sense  of  weight  over  the  stomach  and  by  belching 
large  quantities  of  inodorous  gas.  It  is  to  be  remembered  that  gastric  ulcer 
is  frequently  met  with  in  chlorotic  females.  Chlorotic  girls  are  usually 
melancholy,  abstracted  and  irritable.  In  some  cases  they  have  attacks 
of  nervousness,  so  that  the  term  chlorotic  hysteria  is  used  to  denote  a 
hysteroid  attack  in  young  females.  The  sexual  desires  are  diminished 
rather  than  increased.  The  rapid  breathing,  dyspnoea,  and  palpitation  are 
undoubtedly  in  most  cases  purely  nervous.  Dyspnoea  is  often  a  very  promi- 
nent symptom  and  is  accompanied  by  a  short,  dry  cough  ;  the  respiratory 
murmur  is  feeble,  and  a  full  inspiration  causes  a  fit  of  coughing,  which 
may  lead  to  the  suspicion  of  phthisis.  There  is  rarely  fever  ;  when  fever 
occurs  there  is  something  more  than  chlorosis.  Often  late  in  the  disease, 
oedema  of  the  feet  and  ankles  occurs. 

The  urine  is  pale  and  watery.  The  specific  gravity  is  below  normal.  Urea 
and  coloring  matter  are  deficient  in  quantity.  Leucorrhoea,  and  amenor- 
rhoea  or  menorrhagia  are  common  attendants  of  chlorosis.  The  heart  is 
feeble  and  excitable.  A  systolic  haemic  murmur  is  present  which  is  heard 
in  the  carotids  as  in  anaemia,  but  the  venous  hum  in  the  neck,  though  not 
infrequent,  is  still  not  so  common  as  in  angemia. 

DiflFerential  Diagnosis. — Chlorosis  may  be  mistaken  for  progressive  perni- 
cious ancemia,  for  simple  aiicemia,  Brighfs  and  cardiac  disease. 

In  ancemia  emaciation  is  marked  ;  in  chlorosis  there  is  no  loss  of  flesh. 
The  peculiar  greenish  color  and  the  mental  state  are  important  points  in  its 
differental  diagnosis.  The  age,  sex,  and  presence  of  uterine  complications 
are  all  important  in  distinguishing  chlorosis  from  ansemia. 

An  examination  of  the  urine  in  the  one  case  and  a  physical  exploration 
of  the  chest  in  the  other,  will  soon  decide  as  to  the  existence  of  kidney  or 
cardiac  disease. 

Prognosis. — The  course  of  chlorosis  is  influenced  by  the  hygienic  and  social 
surroundings  of  the  patient,  and  by  the  treatment  employed.  It  is  not  a 
self-limiting  disease,  and  shows  no  tendency  to  spontaneous  cure.  Its  dura- 
tion is  very  uncertain.  As  a  rule  the  prognosis  is  unfavorable,  on  account 
of  the  liability  to  serious  complications,  as  phthisis,  valvular  endocarditis, 
ulcer  of  the  stomach  and  thrombotic  formations.  Eheumatism,  septicaemia, 
typhoid  fever,  and  pneumonia  are  nearly  always  of  a  malignant  type  and 
fatal  in  one  who  is  chlorotic.  Hysteria,  chorea,  paralysis,  and  epilepsy 
sometimes  complicate,  and  sometimes  are  sequelae  of  chlorosis.'  It  is  to  be 
remembered,  in  giving  a  prognosis,  that  relapses  are  common  after  intervals 
of  seeming  health. 

Treatment. — When  a  cause  can  be  reached,  such  as  self-abuse,  masturba- 
tion, or  disease  of  the  functions  of  the  uterus  or  its  appendages,  the  removal 
of  such  cause  will  be  the  first  step  in  the  treatment.  Chlorotic  patients 
should  have  an  out-of-door  life  with  cheerful  companions  and  surroundings  ; 

1  Friedreicli  and  others  state  that  BasedotJo's  Disease  is  unmistakably  connected  with  chlorosis 


888  CHRONIC   GE]srEEAL   DISEASES. 

they  should  eat  regularly  of  a  diet  of  which  meat  and  vegetables  form  the 
chief  part.  Late  hours  and  bad  air  and  gaslight  should  not  be  allowed. 
Mental  is  as  important  as  physical  hygiene.  The  patient  should  not  be  idle; 
something  pleasant  must  always  occupy  the  mind.  I  have  found  that  iron 
does  not  act  as  well  here  as  in  ansemia  ;  indeed,  in  many  instances  it  is  not 
well  borne.'  When  there  is  a  tendency  to  fulness  about  the  head  it  does 
harm  ;  some  authorities  state  that  only  small  quanities  of  iron  are  absorbed 
by  this  class  of  patients,  others  say  that  large  doses  are  of  much  more  service 
than  small. 

Arsenic  I  regard  as  the  most  valuable  medicinal  agent,  either  alone  or 
combined  with  iron.  Constipation  is  to  be  overcome  by  the  careful  but 
persistent  use  of  small  doses  of  aloes  and  nux  vomica.  Quinine,  calumba 
and  quassia  may  be  given  alone,  or  in  combination  with  ferric  preparations. 
Zinc  and  the  mineral  acids  will  often  prove  valuable  adjuvants  to  the 
iron  plan  of  treatment.  In  cases  of  long  standing  the  rest  treatment  com- 
bined with  massage  are  followed  by  good  results  when  all  other  means 
have  failed. 

PEOGEESSIVE    PERNICIOUS    ANEMIA, 

This  form  of  anaemia  has  received  many  names  ;°  but  progressive  perni- 
cious anaemia  is  the  term  now  most  generally  accepted.^  It  may  be  de- 
fined as  that  form  of  anaemia  which  occurs  without  discoverable  cause,  re- 
sists all  treatment,  and  steadily  progresses,  with  greater  or  less  rapidity,  to 
a  fatal  termination.  The  degree  of  oligocythaemia  is  greater  than  in 
simple  anaemia. 

Morbid  Anatomy. — The  Hood  is  scanty  and  pale  with  a  specific  gravity  in 
some  cases  as  low  as  L030,  and  shows  but  slight  tendency  to  coagulate. 
The  number  of  red  corpuscles  is  greatly  diminished  and  their  size  and  out- 
line are  altered.  There  is  no  increase  in  the  white  corpuscles,  but  they 
seem  to  be  in  excess,  solely  from  the  great  loss  in  the  red.  It  is  stated 
that  the  amount  of  haemoglobin  in  each  red  disc  is  diminished  ;  and  that 
the  white  globules  contain  traces  of  it.  Myelogenic  pseudo-leukaemia  was 
the  name  proposed  by  those  who  found  that  in  this  disease  the  adult  mar- 
row became  fcetal,  red  and  adenoid."  But  the  change  in  the  medullary 
structure  of  the  bones  is  a  secondary,  not  a  primary  change.  Large  nucle- 
ated embryonic  corpuscles,  lymphoma,  and  multiple  sarcomatous  growths 
have  been  found  in  the  marrow.^  Secondary  to  the  anaemia  the  heart  un- 
dergoes circumscribed  or  diffuse  fatty  degeneration.  When  this  is  partial 
the  papillary  muscles  and  inner  part  of  the  heart  seem  to  suffer  most.     In 

'  Immermann  and  Niemeyer  both  regard  all  else  as  subservient  to  iron.  The  former  says  a  couple  of 
boxes  of  iron  pills  do  more  good  than  anything  else.  They  both  regard  iron  as  of  more  benefit  than  in 
any  other  (allied)  malady. 

^  Addison  called  it  idiopathic  ansemia ;  Lebert,  essential  anaemia  and  puei^eral  chlorosis  ;  and  Ponflck 
the  ancemia  of  fatty  heart.    Ansmatosis  and  pseudo-leucocythemia,  have  also  been  proposed  for  it. 

3  Andral,  Wilks  and  Wagner  describe  it  under  other  names. 

*  Cohnheim,  Gardner,  Litten,  Fede,  Pepper  and  Eichhorst  all  found  the  bone-changes  prominent  in 
this  disease  ;  and  the  last  named  found  microaytes  in  the  marrow. 

»  See  a  case  described  clinically  by  Ehrlich,  and  pathologically  by  Growitz,  in  Charite-Annalen,  1880. 
Berlin. 


PROGRESSIVE    PERNICIOUS   AN^IIMIA.  889 

many  cases  there  is  more  or  less  dilatation,  but  no  change  occurs  in  the 
valvular  apparatus.  The  inner  coat  of  the  larger  arteries  and  certain 
capillary  tracts  also  exhibits  fatty  degeneration. 

The  liver,  spleen,  kidney  and  stomach  are  ansemic, — even  bloodless  in 
severe  cases — and  their  epithelial  elements  present  similar  fatty  changes. 
In  the  kidney  multiple  sarcomatous  formations  have  been  found.'  The 
liver  and  spleen  may  be  enlarged  ;  although  some  observers  maintain  that 
anemia  attended  by  splenic  enlargement,  disease  or  swelling  of  the  lym- 
phatics, or  any  change  in  the  medulla  of  the  bones  is  to  he  excluded  from 
the  class  called  progressive  pernicious  ancemia.  The  body  is  commonly 
covered  with  small — rarely  large — spots  of  ecchymosis,  and  internal  hem~ 
orrhages  are  not  uncommon. 

Retinal  Jiemorrliage,  demonstrable  during  life,  is  so  common  as  to  have 
been  regarded  as  affording  almost  positive  proof  of  its  existence.  These 
hemorrhages  are  due  to  fatty  degeneration  of  capillary  aneurisms.  The 
serous  sacs  of  the  body  contain  more  or  less  blood-stained  fluid,  and  may 
also  exhibit  ecchymotic  spots.  There  is  not  much  emaciation,  though  the 
skin,  membranes,  and  internal  viscera  are  much  paler  than  in  simple  anae- 
mia ;  and  rigor  mortis  is  late  and  slight.^ 

Etiology. — The  essential  nature  of  progressive  pernicious  anaemia  is  un- 
known. It  has  been  suggested  that  at  times  an  endemic  and  specific  cause 
may  be  at  work,  since  the  disease  has  been  found  to  occur  with  compara- 
tive frequency  in  certain  localities.^  "Women  suffer  more  than  men,  and 
are  liable  to  it  especially  during  pregnancy.^  The  period  between  twenty 
and  forty  is  the  age  when  most  cases  occur  ;  the  disease  being  rarely  seen 
in  early  youth  or  extreme  age.  When  no  cause  can  be  found  for  extreme 
anaemia,  and  when  no  treatment  retards  its  progress,  the  case  is  probably  one 
of  progressive  pernicio us  ancem ia. 

Symptoms. — It  comes  on  insidiously.  Whether  the  patient  has  been  ill 
or  in  perfect  health,  the  course  is  the  same,  and  it  begins  with  a  sense  of 
languor,  which  increases  from  day  to  day.  The  skin  and  mucous  membranes 
become  very  pale  and  assume  a  dusky  yellow  color  quite  distinct  from  the 
green  of  chlorosis.  The  muscles  are  soft  and  relaxed,  and  muscular  weakness 
may  be  so  extreme  as  to  force  the  patient  to  take  to  his  bed  ;  and  yet  there  is 
often  little  or  no  emaciation.  Cardiac  palpitation,  dyspncea,  and  attacks 
of  syncope  are  the  results  of  the  oligocythemia  and  attendant  exhaustion. 
More  or  less  cedema  and  puffiness  appear  about  the  legs  and  ankles,  as- 
sociated with  hemorrhages  from  the  nose,  gums,  bronchi,  and  female  gen- 
itals. At  the  same  time  the  body  exhibits  ecchymotic  and  petechial  spots 
and  vibices,  due  to  subcutaneous  or  external  hemorrhage/  Ketinal  apo- 
plexy is  not  uncommon,  and  an  ophthalmoscopic  examination  should  never 

>  Quincke  found  an  abnormal  quantity  of  iron  in  the  liver,  and  regarded  that  as  a  proof  of  great  destruc- 
tion of  red  discs. 

*  Brigidi  found  that  the  coeliac  ganglia  showed  fatty  and  pigmentary  degeneration  of  the  nerve  cells. 
Le  Sperimentale.    May,  1878. 

'  Cf.  Biermer  In  the  Zuch  Canton, 

*  Gusserow  proposes  the  name  "  extreme  anaemia  of  pregnant  women."  Lebert  also  calls  it  "  puer- 
peral chlorosifi." 

*  Immermann  says  the  bleedings  are  due  to  the  intense  oligocythfemia. 


890  CHRONIC    GEISTEEAL    DISEASES. 

be  omitted  in  any  suspected  case.  Persistent  diarrhoea  is  often  present  quite 
early,  and  the  urine  is  darker  than  normal. 

There  are  early  signs  of  atonic  dyspepsia ;  and  anorexia,  nausea,  and 
vomiting  evidence  the  great  irritability  of  the  gastro- intestinal  tract.  To- 
ward the  end  there  are  periods  of  pyrexia  during  which  the  temperature 
is  remittent  and  may  reach  104°  F.  The  rise  in  temperature  is  attended 
by  other  febrile  phenomena,  such  as  thirst,  furred  tongue,  etc.,  etc.  Still 
later  there  is  a  time  of  absolute  apyrexia,  and  toward  the  very  last  moments 
of  life  the  temperature  runs  far  below  normal.  Cardiac,  venous,  and  arterial 
murmurs  are  present  and  are  far  more  intense  than  in  simple  anaemia.  The 
cardiac  systolic  murmur  is  associated  with  the  fremissement  cataire.  The 
heart  is  always  feeble,  and  in  severe  cases  intermittent ;  sometimes  it  is- 
slightly  dilated  from  fatty  degeneration. 

Differential  Diagnosis. — Progressive  pernicious  anaemia  may  be  mistaken 
for  simple  ancemia,  leucocytlicBmia,  pseudo-leukcemia,  and  chlorosis. 

Ordinary  ancemia  presents  a  discoverable  cause,  is  attended  by  marked 
emaciation,  has  no  febrile  symptoms  and  no  evidence  of  retinal  hemorrhages 
or  purpuric  spots.  In  progressive  pernicious  anasmia  the  case  is  Just  the 
reverse.  Finally,  simple  anaemia  is  amenable  to  treatment,  while  pernicious- 
anaemia  is  not. 

In  leucocythcemia  the  spleen  and  lymphatics  are  enlarged,  often  enor- 
mously ;  and  the  bones,  especially  the  sternum,  may  be  tender  and  some- 
what swollen,  and  the  blood  will  contain  an  actual  as  well  as  relative — 1-20 
excess  of  white  globules.  None  of  these  conditions  are  present  m  progres- 
sive pernicious  anaemia. 

In  pseudo-leukcemia  the  spleen  and  lymphatics  undergo  the  same  en- 
largements as  in  leucocythaemia,  but  there  are  no  blood  lesions,  while  in 
pernicious  anaemia  there  is  no  enlargement  of  lymph-structures,  and  the 
diminution  of  red  discs  is  greater  than  in  a.ny  other  disease. 

Chlorosis  is  a  disease  of  young  females  ;  it  is  uncommon  except  at  the 
time  of  puberty.  Pernicious  anaemia  is  common  among  women  in  the  pu- 
erperal state,  and  occurs  between  twenty-five  and  forty  as  a  rule.  Chlorosis 
is  unattended  by  dropsy,  while  dropsical  symptoms  are  common  in  perni- 
cious anaemia.  Hemorrhages,  spots  of  extravasation,  and  febrile  phenomena 
form  no  part  of  the  natural  history  of  chlorosis  ;  while  they  are  constant 
symptoms  in  pernicious  anaemia.  Chlorosis  is  curable  and  does  not  pro- 
gress beyond  a  certain  point ;  pernicious  anaemia  is  incurable  and  progres- 
sive. In  chlorosis  the  face  has  a  yellow-green  hue  ;  in  progressive  pernicious 
anaemia  it  is  of  a  dusky  yellow. 

Prognosis. — Death  occurs  in  90  per  cent,  of  all  cases.  Of  course  those 
who  make  death  a  necessary  factor  in  their  acceptation  of  the  definition, 
justly  hold  that  it  is  a  fatal  malady.  The  duration  varies  from  six  weeks 
to  six  months.  Whether  it  may  supervene  on  a  benign  ansemia  or  a  chloro- 
sis is  uncertain.  In  very  rapid  cases  hemorrhage  and  diarrhcea  will  be  ex- 
cessive. Death  may  occur  from  inanition,  exhausting  hemorrhages  or  apo- 
P^exy.' 

1  Bramwell  states  that  the  end  is  often  ushered  in  by  diarrhoea,  coma,  or  dehriuin. 


LEUCOCYTH^MIA. 


891 


Treatment. — The  treatment  is  purely  symptomatic  and  supporting.  Iron, 
quinine,  strychnia  and  arsenic,  in  combination  with  a  highly  nutritious, 
mostly  fluid  diet,  will  be  found  the  most  available  moans  in  such  a  line  of 
treatment.  Change  of  air  and,  when  the  strength  allows,  sea-bathing  are 
highly  recommended.  Transfusion  of  blood  has  been  tried,  and  has  failed. ' 
One  case  was  reported  as  cured  by  transfusion  of  two  ounces  of  human 
blood  by  the  Dieulafoy  aspirator.^  Though  the  outlook  is  discouraging 
from  the  onset,  yet  vigorous  supporting  treatment  should  be  the  rule  from 
first  to  last. 

LEUCOCYTHJEMIA. 


Leucocythsemia  is  an  abnormal  blood  condition  marked  by  increase  in 
the  number  of  the  colorless  corpuscles,  and  associated  with  new  formation 
of  cytogenic  tissue  in  different  parts  of  the  body.'  It  may  assume  either  a 
splenic  or  lymphatic  form,  associated,  in  some  cases,  with  a  myelogenous 
leukgemia,  in  which'  the  medulla  of  the  bones  is  involved.  When  two  of 
the  adenoid  structures  are  simultaneously  involved,  it  is  spoken  of  as 
medullo-splenic  or  lymphatico-splenic  leucocythsemia. 

A  temporary  increase  in  the  colorless  corpuscles  (leucocytosis)  is  not  in- 
frequent during  and  immediately  after  full  digestion,  in  pregnancy  and 
fevers.     It  is  not  leucocythsemia. 

Morbid  Anatomy. — The  blood  in  leucocythgemia  is  pale,  its  specific 
gravity  is  diminished,  and  it  does  not  readily  coagulate,  although  the 
amount  of  fibrin  is  said  to  be 
increased.  These  changes  are 
due  to  a  very  marked  increase 
in  the  number  of  white  corpus- 
cles, which  sometimes  equal  the 
red.  In  splenic  leukaemia  the 
white  discs  are  larger  and  more 
granular  than  normal ;  while  in 
the  lymphatic  form  they  are 
smaller.  In  some  instances  cor- 
puscles containing  several  nuclei 
preponderate ;  in  others  the 
white  discs  are  found  with  only 
one  nucleus.  Fat  is  sometimes 
found  in  the  white  discs.  The 
red  blood  globules  are  dimin- 
ished in  number,  and  they  lose 
their  normal  outline.  When 
leuksemic  blood  is  defibrinated 
the  corpuscles  sink  and  form  two 
distinct  layers — an  upper  wliite  layer,  and  a  subjacent  red. 


Fig.  184. 
Blood  from  a  case  of  Leucocythsemia. 

A.  A.  White  Blood  Corpuscles. 

B,  B.  Red  Blood  Corpuscles,   x  300. 


Some  state 


'  Dr.  Weldon  states  that  he  has  cured  four  cases  by  the  intra-venous  injection  of  milk. 
*  Dr.  Cary,  in  the  Buf.  Med.  and  Surf/.  .lour.,  Jan.,  1881. 

3  Prof.  J.  Hughes  Bennett,  in  184.5,  described  this  condition  as  suppuration  of  the  blood.    Virchow,  the 
eame  year,  called  it  Icukcerrda.    Six  years  later,  Prof.  Bennett  used  the  name  leucocythsemia. 


892 


CHROKIC    GENERAL   DISEASES. 


that  the  reaction  of  leuksemic  blood  is  acid,  others  that  it  is  alkaline. 
Elongated,  octahedral,  colorless  crystals  of  albuminoid  material  are  often 
found  in  the  blood ;  chemical  analyses  have  resulted  in  the  discovery  of 
multifarious  ingredients,  as  lactic,  uric,  formic,  acetic,  and  glycerin-phos- 
phoric acids,  leucin,  tyrosin,  etc.,  etc.,  some  of  which  are  present  (nor- 
mally) in  the  spleen.'  It  is,  however,  only  when  the  blood  persistently 
shows  a  proportion  of  white  to  red  of  one  to  twenty  that  leukaemia  can  be 
diagnosticated. 

The  spleen  usually  uniformly  enlarges  in  all  cases,  and  it  may  reach 


Fig.  185. 
Section  of  a  Leucocythsemic  Spleen. 

A,  A.  Fibrous  trabeculce  of  the  vascular  sim/ses—f>Hg/My  thickened. 

B,  B.  Dilated  venous  sinuses  cotitaining  hjmphoid.  cells  C,  C.  swolkn  and  proliferating 

D,  D,  and  large  multinucleated  cells  E,  E. 


endotMM  ceUs 


eighteen  pounds  in  weight.  It  is  usually  fii-mer  than  normal  ;  never 
softer.  On  its  cut  surface  the  trabeculae  stand  out  as  whitish  striae,  and  the 
Malpighian  bodies  as  whitish  dots.  These  last  are  lymphadenomata  of  the 
Malpighian  bodies,  which  resemble  hypertrophies,  the  tumors  having  an 
encephaloid  look,  and  yielding  a  cancer-like  juice.^  The  organ  is  some- 
times "  mottled "  with  infarctions,  the  vessels  being  plugged  by  white 
blood-cells.  In  these  cheese-like  islands  the  vessels  are  changed  into 
granulo-fatty  tracts.  Large  multinuclear  cells  and  many  lymphoid  ele- 
ments are  found  in  the  venous  sinuses.  The  capsule  is  somewhat  thicker 
than  normal,  and  inflammatory  adhesions  may  bind  it  to  surrounding 
parts.  In  the  hilus  of  the  organ  lymphomata  the  size  of  an  egg  are 
sometimes  found. 

Virchow  thus  sums  up  the  splenic  changes  :  "Hyperplasia  of  this  lym- 

^  Physiology,  M..  Foster.     "  Metabolic  Phenomena,"  etc. 

*  Cornil  and  Ranvier  saj'  that  the  diagnosis  of  lymphadenomata  (which  may  affect  other  glands  than 
the  splenic  Malpighian  bodies)  is  to  be  made  from  cancer,  by  the  fact  that  the  capillaries  in  leukcemia  are 
full  of  white  discs  which  carmine  stains. 


LEUCOCTTH^MIA.  893 

phatic  organ  induces  chemical  and  morphological  changes  in  the  blood." 
In  the  lymphatic  variety  the  splenic  enlargement  is  slight,  and  the  princi- 
pal change  is  hyperplasia  of  the  lymphatics.  The  inguinal,  axillary,  and 
cervical  glands  are  enlarged  and  soft,  and  present  a  red,  pulpy  appearance. 
The  meshes  of  their  connective-tissae  are  crowded  with  lymphoid  elements. 

In  myelogenic  leukmmia  the  marrow  in  the  long  bones  and  the  spongy 
tissue  of  the  sternum,  ribs,  and  vertebra  is  changed  to  a  creamy-white 
]niruloid  mass.  lu  some  cases  this  hyperplasia  produces,  or  is  attended  by, 
a  red,  fleshy  appearance,  like  foetal  marrow.  The  larger  vessels  in  these  cases 
have  their  walls  infiltrated  with  lymph-cells,  and  the  small  vessels  that  re- 
main in  the  changed  marrow  are  chiefly  filled  with  red  cells.' 

Between  the  liver  cells  are  found  circumscribed  or  diffused  patches  of 
white  blood  cells  that  have  escaped  from  the  overfull  capillaries — this  is 
called  "  apoplexy  of  the  white  blood  corpuscles  " — and  in  connection  with 
connective-tissue  hyperplasia  form  the  whitish  masses  found  in  the  organ. 
The  liver  is  enlarged  from  hypersemia  and  from  inter-lobular  and  inter- 
cellular infiltration. 

In  the  kidneys  the  infiltration  of  lymphoid  elements  appears  in  lines 
parallel  to  the  tubules.  Here  also  lymphadenomata  start  from  the  con- 
nective-tissue. Similar  new  growths  are  common  in  the  stomach  and 
intestines,  often  measuring  from  1  to  1^  inches  in  diameter,  and  present- 
ing many  of  the  characteristics  of  cancer. 

The  lungs,  brain,  skin,  testicle,  and  retina  are  sometimes  the  seat  of  the 
leuksemic  developments.  The  heart  may  suffer  fatty  degeneration,  and 
there  may  be  effusions  into  the  pericardium.  Indeed,  effusions  are  fre- 
quent in  all  the  serous  cavities.  Cerebral  embolism  occurs  in  about  five 
per  cent,  of  all  cases.  Hemorrhage  from  mucous  surfaces  or  into  serous 
sacs  is  a  very  common  pathological  accompaniment  of  leucocythfemia. 

Etiology. — Leucocythgemia  occurs  at  all  ages  and  conditions,  but  it  is 
most  frequent  in  early  adult  life.  It  is  twice  as  frequent  in  men  as  in 
■women.  In  women  there  is  a  notable  connection  between  the  generative 
functions  and  leucocythaemia.  Cold,  wet,  and  all  anti-hygienic  conditions 
predispose  to  it.  When  the  Peyerian  patches  are  lymphadenoraatous,  it  is 
possible  that  previous  intestinal  catarrh  was  the  etiological  factor.  In  the 
majority  of  instances  the  etiology  cannot  be  determined. 

Symptoms. — The  early  symptoms  of  leucocythaemia  are  almost  identical 
with  those  of  simple  anmmia,  accompanied  by  swelling  of  the  abdomen  with 
a  sense  of  fulness  in  the  left  hypochondrium  and  wandering  pains  in  the 
splenic  region.  The  splenic  enlargement  may  or  may  not  be  attended  by 
fever. 

In  the  lymphatic  variety,  enlargement  of  the  glands  in  the  groin,  neck, 
and  axillary  regions  may  be  the  first  symptoms  which  will  attract  atten- 
tion, and  may  exist  for  months  before  the  blood  changes  can  be  detected. 

In  the  myelogenic  variety,  the  bones,  especially  the  ribs  and  sternum,  be- 


1  Neuman  regards  the  myelogenous  chnnges  as  primary,  and  states  that  hyperplasia  of  the  man-ow 
canses  immature  corpuscles  to  enter  the  blood.  TJeber  Myelogene  Leukcemie,  Berlin,  Klin.  Woch.,  1878, 
(6-10). 


894  CHRONIC    GEiq-ERAL   DISEASES. 

come  tender  upon  pressure,  and  as  the  disease  advances  the  patient  becomes 
pale  and  assumes  a  waxy  appearance.  There  will  be  more  or  less  pyrexia 
with  evening  exacerbations,  the  fever  being  usually  in  proportion  to  the 
rapidity  of  the  leuksemic  development.  The  pulse  is  accelerated,  feeble, 
and  marked  by  a  peculiar  throb.  The  appetite  is  capricious,  and  the  tongue 
and  pharynx  may  be  the  seat  of  ulcerations.  Early  in  the  disease  the 
bowels  are  constipated  ;  but  its  late  stages  are  attended  by  exhausting 
diarrhoea.  Dyspnoea,  arising  from  the  blood  condition  and  from  the 
splenic  enlargement,  is  associated  with  a  chronic  bronchitis.  As  a  result 
of  the  blood  changes,  a  hemorrhagic  tendency  is  developed,  which  may 
cause  hemorrhages  from  any  mucous  surface,  or  apoplexy.  Eetinal  hem- 
orrhages and  whitish  patches  due  to  apoplexy  of  the  white  blood  corpuscles 
can  be  detected  by  the  ophthalmoscope.  Ecchymotic  spots  often  appear 
over  the  body,  and  the  fatal  termination  is  hastened  by  this  hemorrhagic 
tendency. 

If  a  hemorrhagic  diathesis  is  not  developed  the  disease  runs  a  tedious 
course.  In  such  cases  the  enlargement  of  the  spleen  and  lymphatics  is  very 
great  and  leads  to  symptoms  of  pressure.  General  anarsarca  is  of  frequent 
occurrence  toward  the  end  of  the  disease,  and  under  these  circumstances  the 
dyspnoea  becomes  extreme.  The  urinary  symptoms  are  not  important, 
though  the  abnormal  constituents  present  the  greatest  variety.  The 
amount  passed  diminishes  with  the  progress  of  the  disease.'  As  leuksemic 
patients  emaciate  the  dyspnoea  increases,  and  the  fever,  which  was  at  first 
intermittent,  becomes  continuous.  If  no  complication  occur  death  results 
from  exhaustion,  preceded  by  delirium,  stupor,  and  coma. 

Differential  Diagnosis. — Leucocythaemia  may  be  mistaken  for  progressive 
pernicious  anmmia,  for  chlorosis,  and  in  its  early  stages  for  infiammatory 
and  cancerous  enlargements,  and  for  pseudo-leukaemia,  or  Hodghin's 
disease. 

In  all  cases  the  difEerential  diagnosis  rests  upon  the  result  of  a  micro- 
scopic examination  of  the  blood.  When  the  ratio  between  the  white  and 
red  globules  reaches  one  to  twenty  the  case  must  be  regarded  as  one  of 
leucocythsemia. 

Prognosis.— No  case  of  recovery  from  leucocythaemia  has  yet  been  re- 
corded. It  varies,  however,  in  its  duration.  If  it  comes  on  abruptly  with 
active  symptoms  it  may  prove  fatal  in  three  or  four  months  ;  but  when  in- 
sidious in  its  approach  three  or  four  years  may  elapse  before  the  fatal 
result  is  reached.  The  average  duration  of  the  cases  under  my  observa- 
tion has  been  about  fourteen  months.  Sometimes  the  disease  does  not 
progress  steadily,  but  advances  by  stages,  progressing  rapidly  for  a  few 
months,  and  then  remaining  stationary  for  as  long  a  period. 

The  more  rapidly  the  patient  emaciates,  the  more  frequent  and  profuse 
the  hemorrhages,  and  the  higher  the  temperature,  the  more  unfavorable  the 
prognosis.  Dropsy  is  always  an  unfavorable  symptom.  The  most  frequent 
complications  are  effusions  into  the  serous  cavities  and  hypostasis  in  the 


'  A  number  of  cases  are  recorded  where  priapism,  venereal  excess,  and  seminal  emissions  have  marked 
the  onset  and  course  of  the  disease,  but  the  value  of  such  symptoms  is  yet  to  be  determined. 


hodgkin's  disease.  895 

lungs.  Pneumonia,  pleurisy,  and  intestinal  catarrh  stand  next ;  then  follow 
a  long  list  of  visceral  diseases  which  appear  as  coincidences,  rather  than 
complications.  Death  may  occur  from  profuse  hemorrhage,  from  cerebral 
apoplexy,  from  pulmonary  and  serous  inflammation,  or  from  exhaustion. 

Treatment.  — None  of  the  many  measures  proposed  and  tried  have  as  yet 
produced  a  cure  or  proved  successful  in  arresting  its  progress.  Quinine  in 
large  doses  is,  however,  advocated  by  all ;  it  is  tonic,  and  also  has  a  direct 
influence  upon  the  spleen.  Arsenic  and  iron  should  also  be  steadily  given, 
either  alone  or  in  combination  with  quinine.  Faradization  of  the  spleen, 
extirpation  of  the  spleen  and  transfusion  of  blood  have  been  tried,  the 
latter  witJi,  the  two  former  without,  success.  Mtric  and  nitro-muriatic 
acid,  internally  and  in  the  form  of  baths  (locally)  are  recommended. 
Iodine  preparations  do  not  seem  to  have  any  efficacy,  and  the  water-cure 
plan  has  been  abandoned.  The  malady  is  delayed  hj  cheerful  surround- 
ings and  simple  and  nutritious  diet.  Ood-liver  oil  and  phosphorus  are 
valuable  adjuvants  to  the  dietetic  plan.  But  the  chief  indications  for 
treatment  are  found  in  the  accidental  complications. 


(Pseudo-Leukcemia.) 

Pseudo-leukaemia  is  a  disease  resembling  leucocythaemia  in  all  its  ana- 
tomical characteristics  except  the 'blood  changes.  It  consists  in  enlarge- 
ment of  the  lymphatic  structures  and  development  of  lymphotnata  ;  it  so 
invaribly  terminates  fatally  that  the  term  malignant  lymphoma  has  been 
suggested  for  it. ' 

Morbid  Anatomy. — Histologically  the  lesions  of  this  disease  in  no  wise 
differ  from  lymphomata.  They  are  divided  into  hard  and  soft  tumors. 
The  soft  lymphomata  are  of  encephaloid  consistency.  Their  color  is  a 
reddish  gray,  studded  with  spots  of  extravasation.  The  glands  undergo 
simple  hy23erplasia,  and  as  they  enlarge  become  confluent,  forming  a 
large,  soft,  fluctuating,  lobulated  tumor.  The  capsule  is  in  some  cases 
attacked  ("periadenitis"),  and  then  the  process  is  not  confined  to  the 
lymphatics,  but  extends  to,  and  infiltrates  the  adjoining  tissues.  The  fluid 
expressed  from  a  cut  surface  resembles  cancer- juice.  Hard  tumors  have 
a  fibrous  feel,  and  on  section  exhibit  a  shining,  waxy  appearance.  The 
capsule  and  medullary  structure  are  indistinguishable  and  no  fluid  can  be 
expressed.  Many  regard  the  extensive  hyperjolasia  of  the  soft  as  the 
initial  stage  of  the  hard ;  while  others  consider  the  greater  proportion  of 
cellular  elements  as  the  cause  of  the  difference.  These  tumors  are  rarely 
larger  than  a  hen's  egg.  Unlike  scrofulous  glandular  enlargement  they 
undergo  no  caseation,  suppuration,  or  retrogressive  changes. 

As  a  sequela  of  this  disease  the  number  of  red  globules  in  the  blood  is 
diminished.     The  disease  first  attacks  one  group  of  lymphatics  and  later 

1  Hodgkin,  whose  name  the  disease  bears,  was  the  first  to  describe  these  peculiar  Ij'niphatic  changes 
0832).  Trousseau  called  it  "  Adene."  Anaemia  lymphatica,  Lymph o-sarcoma,  Progressive  glandular 
hypertrophy,  and  Lymphadenosis  are  terms  also  applied  to  it. 


896  CHRONIC    GENERAL   DISEASES. 

invades  those  of  the  whole  body.     The  glands  at  the  angle  of  the  jaw,  in 
the  axilla  and  groin  are  usually  first  affected. 

The  spleen  is  enlarged,  but  rarely  to  such  a  degree  as  in  leucocythaemia. 
On  section,  it  is  seen  studded  with  grayish  nodules,  the  Malpighian  bodies 
having  undergone  hyperplasia.  The  lymphatic  enlargements  may  be  fol- 
lowed by  similar  developments  in  the  liver,  kidney,  stomach,  lungs,  ovaries, 
testicles,  brain,  retina,  muscles,  subcutaneous  tissue,  and  in  the  serous 
membranes.  These  are  called  metastatic  or  secondary  deposits  ;  and  de- 
velop especially  in  and  along  vascular  walls. 

Etiology. — Lympho-sarcomata  were  formerly  thought  to  be  carcinoma- 
tous or  a  malignant  form  of  tuberculosis.  There  is  no  connection  between 
pseudo-leuksemia  and  scrofulosis,  or  between  it  and  syphilitic  affections  of 
the  lymphatics.  The  disease  has  been  found  in  men  oftener  than  in  women  ; 
but  no  etiological  relations  have  been  established. 

Symptoms. — When  pseudo-leukaBmia  runs  its  regular  course,  and  begins 
by  swelling  of  the  glands  in  the  neck,  armpit,  or  groin,  it  can  be  recognized 
without  difficulty,  and  the  time  of  its  commencement  can  be  fixed  with 
considerable  certainty.  But  when  the  enlargement  commences  in  the  ton- 
sils, the  retroperitoneal,  mediastinal,  or  other  deep-seated  and  impalpable 
glands,  its  diagnosis  is  difficult.  In  all  forms,  however,  emaciation  and 
anaemia  are  marked  and  progressive.  In  the  majority  of  cases  the  spleen 
will  be  more  or  less  enlarged  ;  and  d\iH  pains,  with  a  sense  oi  fulness  and 
distention,  will  be  felt  in  the  left  hypochondrium.  Attacks  of  cardiac  pal- 
pitation are  common.  The  pulse  is  small  and  rapid.  In  the  majority  of 
cases  there  is  a  steady  pyrexia  (100°  to  101"  F.)  towards  the  end,  attended 
by  slight  evening  exacerbations.  With  the  increasing  anaemia  there  will 
be  dropsy,  and  when  the  disease  is  well  advanced  the  muscular  weakness  is 
marked.  When  nausea,  vomiting,  and  diarrhoea  are  prominent  symptoms, 
lymphadenomata  of  the  stomach  or  intestines  may  be  suspected.  When 
dyspnoea,  cough,  impeded  venous  return,  and  all  the  signs  of  a  bronchitis 
exist,  the  bronchial  or  mediastinal  glands  are  probably  so  enlarged  as  to 
diminish  the  calibre  of  the  bronchial  tubes  or  venous  trunks  near  them. 
The  symptoms  of  laryngeal  paralysis  may  be  induced  by  a  lymphadenoma 
pressing  upon  the  recurrent  laryngeal.  Pressure  on  sensory  nerves  will 
cause  more  or  \e&&  pain  in  the  regions  supplied. 

The  impoverished  blood  condition  is  evinced  by  hemorrhages  from  the 
various  mucous  surfaces  and  by  the  appearance  of  petechise  over  the  sur- 
face of  the  body  ;  or  in  children  by  the  occurrence  of  convulsions  or  coma. 
Jaundice  has  occurred  in  a  few  cases  from  pressure  on  the  common  bile- 
duct.  A  large  inguinal  tumor  may  exert  such  pressure  on  the  femoral  vein 
as  to  cause  oedema  of  the  legs.' 

LifFerential  Diagnosis. — Pseudo-leukaemia  may  be  confounded  with  leuco- 
cytJicsmia ;  the  points  of  differential  diagnosis  have  been  considered  in  leu- 
cocythsemia.  It  is  to  be  remembered  that  pseudo-leuksemia  has  all  the 
symptoms   of  leucocythaemia   except   blood  changes  mentioned  ;   and  in 

1  A  rare  case  is  reported  where  a  lymphadenoma  about  the  Eustachian  tube  caused  deafness.    Another 
is  mentioned  where  paraplegia  resulted  from  tumors  pressing  on  the  cord. 


Addison's  disease.  897 

ctridition  the  cervical,  axillary  and  inguinal  glands  are  early  and  notably 
enlarged. 

Prognosis. — No  case  of  recovery  is  reported  where  the  diagnosis  has  been 
cprtain.  One  year  is  its  average  duration ;  two  months  and  three  years  are 
it^  extremes.  As  in  leukaemia,  so  in  pseudo-leukaemia  the  course  may  be 
rapid  and  attended  by  pyrexia  and  well  marked  constitutional  symptoms  ; 
or  it  may  be  slow  and  essentially  chronic.  Pseudo-leukaemia  is  frequently 
complicated  by  pleurisy,  pneumonia,  so-called  diphtheritic  sore  throat,  ne- 
phritis, lardaceous  degeneration  of  the  lymphatic  glands,  and  pulmonary 
tuberculosis.  Death  may  occur  from  asthenia,  exhaustion,  anaemia,  or  from, 
complications. 

Treatment. — The  general  treatment  of  this  disease  has  been  mainly  surgi- 
cal, the  theory  being  that  if  the  glands  are  excised  the  disease  will  be 
checked.  It  is  true  that  the  removal  of  the  enlarged  glands  relieves  the 
pressure  symptoms,  which  are  often  exceedingly  painful,  but  it  is  of  no 
permanent  service.  Electrolysis,  galvano-puncture,  the  injection  of  caus- 
tics, iodine,  arsenic,  and  phenic  acid  have  been  tried  without  avail.  If 
excision  is  practised,  it  should  be  when  there  is  little  or  no  anaemia  and  no 
fever.  All  forms  of  topical  remedies  have  been  tried,  but  to  no  purpose. 
Internally,  arsenic  seems  to  have  some  controlling  effect. '  Iron  and  cod- 
liver  oil  should  be  given  in  all  cases,  and  sea-bathing  sometimes  arrests  for 
a  time  the  progress  of  the  disease. 

ADDISOlSr's    DISEASE. 

Addison's  disease,  or  melasma  suprarenalis,  is  a  cachexia  accompanied 
or  caused  by  degenerative  changes  in  the  suprarenal  capsules,  that  re- 
semble tubercular  infiltration.  Many  believe  that  any  of  the  three  condi- 
tions, viz. :  tuberculosis,  chronic  interstitial  inflammation,  or  fibro-caseous 
metamorphosis,  or  the  three  combined,  may  be  present  in  this  disease.  But 
its  real  pathogenesis  is  still  in  obscurity,  for  the  reason  that  the  physiology 
of  the  suprarenal  capsules  is  still  unsettled.  Histologically  Miese  capsules 
closely  resemble  a  lymphatic  structure.^ 

Morbid  Anatomy. — In  the  early  stages  of  this  disease  the  capsules  are 
enlarged.  In  the  centre  of  the  medullary  portion  of  the  glands  are  found 
small,  gray,  tubercle-like  granules.  As  the  development  of  these  masses 
progresses  towards  the  cortex,  those  at  the  centre  become  fused  and  suffer 
caseous  metamorphosis.  This  change  may  be  so  uniform  that  the  ivliole 
capsule  becomes  a  uniform  caseous  mass.  At  other  times  the  process,  be- 
ginning in  several  foci  at  the  same  time,  causes  the  gland  to  assume  a  more 
or  less  lobulated  appearance.  The  line  of  demarcation  between  the  corti- 
cal and  medullary  portions  of  the  gland  is  lost,  and  either  the  whole  cut 
section  may  be  of  a  yellow  color,  or  yellow  masses  may  be  entwined  by  gray 
tuberculoid  fibrous  tissue.     The  gray  or  yellow  color  predominates,  ac- 

1  Warfynge  reports  improvement  in  four  cases  from  its  use. — London  Medical  Becord,  March  15,  1881. 

2  Kollikcr  describes   the  renal   capsules  as  both  vascular  glands  and  as  appendages  to  the  nervous 
system.    Brown-Sequard's  jihysiological  experiments  accord  with  tliese  views  of  Kolliker. 

57 


898  CHEOKIC   GEN'ERAL  DISEASES. 

cording  as  the  condition  has  existed  for  a  sliort  or  a  long  time.  As  the  proc- 
ess extends  to  the  cortex  the  centre  begins  to  soften.  In  some  cases- the 
gland  is  a  shell  of  hard,  cheesy  material,  with  diffluent  creamy  contents. 
Instead  of  this  liquefaction  it  is  not  uncommon  to  find  the  centre  of  the 
capsule  in  a  state  of  calcification.  In  either  case  no  sign  of  normal  gland 
structure  remains.'  In  the  stage  where  gray  matter  predominates  the 
capsules  are  enlarged  ;  where  yellow  material  is  in  excess,  especially  if  as- 
sociated with  chalky,  degenerative  changes,  the  gland  is  hard  and  indurated. 

In  some  cases  the  suprarenal  glands  may  become  a  mass  of  cicatricial 
tissue,  the  central  portion  of  which  is  in  a  state  of  caseous  degeneration. 
The  capsules  are  usually  bound  to  all  the  surrounding  organs  or  parts  by 
^rm  connective-tissue. 

The  sTcin  is  discolored.  In  the  lower  layers  of  the  rete  MalpigMi  there 
are  granules  of  pigment  matter  which  vary  in  color  from  a  very  light  to  a 
dark  brown.  The  coloration  is  deepest  in  those  parts  in  which  the  pigment 
is  normally  most  abundant.  In  some  instances  granular  pigment  is  found 
in  the  papillae  and  in  the  cuticular  connective-tissue  cells.  It  may  be  dis- 
tributed along  the  line  of  the  nerves  and  blood-vessels. 

The  spleen  may  be  enlarged  and  softened.  The  adjacent  mesenteric  and 
retroperitoneal  glands  are  often  tuberculous  or  in  a  state  of  cheesy  meta- 
morphosis. Peyer's  patches  and  the  solitary  glands  of  the  intestine  are 
enlarged,  and  the  testicles  and  the  prostate  are  in  some  cases  tuberculous. 
The  same  changes  occur  in  the  liver  as  in  the  spleen.  Scattered  tubercu- 
lous nodules  are  often  found  in  the  brain  and  apices  of  the  lungs.  The 
heart  may  undergo  fatty  change  and  the  kidneys  are  occasionally  the  seat 
of  parenchymatous  degeneration.  Connective-tissue  hyperplasia  is  marked 
about  the  nerve-sheaths  in  the  sympathetic  nerves  near  the  capsules.  There 
is  hypersemia  of  the  nerve  trunks  and  ganglia  of  the  large  adjoining  plex- 
uses." The  blood  is  ansemic,  fibrin  is  diminished,  the  red  discs  are  altered 
in  size  and  form,  and  do  not  run  together  in  rouleaux  as  normal  discs  do. 
The  white  blood  globules  are  increased. 

Etiology. — There  is  an  undoubted  connection  between  tuberculosis  and 
morbus  Addisonii.  In  over  80  per  cent,  of  reported  cases,  tuberculosis  ex- 
isted in  the  capsules  or  in  other  organs.'  The  latest  and  by  far  the  most 
reasonable  theory  is  that  the  highly  nervous  capsule  contains  gland-cells 
which  have  a  close  connection  with  the  vascular  and  liaBmatopoetic  system.* 
Buhl  thinks  that  not  only  is  it  a  blood  disease,  but  that  it  is  infectious. 
It  has  been  regarded  as  analogous  to  leukaemia  and  pernicious  anaemia. 

1  G.  Merkel  states  that  there  is  cell  proliferation  attended  by  the  formation  of  a  delicate  reticulated 
structure  containing  many  furiform  lymphoid  and  giant  cells.  In  opposition  to  most  anthorities,  Cornil 
and  Ranvier  affirm  that  the  process ./??•«<  invades  the  cortex,  and  the  medullary  portion  suffers  secondarily. 
Upon  microscopical  examination  the  yellow  and  gray  matter  present  the  same  pathological  aspects  as 
tubercle. 

2  Cornil  and  Ranvier  say  that  "the  lesions  of  the  nerve  centres  of  the  suprarenal  capsules  and  of  the 
great  sympathetic  in  part  account  for  the  phenomenon  of  pigmentation." 

3  Letnlle  points  to  its  association  with  tnberctilous  disease  of  the  spinal  column.  Wilks  and  Moson 
found  pulmonary  tuberculosis  in  80  per  cent,  of  their  cases.  Riesel  claims  that  there  is  a  paralytic  state  of 
the  vaso-motor  fibres  of  the  sympathetic,  and  as  a  consequence  the  blood  is  imperfectly  and  unequally  dis- 
tributed. La  France  Medicale,  No.  40, 1880.  Also  see  Ziir  Pathologic  des  morbus  Addisonii.  Deut.  Arch, 
fur  Klin.  Med.  18^0,  Be.  7. 

4  Henle  and  Von  Brunn. 


Addison's  disease.  899 

It  attacks  males  oftener  than  females,  and  is  essentially  a  disease  of  adult 
life.  It  has  been  found  associated  with  cancer,  apoplexy,  fatty  and  waxy 
degeneration  of  the  suprarenal  capsules,  and  in  some  cases  the  suprarenal 
capsules  have  been  found  perfectly  normal. 

Symptoms. — This  disease  may  come  on  so  insidiously  that  the  patient 
will  be  unable  to  determine  the  date  of  its  commencement.  A  feeling  of 
extreme  languor  is  its  most  constant  symptom.  Its  progress  may  be  unin- 
terrupted, either  slow  or  rapid  ;  or  it  may  progress  by  stages ;  in  the  lat- 
ter case  there  will  be  periods  when  the  disease  remains  stationary  for 
months.  The  countenance  becomes  pale,  the  muscles  flabby,  the  pulse  fee- 
ble ;  there  is  extreme  muscular  weakness,  asthenia,  indigestion,  anorexia, 
dyspnoea,  and  fits  of  palpitation.  Melancholia  is  not  uncommon  ;  the  pa- 
tient is  not  easily  aroused  from  a  drowsy,  dreamy  languor  into  which  lie 
habitually  falls.  Dizziness  and  long  fits  of  syncoj^e  are  not  infrequent. 
Gastric  irritability,  nausea,  and  vomiting  are  common.  There  is  a  sense 
of  distention  over  the  epigastrium,  acid  eructations,  and  fits  of  cardialgia. 
The  tongue  remains  normal  in  appearance  throughout.  Sometimes  there 
is  obstinate  diarrhoea.'  In  most  cases  there  is  intense  pain  in  the  joints, 
and  along  the  spine  and  sacrum.  As  the  disease  advances  the  heart  action 
becomes  more  and  more  feeble,  the  pulse  more  rapid  and  weak,  and  arte- 
rial anaemic  murmurs  are  heard. 

Meanwhile  the  skin  changes  its  appearance.  At  first  its  hue  is  like 
that  of  melansemia,  then  it  is  distinctly  icteroid,  then  it  j)resents  the 
color  of  a  mulatto ;  finally,  it  becomes  a  lustreless  bronze.  Not  only 
the  whole  cutaneous  surface,  but  the  mucous  membranes  of  the  lips, 
tongue,  gums  and  mouth  are  strongly  pigmented.  The  parts  most  exposed 
change  in  color  first,  then  the  parts  subjected  to  pressure  and  the  flexures  of 
the  joints.  Superficial  cicatrices  are  strongly  pigmented,  while  deep  ones 
remain  unaltered.  The  roots  of  the  nails  and  the  sclerotic  remain  un- 
changed, and  the  soles  of  the  feet  and  palms  of  the  hands  are  not  discolored 
until  late,  and  then  not  markedly.  As  these  patients  approach  death, 
sight  and  memory  fail,  convulsions  and  choreic  symptoms  and  delirium  are 
followed  by  comatose  jieriods.  But  even  when  they  reach  a  state  of  com- 
plete asthenia  there  is  but  slight  emaciation  ;  the  body  often  presents  the 
appearance  of  obesity. 

The  temperature  is  slightly  sub-normal  throughout  its  course.  The 
urine  is  normal  in  amount;  uric  acid,  coloring  matter,  and  indican  are 
in  excess,  and  urea  is  decreased. 

DifFerential  Diagnosis. — It  may  be  mistaken  for  ptyriasis  nigra,  but 
the  itching  of  the  surface  and  the  desquamation  of  the  cuticle  in  the  latter 
disease  readily  distinguish  it  from  Addison's  disease.  Anaemic  jaundice, 
and  the  discoloration  of  the  skin  from  nitrate  of  silver  or  from  exposure  to 
the  sun  will  readily  be  distinguished  from  the  bronzed  skin. 

Prognosis. — It  is  an  incurable  disease,  and  no  case  of  recovery  has  been  re- 
ported.    Its  duration  varies  from  sixteen  to  eighteen  months  to  four  or  five 

'  In  1871  Prof.  Flint  stated  that  degenerative  changes  in  the  gastric  and  intestinal  tubules  were  prob- 
ably the  cause  of  the  intense  ansemia.    N.  T,  Med.  Journal,  March,  1871. 


900  CHRONIC    GENERAL   DISEASES. 

years.      Death  may  occur  from  asthenia,  diarrhoea,  convulsions  or  coma, 
or  from  complications. 

Treatment.— All  remedial  measures  have  thus  far  proved  unavailing.' 
Faradization  and  galvanism  of  the  sympathetic  have  been  proposed.  Qui- 
nine combined  with  iron,  and  iodide  of  potassium  have  been  strongly  rec- 
ommended. In  all  cases  perfect  rest,  quiet  and  good  hygienic  surround- 
ings are  important.  It  must  be  remembered  that  sudden  and  unexpected 
death  at  any  period  of  the  disease  may  occur  when  treatment  is  apparently 
arresting  its  progress.  I  have  never  obtained  any  positive  beneficial  results 
from  any  plan  of  treatment. 

AMMOlSTiBMIA. 

Ammonaemia  is  a  condition  in  which  an  excess  of  carbonate  of  ammonia 
is  found  in  the  blood,  the  result  of  the  decomposition  of  urine  retained  in 
the  urinary  tract. 

Morbid  Anatomy. — The  intestines  are  the  seat  of  chronic  catarrh  and 
contain  a  greenish  yellow  alkaline  fluid.  Sometimes- ulcers  are  found  in 
the  intestines  similar  to  dysenteric  ulcers.  When  ammongemia  occurs  with 
anmmia,  it  is  possible  for  the  urea  excreted  by  the  intestines  to  change  into 
carbonate  of  ammonia.^  K  ferment  has  been  obtained  from  cystitic  urine 
that  is  said  to  be  capable  of  changing  urea  into  carbonate  of  ammonia.' 

Etiology. — The  one  essential  condition  necessary  for  the  development  of 
ammonaemia  is  the  retention  of  urine  in  the  body  sufficiently  long  for  the 
urea  to  undergo  decomposition.  The  conditions  under  which  it  most  fre- 
quently occurs  are,  stricture  of  the  urethra,  enlargement  of  the  jDrostate 
gland,  atony  and  paralysis  of  the  bladder,  pyelitis,  pyonephrosis,  hydro- 
nephrosis, sacculated  kidney  and  chronic  cystitis. 

Symptoms. — There  are,  clinically,  two  forms  of  ammonsemia  ;  in  one  the 
conditions  which  give  rise  to  it  come  on  suddenly  ;  in  the  other  the  causa- 
tive condition  comes  on  slowly  but  continuously. 

In  the  first,  or,  as  it  is  called,  acute  ammoncBmia,  there  are  nausea  and 
vomiting,  intermittent  and  irregular  chills,  acceleration  of  the  pulse,  and 
rapid  rise  of  temperature.  Diarrhoea  and  vomiting,  if  excessive,  lead  to 
exhaustion  and  a  typhoid  condition.  The  complexion  assumes  a  dingy 
bronzed  hue ;  there  is  great  muscular  weakness  with  a  tendency  to 
lethargy.  (Edema  of  the  face  and  ankles  is  of  very  rare  occurrence.  De- 
lirium may  occur.  The  tongue  is  dry,  brown  and  shining — the  beefy 
tongue — and  the  mucous  membranes  that  are  exposed  to  the  air,  that  of 
the  throat  especially,  are  remarkably  dry.  The  breath  and  the  perspira- 
tion are  ammoniacal. 

Chronic  ammonaemia  which  accompanies  atony  and  paralysis  of  the  blad- 

1  Greenhow  asserts  that  glycerine  3  ij.  combined  with  spts.  chlorof onn.  et  tr.  ferri  chloridi,  aa  tii,xv., 
is  highly  advantageous. 

sRosenstein  denies  any  connection  between  ammonsemia  and  carbonate  of  ammonia  ;  but  the  weight  of 
opinion  is  in  favor  of  it.  Rosenstein,  "  xieber  Ammon(Bmia, "  Deutsche  Zeitschrift  f.  pr.  Med.  No. 
20:  1874. 

3  Pasteur  only  succeeded  in  finding  a  ferment  when  bacteria  were  present ;  but  those  who  follow  PaS' 
teur's  teachings  claim  that  a  specific  ferment  is  the  cause  of  amraonasmia. 


AMMON^MIA.  901 

der  and  enlargement  of  the  prostate  gland,  comes  on  very  insidiously.  The 
complexion  becomes  sallow,  then  of  a  dingy  brown  hue.  There  is  pro- 
gressive emaciation  and  restlessness,  headache  and  insomnia.  Irregular 
chills  occur  at  infrequent  intervals  ;  the  temperature  is  constantly  above 
normal,  and  the  pulse  is  accelerated.  Vomiting  is  persistent.  The 
mucous  membranes  assume  a  dry,  glazed,  shining  apj^earance  ;  the  skin  be- 
comes dry  and  harsh  ;  the  breath  and  persjiiration  are  distinctly  ammo- 
niacal.  JBut  it  should  be  remembered  that  the  amount  of  perspiration  in 
ammongemia  is  probably  less  than  in  any  other  disease.  When  the  disease 
is  far  advanced  convulsions  may  occur.  At  this  time  the  complexion  may 
become  quite  dark,  and  emaciation  is  marked.  Diarrhoea  alternates  with 
constipation. 

As  a  cachexia  develops,  insomnia  and  restlessness  give  place  to  som- 
nolence, delirium,  lethargy,  stupor,  or  coma,  and  the  patient  passes  into  a 
typlioid  state.  Old  men  with  enlarged  prostates  pass  into  a  condition  of 
stupor  ;  and  then  low  muttering  delirium,  rapid,  feeble,  and  irregular 
pulse  and  subsultus  tendinum  terminate  in  a  fatal  coma. 

The  urinary  symptoms  are  important.  The  urine  is  ammoniacal  and 
strongly  alkaline  when  passed.  It  often  contains  pus,  and  there  is  a  deposit 
of  amorphous  phosphate  of  lime  with  crystals  of  ammonio-magnesian  phos- 
phate.    The  odor  is  offensive  and  pungent. 

Differential  Diagnosis. — Ammonsemia  may  be-  mistaken  iov  typlioid  fever, 
sub-acute  gastritis,  pycemia,  or  septicmmia.  In  gastritis  the  urinary  symp- 
toms are  negative,  while  in  ammonasmia  they  are  diagnostic.  Nausea  and 
vomiting  are  persistent  in  ammonaemia,  and  intermittent  in  gastritis.  Ca- 
theterization, or  a  rectal  examination,  will  rarely  fail  to  discover  some 
organic  genito-urinary  obstructive  cause  for  urinary  retention;  while  a 
physical  exploration  in  gastritis  gives  negative  results. 

In  pycBinia  there  will  be  an  initiatory  chill,  profuse,  exhausting,  and  re- 
curring siveats,  a  high  temperature  (103°  to  104°  F.),  a  sweet,  sickly  odor 
to  the  breath,  and  the  evidence  of  thrombi,  infarctions,  and  multiple  ab- 
scesses in  some  central  organ  or  organs.  All  these  symptoms  are  absent  in 
ammongemia  ;  and  the  ammoniacal  breath  and  urine,  and  i\\e  parched,  diy 
skin  are  in  direct  contrast  to  the  symptoms  of  pysemia. 

In  septicmmia  the  temperature  is  very  high— 105°  to  107°  F.  Besides 
there  is  no  ammoniacal  odor  to  the  breath  or  urine;  the  skin  is  not  dry, 
and  genito-urinary  obstructive  conditions  will  not  be  found.  The  history 
of  the  case  will  also  greatly  aid  in  making  a  diagnosis. 

Prognosis. — The  prognosis  in  ammonaemia  is  determined  to  a  great  extent 
by  the  condition  which  causes  it ;  when  it  is  possible  to  remove  the  cause 
the  prognosis  is  good,  but  when  the  cause  cannot  be  removed  the  prognosis 
is  very  bad.  In  all  cases  there  is  slow  but  progressive  impairment  of  the 
general  health.  Aged  patients  rapidly  become  exhausted,  and  sink  into  a 
typhoid  state  if  the  causative  condition  cannot  be  speedily  removed. 

Treatment. — The  most  important  thing  to  be  accomplished  in  the  treat- 
ment of  this  condition  is  the  removal  of  its  cause.  And,  since  atony  of 
the  bladder  and  enlarged  prostate  are  its  most  common  causes,  the  first 


902  CHROI«riC   GE^^TERAL  DISEASES. 

step  is  to  empty  and  wash  out  the  bladder.  Very  often  when  the  patient 
seems  to  be  sinking  into  a  typhoid  state,  when  there  has  been  nothing 
to  direct  attention  to  the  bladder,  on  the  introduction  of  a  catheter  a  large 
quantity  of  stinking  urine  will  be  evacuated ;  and  after  having  thoroughly 
washed  out  the  bladder,  rapid  improvement  takes  place,  and  the  gastric 
symptoms  subside.  The  diet  should  always  be  supporting  and  stimulating. 
If  tepid  water  is  used  to  wash  out  the  bladder,  carbolic  acid,  bicarbonate 
of  soda,  borax,  or  glycerine  may  be  added ;  and  the  washing  should  be 
continued  till  the  withdrawn  fluid  is  perfectly  clear  and  free  from  odor. 
Iron  and  vegetable  tonics  are  indicated. 

HEMOPHILIA. 

The  hemorrhagic  diathesis  is  an  hereditary  disease  marked  by  a  tendency 
to  immoderate  bleedings — spontaneous  or  traumatic — and  to  obstinate 
swelling  of  the  Joints. 

Morbid  Anatomy. — No  changes  in  the  blood  or  vessels  have  been  found 
in  the  few  post-mortems  that  have  been  made.  The  swellings  of  the  joints 
are  probably  due  to  blood  extravasations  within  the  articulation. 

Etiology. — Its  most  marked  cause  is  hereditary  predisposition.  It  attacks 
men  far  oftener  than  women.'  The  tendency  descends  to  sons  through 
the  mother,  who  herself  may  give  no  evidence  of  the  disease.  Fathers  do 
not  transmit  the  tendency  to  their  sons.  Pregnancy  is  said  to  be  a  devel- 
oping cause.  There  is  often  nothing  to  indicate  the  existence  of  this  dia- 
thesis prior  to  the  occurrence  of  the  hemorrhage.  Whether  the  hcemophilia 
of  the  new-born  is  a  distinct  disease  is  an  unsettled  question.  Their  blood 
has  been  found  to  contain  fungoid  organisms  which  afford  an  apparent 
explanation  of  the  hemorrhages.  The  hemorrhagic  diathesis  has  been  re- 
garded as  allied  to  scrofula,  chlorosis,  gout,  and  similar  dyscrasise,  and 
again  as  a  pronounced  manifestation  of  a  rheumatic  diathesis,  as  both  these 
conditions  occur  under  the  same  influences.  One  of  the  most  recent  theories 
is  that  it  is  dependent  on  deficient  capillary  innervation  with  resulting 
dilatation.  This  neurotic  theory  is  favored  by  the  frequency  of  nervous 
disorders  in  bleeders  and  the  fact  that  neurotic  remedies  exert  the  greatest 
control  over  it.^  In  its  transmission  from  parent  to  offspring  it  often  skips 
one  generation. 

Symptoms. — The  symptoms  appear  as  a  rule  during  the  first  or  second 
year  of  life.  There  is  nothing  about  the  appearance  that  indicates  the  ex- 
istence of  any  diathesis.  The  disease  remains  latent  until  a  cut,  a  fall 
on  the  nose,  or  the  pulling  of  a  tooth  starts  a  hemorrhage,  which  at  times 
is  uncontrollable.  The  blood  will  ooze  for  days,  and  death  from  acute 
anaemia  may  result.  Usually  the  bleeding  slowly  ceases  and  after  a  long 
time  the  patient  recovers.  The  bleedings  may  come  on  spontaneously. 
Then  there  may  be  prodromata :  signs  of  plethora,  of  cerebral  congestion. 


'  Legg  (in  QuaMs  Dictionary,  p.  569)  gives  the  proportion  as  high  as  11  to  1. 

*  Mosler  states  that  over  fifty  per  cent,  of  his  cases  of  leiilifemia  were  complicated  by  it,  and  in  one 
hundred  and  fifty  cases  collected  by  Gowers,  eighty  were  bleeders. 


SCURVY.  903 

stupor,  cardiac  palpitation,  and  painful  swellings  of  the  joints.  In  child- 
hood bleeding  from  the  nose  is  the  commonest  form  of  hemorrhage.  The 
joints  affected  are  the  larger  ;  the  knee  is  most  frequently  attacked. 

In  bleeders  a  slight  bruise  will  be  followed  by  extensive  blood  extrava- 
sations into  the  connective-tissue.  Hemorrhages  may  take  place  into  the 
stomach,  intestines,  lungs,  bronchi,  kidney  and  brain.  Extensive  blood 
tumors  may  form  in  any  part  of  the  body. 

DiiFerential  Diagnosis. — There  is  no  condition  which  is  liable  to  be  mis- 
taken for  haemophilia,  if  the  history  of  the  patient  is  accurately  taken. 

Prognosis. — Complete  recovery  is  rare,  but  life  may  be  prolonged  by  ju- 
dicious management ;  an  example  of  which  can  be  cited  in  the  case  of 
Prince  Leopold,  who  was  thirty-two  when  he  died  of  haemophilia. 

Treatment. — For  tlie  traumatic  forms  styptics  and  mechanical  surgical 
measures  should  be  promptly  made  use  of.  When  hemorrhage  arises  spon- 
taneously little  can  be  done.  The  diet  of  bleeders  should  consist  largely 
of  animal  food.  Chalybeate  tonics  should  be  constantly  administered,  and 
the  patient  should  lead  a  quiet  life  in  a  warm  climate.  Niemeyer  rec- 
ommends cathartic  doses  of  Glauber's  salts  and  ergot.  Harkin,  of  Bel- 
fast, recommends  the  chlorate  of  potash, — one  ounce  of  the  saturated 
solution  three  times  a  day — combined  with  the  muriated  tincture  of  iron, 
and  claims  to  have  had  excellent  results.  He  states  that  this  plan  will 
eradicate  the  constitutional  tendency. 

SCTJEVT. 

Scurvy  or  scorbutus  is  a  chronic  blood  disease,  which  may  be  regarded 
as  a  peculiar  form  of  anaemia  arising  from  deficiency  of  vegetable  diet. 
Until  recently  it  prevailed  very  extensively  in  armies  and  among  crews  of 
sailing  vessels.  Improved  means  for  the  preservation  of  supplies  have  ren- 
dered it  of  much  less  frequent  occurrence,  and  greatly  mitigated  its  severity 
even  during  long  campaigns,  and  at  the  present  time  it  is  seen  but  infre- 
quently among  sailors. 

Morbid  Anatomy. — The  red  blood  corpuscles  are  diminished  and  the  al- 
bumen and  fibrin-factors  are  increased,  although  the  albumen  does  not 
coagulate  readily,  and  there  is  a  peculiar  viscidity  to  the  blood.  There 
is  said  to  be  a  deficiency  of  potash  salts.'  The  capillaries  have  been  found 
choked  with  red  corpuscles  and  their  endothelial  cells  altered.  Some  de- 
scribe the  blood  as  thicker,  others  as  thinner  than  normal — at  one  time 
lighter,  at  another  darker.  Ecchymoses  are  very  characteristic  of  scurvy, 
and  occur  in  and  beneath  the  skin,  in  the  muscles,  between  the  periosteum 
and  the  bone,  and  within  the  joints.  In  these  situations  they  may  be  very 
extensive.  They  are  also  found  on  all  the  mucous  and  serous  membranes 
and  may  partially  fill  the  pleura  or  pericardium. ° 

The  heart,  kidney,  and  liver  often  undergo  fatty  or  parenchymatous  de- 

'  Cornil  and  Ranvier. 

^Dr.  Ralfe  regards  diRproportion  bptween  the  various  acids  and  bases  of  the  blood  as  the  cause  of  the 
disorganization  of  the  blood  corpuscles  and  subsequent  mucous  ecchymoses. 


904  CHKOKIC   GENERAL   DISEASES. 

generation.  The  spleen  is  enlarged,  softened,  and  exceedingly  friable. 
Ulcers  occasionally  form  on  tlie  mucous  surface  of  the  large  intestine,  re- 
sembling those  of  dysentery.  The  changes  in  the  gums  are  even  more 
characteristic  lesions.  In  nearly  all  cases  they  become  soft,  spongy,  and 
•oedematous,  and  ulcerated  masses  overhang  the  teeth  and  bleed  upon  the 
slightest  provocation. 

The  bodies  of  those  who  have  died  of  scurvy  are  emaciated,  the  skin  is 
ashen  gray,  and  there  is  more  or  less  oedema,  especially  of  the  lower  ex- 
tremities. 

Etiology. — Deprivation  of  fresh  vegetable  food  for  a  long  time  will  very 
surely  induce  scurvy,  independent  of  climate,  latitude,  race,  or  sex. '  It  is 
rarely  met  with  from  any  other  cause,  although  an  unvaried  diet  of  poor 
quality  may  induce  it.  Sudden  atmospheric  changes,  mental  disturbance, 
severe  and  prolonged  physical  labor  with  insufficient  food,  and  bad  hygi- 
enic surroundings  may  predispose  to  scurvy,  but  seldom  develop  it  so  long 
as  fresh  vegetables  in  moderate  amounts  are  eaten. 

The  theory  that  scurvy  is  due  to  a  specific  infection,  while  improbable, 
cannot  absolutely  be  rejected.^ 

Symptoms. — The  earliest  noticeable  changes  are  in  the  skin  of  the  face 
and  eyelids,  which  changes  color  and  appears  bruised  and  swollen.  The 
pulse  is  soft  and  the  temperature  lower  than  normal.  The  patient  rapidly 
becomes  less  and  less  capable  of  mental  or  physical  labor,  the  face  grows  pale 
and  bloated,  there  is  great  despondency  and  a  sense  of  weight  in  the  lower 
limbs.  The  skin  is  dry,  rough,  and  of  a  muddy  pallor  ;  later  it  becomes 
sallow  and  leaden.  The  conjunctivae  are  pearly  white,  the  tongue  is  clean 
and  pale,  the  teeth  loosen  and  are  surrounded  by  bright  red  ulcerated  or 
fungous-looking  gums  that  present  a  purple  line  where  they  join  the  teeth, 
and  contrast  strongly  with  the  pale  or  livid  lips.  The  breath  is  exceed- 
ingly offensive,  frequently  from  necrosis  of  the  jaws.  The  eyes  are  sunken 
and  surrounded  by  a  dark  blue  circle. 

Ecchymoses  and  petechial  spots  cover  the  body  and  extend  over  a  large 
surface  on  the  slightest  blow  or  injury.  Severe  darting  pains  which  simulate 
rheumatism  are  felt  in  the  limbs,  about  the  calf  of  the  leg  and  the  popliteal 
space.  The  legs  may  become  fixed,  owing  to  the  hardness  of  the  muscles 
of  the  calf  and  thigh.  Node-like  swellings  occur  over  the  tibia  from  sub- 
periosteal ecchymoses.  The  pulse  is  slow  except  upon  excitement,  when 
palpitation  and  dyspnoea  are  also  marked.  Slight  exertion  may  occasion 
syncope  in  those  in  whom  the  disease  is  advanced.  Ansemic  murmurs  are 
heard  upon"  auscultation.  The  bowels  are  constipated,  unless  there  be  scor- 
butic dysentery.  The  urine  is  high  colored,  sometimes  albuminous,  and 
there  is  a  diminution  in  its  normal  ingredients  except  potash  salts  and 
phosphoric  acid.  The  chlorides  are  abundant.  Insomnia  and  disordered 
vision  are  common. 

Differential  Diagnosis. — The  history  of  a  case  and  a  close  inspection  of 

1  In  the  Crimean  war  more  died  from  scurvj^  than  from  any  other  cause.    It  was  the  cause  of  death  in  a 
large  proportion  of  those  who  died  during  the  potato  famine  in  Ireland. 
*  Fabre  regards  scorbutus  as  a  miasmatic  afEection  which  especially  affects  the  nervous  system. 


PURPURA.  905 

tlie  gums  will  enable  one  to  clistingoiisli  scurvy  from  mercurial  poisoning. 

Scurvy  is  distinguished  from  purp^ira  by  the  sjiongy  gums,  painful 
swellings,  and  more  j^rofuse  though  less  numerous  hemorrhages.  Purpura 
frequently  occurs  in  those  whose  health  has  not  been  impaired  by  faulty 
nutrition  ;  scurvy  very  rarely  Purpura  is  not  affected  by  lime  juice  or 
change  in  diet,  while  either  will  at  once  produce  marked  improvement  in 
scurvy.  Purpura  occurs  in  isolated  cases  ;  the  vital  powers  are  not  as  de- 
pressed as  in  scurvy,  and  muscular  swellings  are  aljsent. 

Prognosis. — Scurvy  is  not  a  fatal  disease  ;  appropriate  treatment  in  un- 
complicated cases  always  effects  a  cure.  It  may  be  complicated  by  dysen- 
tery, syphilis,  the  various  forms  of  malaria,  typhus,  typhoid,  and  chronic 
alcoholismus.  The  former  diseases  assume  a  scorbutic  character.  Death 
may  occur  from  complications,  exhaustion,  general  dropsy,  hemorrhage, 
diarrhcea,  dysentery,  pleurisy,  pericarditis,  or  pulmonary  oedema.  It  is 
said  that  meningeal  hemorrhage  is  sometimes  a  cause  of  death.  Hemera- 
loj^ia  often  occurs  as  a  sequela. 

Treatment. — In  long  voyages  or  campaigns  lemon  or  lime  juice  or  cit- 
ric acid  should  be  taken  daily  when  fresh  or  preserved  vegetables  cannot 
be  obtained.  By  their  use  in  the  English  navy  scurvy  has  been  diminished 
nearly  ninety  per  cent.  One  who  is  seriously  ill  of  scurvy  should  be  kept 
in  bed,  and  the  diet  at  once  be  made  to  consist  largely  of  fresh  yegetables 
and  acid  fruits  with  fresh  meats  in  such  proportion  as  the  patient  can 
easily  masticate  and  digest.  Mustard,  radishes,  cabbage,  and  water-cresses 
are  anti-scorbutics.  Three  or  four  ounces  of  lime  or  lemon  juice,  largely 
diluted  with  cold  water,  should  be  taken  daily.  If  stimulants  are  required 
malt  liquors  are  to  be  preferred.  A  wash  of  chlorate  of  potash  will  afford 
relief  to  the  oral  symptoms,  and  potash  may  be  given  internally  ;  quinine, 
iron  and  strychnia  act  both  as  tonics  and  appetizers. 

PTJEPUEA. 

Purpura  is  a  general  disease,  characterized  by  sanguineous  effusions  into 
the  upper  layers  of  the  cutis  and  beneath  the  epidermis.^ 

Morbid  Anatomy. — Either  from  changes  in  the  walls  of  the  vessels  or  in 
the  blood  itself  (excess  of  salts,  or  water,  etc.),  or  quite  probably  from  both 
combined,  extravasations  occur  into  the  connective-tissue  spaces  of  the 
rete  mucosum  and  papillary  laj^er  of  the  cutis  or  in  the  spaces  between  the 
ducts  and  hair  follicles.  The  serum  is  soon  absorbed  and  the  more  solid 
elements  may  gradually  undergo  complete  absorption  or  result  in  perma- 
nent pigmentation  of  the  parts.  Similar  lesions  are  found  in  the  mucous 
membranes,  attended  by  hemorrhage  from  the  free  surfaces.  Such  hemor- 
rhages are  more  common  in  the  nares  and  along  the  alimentary  canal. 
Serous  membranes  are  less  frequently  affected,  but  extravasations  have  been 
found  in  the  pleural,  pericardial  and  peritoneal  cavities  and  in  the  meshes 
of  the  pia  mater. 

1  It  may  be  simple,  rJievmatic,  hemorrhagic  or  symptomatic.  Purpura  hemorrhagica  is  also  called 
"  Morbus  MaciUoi'M  WerlhoJU." 


906  CHEONIC    GENEEAL   DISEASES. 

Earely  are  the  muscles,  periosteum,  bones,  conjunctiva,  and  retina  the 
seat  of  extensive  blood  effusions. 

Etiology. — Age  appears  to  have  no  bearing  upon  the  development  of  pur- 
pura, but  it  is  found  more  frequently  in  women  than  in  men.  It  appears 
in  some  cases  without  any  discoverable  cause  in  the  healthy  and  robust  ; 
sometimes  its  causes  seem  almost  identical  with  those  of  scurvy.  Rheu- 
matic purpura  may  complicate  acute  polyarticular  rheumatism  or  occur 
in  those  of  a  rheumatic  diathesis.  Purpuric  spots  are  not  infrequent  with 
valvular  disease  of  the  heart,  Bright's  disease,  phthisis,  cirrhosis  of  the 
liver,  and  various  forms  of  malarial  fever. 

Its  occurrence  with  leucocythsemia  is  interesting  on  account  of  Pen- 
zoldt's  discovery  of  the  peculiar  form  of  the  blood  discs  in  Werlhof's  dis- 
ease/ Purpuric  spots  have  followed  large  doses  of  chloral  and  iodide  of 
potash.  Distinct  exciting  causes,  if  such  exist,  are  obscure  ;  fright,  severe 
coughing  fits,  and  epileptic  attacks  are  said  to  have  induced  it.  There  is 
no  doubt  but  that  the  enfeebled  condition  of  the  vessels  often  depends 
upon  a  state  of  general  debility  either  hereditary  or  acquired. 

Embolism  and  thrombosis  have  been  suggested  as  causes,  while  disor- 
dered vaso-motor  innervation,  which  might  possibly  account  for  its  occur- 
rence after  exhausting  diseases,  has  also  been  considered  the  primary 
lesion." 

Symptoms. — In  many  ^ases  for  days  or  weeks  before  the  eruption  occurs 
there  will  be  a  general  feeling  of  malaise  accompanied  by  digestive  derange- 
ment. In  all  varieties  of  purpura  the  eruption  has  the  same  general  char- 
acters. The  spots  appear  upon  the  extremities  and  trunk  as  a  rule,  but  in 
severe  cases  the}^  cover  the  head  and  face  as  well.  They  vary  in  color  from 
a  bright  red  to  a  livid  or  purple  ;  they  are  round  or  irregular  with  serrated 
edges,  and  vary  in  size  from  a  pin's  head  to  a  large  pea,  or  a  spot  may 
measure  an  inch  or  more  in  circumference.  They  do  not  disappear  upon 
pressure.  The  smaller  extravasations  are  spoken  of  as  petechise,  and  the 
larger  as  fecchymoses,  and  when  they  occur  in  lines  or  stripes  they  are 
called  vibices. 

If  the  hemorrhage  is  so  extensive  or  of  such  a  form  as  to  cause  the  spots 
to  be  elevated  above  the  level  of  the  skin  the  disease  receives  the  name  pur- 
pura papulosa,  or  lichen  lividus  when  they  are  conical  and  located  around 
a  hair  follicle.  The  elevated  wheal-like  nodules  are  designated  as  purpura 
urticans,  and  if  they  form  bullae  containing  serum  and  blood  the  name 
purpura  bullosa  is  given. 

While  the  primary  spots  are  undergoing  absorption,  as  indicated  by  the 
gradual  change  of  color  from  the  dark  blue  through  the  green  to  yellow, 
another  livid  red  crop  is  appearing.  In  ordinary  cases  a  crop  lasts  from  a 
week  to  ten  days.  Desquamation  never  follows,  and  once  formed  a  spot 
does  not  increase  in  size,  except  by  fresh  hemorrhage  in  its  vicinity. 

Sometimes  there  are  no  constitutional  symptoms  whatever  in  jsMrjowrfl! 
simplex;  but  vci purpura  r7ie?i7wa^/ca  slight  fever  and  rheumatic  pains  in 

1  Blufbefvnd  bei  derWeiihofschen  Krankheit,  1878,  Erlanger. 

2  Cavalie  reports  a  case  associated  with  organic  disease  of  the  brain. 


MTXOEDEMA.  907 

the  knees  and  ankles  are  accompanied  by  red  and  swollen  joints,  gastric 
and  intestinal  disturbances,  colicky  pains,  etc.,  in  addition  to  the  usual 
eruption.  In  purpura  hemorrhagica,  preceding  and  accompanying  the 
eruption,  there  is  great  constitutional  disturbance  ;  the  spots  are  large  and 
numerous,  and  invade  the  whole  body  ;  there  are  free  hemorrhages  from 
all  the  mucous  tracts  and  from  the  lungs.  So  extensive  may  these  hemor- 
rhages be  that  acute  ansemia  is  rapidly  followed  by  typhoid  symptoms  and 
death.  The  amount  of  hemorrhage  does  not  depend  upon  the  extent  of 
the  eruption.  Cerebral  symptoms  may  occur  from  ventricular  or  menin- 
geal hemorrhage. 

When  purpuric  spots  accompany  the  exanthems  and  contagious  fevers  the 
usual  symptoms  of  those  diseases  and  the  eruption  are  purely  symjotomatic 
of  the  extensive  degenerative  changes  engendered  by  the  primary  infec- 
tion. 

Differential  Diagnosis. — The  points  of  diagnosis  between  purpura  and 
scurvy  have  already  been  given.  The  fact  that  there  is  no  itching,  no 
desquamation,  no  suppuration  or  discharge,  and  no  change  in  purpuric 
spots  upon  pressure  suffices  to  distinguish  them  from  the  eruption  of  any 
form  of  sTcin  disease. 

Prognosis. — In  uncomplicated  purpura  the  prognosis  is  good  ;  but  when 
venous  thrombosis,  scurvy,  diarrhuea,  or  an  incurable  organic  disease  exists, 
life  is  endangered  by  the  liability  to  hemorrhage  from  mucous  surfaces,  and 
the  occurrence  of  extravasations  into  the  serous  cavities  or  brain.  Anaemia 
and  dropsy  are  often  causes  of  death. 

Treatment. — At  one  time  the  treatment  consisted  in  administering  quinine 
and  sulphuric  acid.  At  the  present  day  rest,  a  highly  nutritious  concen- 
trated diet,  and  moderate  stimulation  with  a  nutritive  wine  are  the  princi- 
pal measures  employed.  Tinctnra  ferri  perchloridi, — 15  to  20  minims 
three  times  a  day, — is  very  efficacious,  and  should  be  given  in  connection 
with  some  one  of  the  mineral  acids,  preferably  sulphuric.  Ergot,  turpen- 
tine, gallic  acid,  and  other  haemostatics  are  all  highly  recommended  when 
the  hemorrhages  become  dangerous.  When  hemorrhage  from  the  lungs 
occurs,  the  treatment  is  the  same  as  in  other  forms  of  bronchial  hemorrhage. 
Eecently,  small  doses  of  mercury  have  been  given,  and  apparently  effected 
a  cure.  Shand  has  obtained  excellent  results  from  Faradization  {Lond. 
Lancet,  July  9,  1879). 

MYXCEDEMA. 

Myxoederaa  is  a  name  given  by  Prof.  Ord  to  a  progressive  disease  where 
the  tissues  of  the  body  are  invaded  by  a  Jelly-like,  mucus-yielding  dropsy. 

Morbid  Anatomy. — All  over  the  body  the  connective-tissue  is  found  ab- 
normally abundant,  the  fibrillar  element  being  especially  increased  and  un- 
usually well  defined.  In  Prof.  Ord's  cases  the  corpuscular  elements  were 
enlarged  and  multiplied,  and  the  interstitial  element  greatly  augmented. 
The  skin  in  myxoedema  yields  many  hundred  times  as  much  mucin  as  nor- 
mal or  ordinarily  dropsical  skin.  Besides  the  overgrowth  of  connective- 
tissue,  it  seems  to  have  undergone  a  retrograde  degeneration.     In  the  skin 


908  CHEONIC   GENEEAL  DISEASES. 

the  mucous  infiltration  causes  swelling,  translucency  and  defective  secre- 
tion. The  connective-tissue  stroma  of  the  mucous  membranes,  of  the  outer 
coat  of  the  arteries,  the  glands,  muscles,  and  the  central  nervous  ganglia 
is  similarly  infiltrated  and  degenerated. 

Prof.  Ord  states  that  the  structure  of  the  thyroid  glands  maybe  entirely 
destroyed  by  the  material  ;  and  he  thinks  its  inroads  on  the  Malpighian 
bodies  and  tub  ales  of  the  kidney  cause  the  albuminuria  which  occurs  late 
in  the  disease.  Dr.  Mahomed,  on  the  other  hand,  argues  strongly  in  favor 
of  the  identity  of  myxoedema  and  Bright's  disease.  Eecently  it  has  been 
almost  conclusively  proven  that  the  central  nervous  system  is  affected,  and 
in  two  cases  marked  bulbar  paralysis  has  been  found. 

Etiology. — Myxoedema,  in  the  few  cases  first  described,  only  occurred  in 
adult  females,  and  of  these  more  married  than  single  women  were  affected. 
Eecently,  however.  Dr.  Andrew  Clark  states  that  in  his  experience  males 
suffer  oftener  than  females,  in  the  proportion  of  seven  to  three.  The 
number  of  recorded  cases  is,  however,  too  small  to  admit  of  positive 
statements. ' 

Symptoms. — The  face  is  swollen  as  in  real  dropsy ;  but  the  skin  has  a 
waxy  anaemic  look,  and  the  oedema  involves  not  only  the  dependent  por- 
tions, but  every  feature  of  the  face.  Both  lips  are  equally  enlarged  ;  the 
nose  is  thickened,  and  the  rounded  cheeks  have  a  pinkish  hue,  contrasting 
peculiarly  with  the  rest  of  the  waxy  white  skin.  There  is  no  pitting  on 
pressure  ;  on  the  contrary,  the  skin  is  rather  elastic.  The  shape  and  form  of 
the  hands  is  lost.^  The  dry,  rough,  translucent  skin  seldom  or  never  per- 
spires. The  thyroid  body  disappears  or  diminishes,  while  there  is  elastic 
tumefaction  of  the  skin  in  the  lower  triangle  of  the  neck  above  the  clavicle. 
The  expression  of  the  face  is  stolid  and  sad ;  the  speech  is  monotonous, 
slow,  and  leathery  ;  the  limbs  move  slowly  and  lazily  ;  a  fixed  attitude 
cannot  be  maintained,  and  consequently  the  patient  is  apt  to  suddenly  fall. 
The  intellect  becomes  dull,  sensation  is  slow  but  finally  sure,  and  the  mus- 
cles are  so  relaxed  at  rest  that  a  long  contraction  occurs  before  a  proper 
equilibrium  can  be  maintained ;  hence  a  quiver  often  runs  through  the 
body  as  one  foot  is  raised  from  the  ground  and  the  body  is  balanced  on 
the  other.  The  muscles  of  the  neck  are  so  lax  that  the  head  droops  on 
the  chest.  Sometimes  the  patella  is  fractured  by  the  forward  bending  of 
the  body.  There  is  no  real  loss  of  muscular  power,  no  wasting,  and  no  loss 
of  sensation. 

Thoughts  and  expressions  are  tardy  and  deliberate,  but  correct.  The 
bodily  temperature  ranges  between  98"  and  94°  F.  These  patients  are 
constantly  chilly.  Late  in  the  disease  patients  grow  morose  and  irritable, 
and  are  subject  to  delusions,  hallucinations,  loss  of  memory,  and  finally 
complete  mental  failure. 

Differential  Diagnosis. — There  is  no  disease  with  which  myxoedema  can 
be  confounded  when  the  mucoid  oedema  is  well  marked. 

^  In  the  sixteen  cases  on  which  Ord  based  his  descriptions,  pregnancy  ia  one  or  two  cases  preceded  the 
myxoedema. 

=  Sir  William  Gull  calls  them  spade  like. 


SCROFULA.  909 

Prognosis. — This  is  always  unfavorable  ;  its  duration  varies  from  six  to 
eight  years.     Death  may  occur  from  coma,  uraemia,  or  inanition. 

Treatment. — Besides  warm  clothing,  tonics,  and  good  food  little  can  be 
done.  Prof.  Ord  found  that  ten  to  sixty  minims  of  the  fluid  extract  of 
jaborandi,  administered  four  times  a  day,  was  followed  by  marked  relief. 
He  says  the  signs  of  myxoedema  almost  entirely  disajopeared  under  this 
treatment.  JSTitro-glycerine  benefited  one  case.  Vapor  baths  are  advo- 
cated. Dr.  Andrew  Clark  says  that  baths,  assiduous  friction,  a  careful 
diet,  and  arsenic  and  iron  as  tonics,  may  sometimes  cure  the  disease. 

SCROFULA. 

Scrofula  is  a  term  applied  to  many  different  physical  conditions  de- 
pending upon  a  diathesis  which  is  regarded  as  identical  with  the  tuber- 
culous. 

Morbid  Anatomy. — The  characteristic  lesions  of  scrofula  are  to  be  found 
in  the  lymphatic  glands,  although  the  skin,  mucous  membranes,  bones, 
joints,  and  organs  of  special  sense  may  be  involved.'  Inflammation  ante- 
dates the  scrofulous  change,  and  whether  occurring  in  the  glands,  skin, 
mucous  membrane,  subcutaneous  connective-tissue,  bones,  joints,  kidney 
or  testicle,  the  inflammatory  product  is  the  same.  When  fresh  it  is  rich 
in  cells,  consisting  of  a  dim,  glistening  protoplasm  with  a  large  single  or 
double  nucleus.  The  exudation  is  either  nodular  or  diffused.  It  may 
undergo  resolution,  suppuration  or  organization  ;  all  taking  place  slowly 
and  imperfectly,  on  account  of  poor  vascularity.  Anemic  necrosis  some- 
times occurs  in  the  glands. 

On  the  skin  the  lesions  appear  as  eruptions.  Impetigo  of  the  eyelashes 
and  external  otitis  are  common  strumous  diseases.  In  one  who  has  this 
diathesis  any  skin  disease  takes  on  a  scrofulous  character.  Scrofulous  in- 
flammation of  mucous  membranes  is  marked  by  a  thick,  sticky  exudation, 
with  a  tendency  to  form  scabs.  The  bones  most  frequently  involved  are 
those  of  the  ankle,  lower  part  of  the  femur,  the  vertebrge,  and  rarely  the 
fingers  and  toes.  The  scrofulous  development  may  assume  the  form  of 
synovitis,  osteitis,  periosteitis,  or  general  arthritis. 

Etiology. — The  scrofulous  diathesis  is  very  largely  an  inherited  condition 
whose  exact  nature  is  unknown,  and  whose  etiology  is  perhaps  equally  ob- 
scure. It  usually  has  been  considered  a  functional  disturbance  of  impaired 
vitality,  but  some  recent'  observations  afford  ground  for  the  suspicion  that 
it  may  possibly  possess  an  anatomical  basis. 

The  children  of  intemperate,  phthisical,  syphilitic,  very  old  or  very 
young  parents  develop  early  all  the  characteristic  features  of  the  scrofulous 
diathesis.     It  is  also  very  apt  to  appear  in  the  children  of  parents  closely 

1  Virchow  taught  that  the  primitive  strumous  lesion  is  a  simple  h}'perplasia  of  the  gland  tissue,  but 
Schiippel  has  proven  ihaX.  a  scrofulous  gland  is  a  tubercvlous  gland.  Tubercles  stud  the  glands,  which 
soon  become  enlarged  and  soft.  When  cut  they  eii her  resemble  a  normal  gland  or  contain  a  white,  soft 
cheesy  mass  mixed  with  thick  pus.  Abscess  or  ulceration  may  ensue  and  leave  an  unsightly  scar.  Simple 
chriinic  hypertrophy  results  in  tlie  formation  of  knotty  groups  of  glands.  Of  all  the  tissues  the  lymphatic 
is  the  most  embryonic,  the  most  plastic  or  potential. 


910  CHRONIC    GENERAL   DISEASES. 

related  by  blood.  Heredity  is  by  no  means  always  present,  however,  for  a 
marked  scrofulous  diathesis  is  acquired  in  early  infancy  by  healthy  children 
from  improper  food,  over-crowding,  and  anti-hygienic  surroundings. 

Lack  of  fresh  air,  exercise,  and  sunlight  exerts  an  equally  powerful  influ- 
ence in  reducing  the  vitality  and  the  reactive  power  of  the  system  under 
irritation.'  Scrofula  and  the  tuberculous  diathesis,  if  not  identical,  are  so 
closely  related  as  to  be  interchangeable.' 

Symptoms. — Scrofula  presents  no  lesions  that  may  not  occur  in  other  dis- 
eases, and  the  scrofulous  inflammation  has  no  characteristics,  beyond  a 
tendency  to  extreme  clironicity  and  to  undergo  caseous  changes.  It  is 
principally  a  disease  of  childhood  ;  rarely,  however,  appearing  before  the 
second  year. 

Children  with  a  scrofulous  habit  are  markedly  different  in  appearance 
from  their  healthier  mates.  Most  of  them  have  a  transparent,  white  skin, 
with  delicate  blue  veins  ;  large,  lustrous  eyes ;  bright  red  lips,  and  alto- 
gether look  more  like  wax  figures  than  healthy  children.  They  are  apt  to 
show  abnormal  mental  development,  with  an  irritable  nervous  system.  On 
the  other  hand,  they  may  have  a  large  head  with  coarse  features,  a  thick 
skin,  which  has  a  flabby,  spongy  feel,  an  enlarged  abdomen  and  cervical 
glands.  About  the  upper  lip  and  the  nose  there  is  frequently  ah  over- 
production of  fat.^  In  their  development  no  two  cases  present  the  same 
characteristics.  Chronic  inflammations  of  the  skin,  especially  about  the 
face  and  scalp  and  at  the  junction  of  skin  and  mucous  membranes,  are 
frequent,  either  alone  or  associated  with  persistent  chronic  catarrh  of  the 
adjacent  mucous  surface.  Coryza,  conjunctivitis,  ulceration  of  the  cornea, 
and  otorrhoea  often  follow  an  eczema  of  the  face  and  neck  or  alternate  with 
it.  Laryngitis  and  bronchitis  are  obstinately  persistent,  and  may  extend  to 
the  alveoli  and  eventuate  in  phthisis.  Pyelitis,  cystitis,  and  vaginal  or 
vulvar  catarrh  are  rarer  indications  of  the  depraved  condition. 

The  articular  manifestations  may  appear  as  a  simple  synovitis  or  tumor 
albiis,  or  some  slight  injury  may  be  the  starting-point  of  caries  and  ne- 
crosis, with  suppuration,  burrowing  of  pus,  and  complete  destruction  of  the 
joint. 

Glandular  enlargements  so  invariably  develop  sooner  or  later  in  scrofulous 
patients  as  to  be  accepted  as  the  most  characteristic  lesion.  This  enlarge- 
ment, which  is  non-inflammatory  and  due  to  cellular  hyperplasia,  is  very 
gradual,  and  forms  a  smooth,  firm  tumor,  which,  with  similar  adjacent 
glands,  may  unite  in  an  irregular,  shapeless  mass.  Occasionally  these 
hypertrophied  glands  subside,  but  more  frequently  they  finally  excite  in- 
flammation with  suppuration  or  caseous  changes. 

The  disease  progresses  slowly  with  periods  of  apparent  well-being,  bub 
toward  puberty  pulmonary  disease  is  apt  to  be  established  ;  or,  if  there  has 
been  much  suppuration,  waxy  degeneration  may  occur  in  the  viscera  or  in- 

1  BuW  favors  a  specific  virus  theory,  but  the  parasitic  origin  rests  on  no  certain  anatomical  facts. 

2  Birch-Hirschf eld  found  tubercles  in  nine  out  of  ten  lymphatic  glands  removed  from  the  necks  of 
scrofulous  patients. 

s  Canstatt  calls  this  latter  the  torpid,  and  the  former  the  erethitic  form  of  scrofulosis. 


RICEETS.  911 

testinal  tract.  Such  a  condition  will  not  long  continue  without  the  devel- 
o^ament  of  extreme  ansemia  and  a  characteristic  cachexia. 

DifiFerential  Diagnosis. — Scrofulous  developments  per  se  can  hardly  be 
mistaken  for  any  other  disease,  and  a  question  of  diagnosis  can  only  arise 
as  to  the  nature  of  chronic  degenerative  changes  other  than  glandular. 
Such  a  diagnosis  can  be  made  from  the  obstinacy  of  the  disease  and  coinci- 
dent evidence  of  the  j)eculiar  diathesis. 

Prognosis. — The  prognosis  is  good  when  the  patient  is  seen  early,  and 
means  exist  for  a  change  of  diet  and  surroundings.  Scrofulous  children 
may  die  from  tuberculous  intestinal  disease,  acute  hydrocephalus,  or  croup. 

Treatment. — The  prophylactic  treatment  embraces  a  consideration  of  all 
the  laws  of  health.  Until  unhealthy,  old  and  closely  related  individuals 
cease  to  marry,  until  children  receive  the  proper  amount  and  kind  of  food 
for  the  first  two  or  three  years  of  life,  scrofula  will  exist. 

The  diet  of  scrofulous  children  should  be  the  same  as  that  advised  in  the 
treatment  of  chronic  phthisis  {q.  v.).  Cod-liver  oil  will  be  the  chief  agent 
for  arresting  its  progress  and  development,  and  should  be  given  daily  dur- 
ing the  greater  portion  of  infantile  and  adult  life.  Iodine  is  no  longer  re- 
garded as  a  specific.  Chloride  of  calcium  and  the  sulphites  have  been  recent- 
ly highly  recommended.  Sea  or  brine  baths  or  even  ordinary  cold  water 
baths  are  frequently  of  the  greatest  benefit.  The  treatment  of  the  skin,  joint, 
and  eye  complications,  and  the  question  of  extirpation  of  scrofulous  glands, 
belong  to  the  domain  of  surgery. 

EICKETS. 

Eickets  or  rachitis  is  a  disease  of  general  malnutrition  with  characteristic 
lesions  in  the  osseous  structures. 

Morbid  Anatomy. — Deficient  ossification  is  the  essential  pathological 
change  ;  bones  already  ossified  are  softened,  and  ossification  in  parts  still 
cartilaginous  is  prevented  or  delayed.  G-rowth  of  the  bone  is  retarded  or 
advances  in  an  irregular  manner,  and  while  the  medullary  cavity  increases 
the  osseous  shell  becomes  deficient,  owing  to  proliferation  of  unossified 
matter  at  its  circumference.  There  is  an  undue  development  of  the  car- 
tilaginous epiphyses  and  fibrous  periosteum,'  causing  the  clumsy  appearance 
of  rachitic  bones.  The  flat  bones  are  greatly  thickened  at  their  circumfer- 
ence, from  proliferation  of  the  periosteum,  but  thinned  at  their  centres, — a 
condition  called  craniotabes: — this  is  especially  marked  in  the  occipital  and 
other  cranial  bones.  In  the  lower  jaw  the  anterior  wall  of  the  alveolus  is 
sometimes  perforated  by  the  milk  teeth. 

The  liver,  kidneys,  sjDleen  and  lymphatic  glands  are  often  enlarged  from 
irregular  hyperplasia  of  their  fibroid  and  epithelial  elements,  conjoined 
with  a  deficiency  in  earthy  salts.  The  brain  enlarges  from  increase  in  its 
neuroglia.    The  muscles  are  small,  pale,  flabby,  and  soft,  and  their  striae  are 

1  Virc'now  thii«  describes  the  changes  in  the  diaphyses: — (1)  Increasing  density  of  perioste'il  prolifera- 
tion and  progressive  rarefaction  of  tlie  substance  in  the  areolje  and  cancellated  tissue.  (2)  Deficient  os- 
eification  of  the  cancellated  tissue  and  continuance  of  the  deep  layers  of  compact  exterior  substance.  (3) 
Partial  formation  of  cartilage  in  tlie  areolae. 


912  CHKOKIC   GENERAL  DISEASES. 

very  indistinct.  The  ligaments  are  also  wasted.  The  fontanelles  close 
very  late  in  rachitic  children,  and,  on  this  account,  chronic  hydrocephalus 
maybe  suspected. 

Etiology. — Our  knowledge  of  the  primary  blood  changes  which  result  in 
deficient  ossification  is  largely  theoretical.  It  has  been  supposed  to  be : 
(1)  the  presence  of  lactic  acid  holding  the  salts  in  sojution  ;  (2)  deficiency 
of  lime  salts  ;  (3)  an  inflammation  of  the  epiphyseal  cartilages  and  perios- 
teum ;'  (4)  some  irritant  in  the  blood.^  Clinically,  rickets  is  caused  by 
anti-hygienic  surroundings.  Poor  or  deficient  food  and  foul  air  are  the 
most  potent  factors.  Acute  disease  and  troublesome  dentition  predispose 
to  it.  It  is  more  apt  to  occur  in  children  of  rachitic,  syphilitic,  or  phthisi- 
cal parents. 

The  disease  usually  develops  during  the  first  year  of  life,  and  is  rare  be- 
fore the  seventh  month  or  after  the  seventh  year  of  life.'  Foetal  and  con- 
genital forms  occur,  and  in  many  cases  no  cause  can  be  ascertained. 

Symptoms. — Usually  gastro-intestinal  disturbances  are  the  earlier  symp- 
toms of  rickets.  There  may  be  vomiting,  and  the  motions  are  frequent, 
pasty  and  offensive.  The  child,  when  awake,  is  listless  and  drowsy,  and 
when  asleep  is  restless  and  sweats  profusely,  mainly  about  the  head  and 
upper  parts  of  the  body,  regardless  of  the  temperature  of  the  room.  He 
dislikes  to  be  disturbed  and  frets  when  any  one  approaches  his  cot.  There 
is  an  intolerance  of  the  bedclothes,  which  the  child  is  constantly  throw- 
ing off. 

The  final  distinct  evidence  of  the  osteal  changes  is  the  enlargement 
of  the  lower  extremity  of  the  radius  and  tibia  and  of  the  corresponding 
portion  of  the  ulna  and  fibula.  The  softened  bones  yield  readily  to 
pressure,  and  if  the  child  is  allowed  to  stand  or  walk,  the  legs  become  bent 
and  twisted,  and  the  gait  unsteady  and  swaying.  The  limbs  may  remain 
perfectly  straight,  though  stunted,  thin  and  flabby,  when  the  disease  oc- 
curs very  early  in  life.  The  head  is  large  and  elongated  antero-posteri- 
orly,  the  fontanelles  are  wide  and  the  sutures  thick.  The  forehead  is  very 
prominent,  while  the  face  is  small  and  wizened,  with  the  skin  wrinkled  as 
in  old  age.  The  lower  Jaw  is  shortened,  so  that  the  upper  teeth  overlap 
the  lower.  The  teeth  appear  late,  the  incisors  may  not  appear  until  the 
end  of  the  first  year,  and  dentition  proceeds  very  irregularly.  The  spine 
is  curved,  and  distortions  of  the  ribs  induce  an  unsymmetrical  or  oblique 
thorax. 

Eachitic  children  are  usually  pigeon-breasted,  and  there  is  often  marked 
deformity  of  the  pelvis.  The  joints  are  large,  loose,  and  lax.  The  child  is 
short  for  his  age,  and  the  limbs  are  short  in  proportion  to  the  trunk 
and  head.  The  abdomen  is  prominent,  and  the  liver  and  spleen  will 
usually  be  enlarged  ;  sometimes  their  enlargement  gives  the  first  indication 
of  rachitis.  The  large  cranium,  thin  face,  and  distorted  limbs  cause  a 
rachitic  child  to  present  the  appearance  of  a  monstrous  deformity,  when 
intellectually  it  is  bright  and  mature  beyond  its  years.  Eachitic  children  are 

'  Niemeyer.  2  Wagner. 

5  Rehn  states  that  lie  never  saw  it  develop  after  the  third  yewc.—  Centralb.f.  Kindr/i.,  1877  to  '78. 


ALCOHOLISM.  913 

anaemic  and  very  sensitire  to  changes  of  temperature.'  The  nervous  sys- 
tem is  very  im  j)ressionable,  and  general  convulsions  or  spasms  of  the  larynx 
are  frequent.  All  rickety  children  do  not  emaciate,  and  some  only  suffer 
pain  when  they  attempt  an  exertion. 

Persons  who  were  rachitic  in  infancy  not  infrequently  become  very 
strong  as  they  reach  adult  life.  They  remain  of  short  stature  and  the 
deformities  persist.  In  foetal  rickets  the  body  is  large  and  plump,  the  ab- 
domen protrudes,  all  the  abdominal  organs  being  large,  the  skin  is  thick, 
and  the  extremities  are  short  and  thick.  In  these  cases  the  chicken- 
breast  is  not  present.  * 

Differential  Diagnosis. — The  nocturnal  sweats  about  the  head,  the  osseous 
changes,  the  enlargement  of  the  spleen  and  liver,  the  weakness  of  the  legs, 
the  rims  around  the  cranial  bones,  the  large,  lax  joints,  and  the  gastro- 
intestinal disturbances  form  a  train  of  symptoms  that  prevent  rickets 
from  being  confounded  with  any  other  disease. 

Prognosis. — As  a  rule,  when  the  cause  is  removed  the  disease  will  dis- 
appear. The  greater  the  thoracic  deformity  and  the  longer  the  disease  has 
existed  the  worse  the  outlook.  Bronchitis,  pneumonia,  enteritis,  laryn- 
gismus stridulus,  convulsions,  difficult  dentition,  diarrhoea  and  chronic 
hydrocephalus  are  not  infrequent  complications.  Death  may  occur  from 
the  wasting  and  anaemia,  from  the  complications,  or  from  asphyxia  due  to 
thoracic  deformity. 

Treatment. — Cleanliness,  fresh  air,  and  nutritious  food  suitable  to  the 
age  of  the  patients  are  of  the  utmost  importance.  Children  kept  too  long 
at  the  breast  often  become  rickety  ;  they  should  be  weaned  at  once  and  have 
liquor  calcis  saccharatus  added  to  their  food.  Cod-liver  oil  should  be  taken 
as  early  and  in  as  large  doses  as  the  child  can  digest.  Scraped  raw  beef^. 
with  a  small  amount  of  wine,  often  produces  marked  improvement.  The 
intestinal  derangements  are  best  corrected  by  castor  oil  or  rhubarb  and 
soda.  In  older  children  quinine,  iron,  and  lime  preparations  may  be  ad- 
ministered.' The  hydrate  of  chloral  is  to  be  used  for  any  nervous  derange- 
ments. Eickety  children  should  not  sleep  on  feather  beds  or  high  pillows, 
and  must  not  be  allowed  to  run  about  or  exert  pressure  on  any  part  thai; 
may  become  deformed.  Orthopaedic  measures  are  treated  of  in  works  on 
Surgery. 

ALCOHOLISM. 

Alcoholismus  may  be  acute  or  chronic.  Acute  alcoholismus  often  mani- 
fests itself  as  delirium  tremens. 

Morbid  Anatomy.  —In  acute  alcoholismus  the  mucous  membrane  of  the 
stomach  and  duodenum  is  intensely  injected.  Patches  of  aphthae  are  found 
upon  it,  and  the  mucous  surface  of  the  stomach  is  covered  with  ropy  mucus 
slightly  tinged  with  blood.  The  gastric  juice  is  altered  in  quantity  and 
quality.     The  brain,  lungs  and  kidneys  are  the  seat  of  active  hyperaemia, 

1  Barthez  regardw  a  blowing  sound  audible  over  the  cranial  sutures,  as  diagnostic  of  the  affection. 
"  Recently  the  phonphates  have  been  more  recommended  than  cod-liver  oil.    The  fluorides  and  arsenic 
are  esteemed  highly  by  German  phytsicians. 
58 


914  CHEOKIC    GENEUAL   DISEASES. 

and  the  pericardium  and  .pleura  are  often  filled  "with  bloody  serum.  In 
chronit  alcoholismus  there  is  chronic  gastritis,  congestion  or  cirrhosis  of 
the  liver,  emphysema  and  bronchitis,  fatty  degeneration  and  dilatation  of 
the  heart,  atheroma  of  the  vessels,  and  Bright's  disease  of  the  kidneys. 
Chronic  meningitis  and  pachymeningitis  are  common.  In  long-standing 
cases  cerebral  softening  occurs,  and  in  such  the  viscera  are  fatty  and  the 
subcutaneous  tissue  and  omentum  are  loaded  with  fat  if  the  subjects  are 
beer  or  wine  drinkers  ;  those  who  drink  s|)irits  are  emaciated  and  grow  pre- 
maturely old,  on  account  of  the  increase  in  connective-tissue.  Frequently 
the  abnormal  accumulation  of  fat  in  the  abdomen  is  in  striking  contrast 
with  tlie  thin,  wasted  limbs. 

The  blood  m  chronic  alcoholismus  contains  more  fat  than  normal ;  one 
of  the  first  effects  of  alcohol  is  a  true  chfimical  combination  with  nerve- 
tissue,  and  as  the  ingestion  of  spirits  is  constant,  the  nerves  progressively 
atrophy  and  harden.  This  is  hastened  by  general  interference  with  nutri- 
tion from  poor  blood.  The  face  of  the  confirmed  toper  shows  turgid  and 
varicose  veins, — especially  about  the  nose,  which  becomes  clubbed, — in- 
jected conjunctivge,  and  pimples  of  acne  rosacea.  Puffiness  under  the 
eyes  indicates  the  changes  taking  place  in  the  kidneys. 

Etiology. — Even  more  deleterious  than  alcohol  itself  are  the  adulterations 
of  fusel  oil,  wormwood,  and  cocculus  indicus.  Delirium  tremens  comes  on 
after  a  prolonged  debauch  in  an  old  drinker,  or  when  one  unaccustomed  to 
alcohol  takes  a  comparatively  large  quantity  of  raw  spirits.  After  ex- 
posure to  cold,  prolonged  abstinence  from  food,  or  some  exhausting  dis- 
ease, a  small  amount  of  alcohol  may  induce  acute  alcoholismus.  Chronic 
alcoholismus  is  often  met  with  in  families  where  epilepsy,  hysteria,  in- 
sanity, and  allied  disorders  show  themselves.  In  such  cases  a  peculiar 
constitutional  condition  which  renders  abstinence  from  alcohol  especially 
difficult,  is  undoubtedly  present. 

Symptoms. — In  acute  alcoholism,  after  a  period  of  exhilaration  and  semi- 
delirium,  acute  coma  is  very  apt  to  supervene  ;  in  this  condition  the  breath- 
ing is  stertorous,  the  face  is  pale,  and  the  pupils  as  a  rule  are  dilated. 
The  skin  is  cold  and  clammy,  and  the  temperature  below  normal.  The 
urine  may  be  albuminous,  and  always  contains  more  or  less  alcohol.  Some- 
times control  over  the  sphincters  is  lost.  In  rare  cases  delirium  tremens 
occurs  after  the  first  debauch. 

In  chronic  alcolioUsmus  there  is  muscular  tremor  and  pyrosis,  or  vomit- 
ing on  waking,  with  entire  loss  of  appetite,  the  sleep  is  disturbed,  and  there 
is  headache  and  vertigo ;  the  will-power  and  memory  are  progressively 
weakened  until  entirely  lost,  the  gait  becomes  ataxic,  the  face  is  flabby  and 
the  eyes  watery.  The  breath  and  sweat  have  a  peculiar,  offensive  odor, 
the  generative  functions  are  enfeebled,  muscular  ti'emors  become  constant, 
and  the  patient  is  in  a  continued  state  of  dread  or  anxiety. 

Delirium  tremens  occurs  most  frequently  in  old  topers  after  a  severe 
drinking  bout : — there  is  complete  anorexia,  marked  tremor,  especially  of 
the  tongue,  insomnia,  or  sleep  disturbed  by  bad  dreams,  disorders  of  vision 
and  hearing,  a  soft,  weak  pulse,  cold  extremities,  and  extreme  mental  de- 


ALCOHOLISM.  915 

jection.  In  a  day  or  two  a  wild  delirium  comes  on  characterized  by  the 
most  terrible  hallucinations,  snakes  and  all  forms  of  repulsive  reptiles 
bemg  seen  and  causing  the  most  intense  horror  and  abject  fear.  The 
patient  talks  incoherently  and  incessantly,  moves  constantly  and  quickly, 
has  a  wild  or  vacant  expression  of  the  eye,  and  all  the  muscles  are  mean- 
while in  a  continual  tremor.  The  pupils  are  contracted,  the  pulse  is  rapid, 
feeble,  and  dicrotic.  Insomnia  is  continuous.  After  a  day  or  two,  coma- 
vigil  and  all  the  typhoid  symptoms  appear  as  the  precursor  of  death,  or  a 
sound  sleep  ends  the  delirium  and  establishes  convalescence. 

Acute  alcoholic  mania,  acute  melancholia,  or  chronic  dementia  with  sui- 
cidal tendencies,  are  common  exhibitions  in  chronic,  but  rare  in  acute 
alcoholismus.  ^ 

Differential  Diagnosis. — The  coma  of  alcoholism  may  be  confounded  with 
urmmic  coma,  which  has  already  been  considered.  Its  diagnosis  from  apo- 
plectic coma  will  be  considered  under  apoplexy. 

It  can  only  be  distinguished  from  opium  poisoning  by  an  examination 
of  the  contents  of  the  stomach,  and  by  an  examination  of  the  uriue. 

The  delirium  of  acute  diseases  will  not  be  confounded  with  delirium  tre- 
mens if  the  history  of  the  case  and  the  j)atient's  temiaerature  be  taken. 

Meningitis  is  distinguished  from  alcoholismus  by  the  firm,  hard  pulse, 
the  pyrexia,  the  projectile  vomit,  the  retracted  abdomen,  the  j)hotophobia 
(absent  in  alcoholismus)  and  the  agonizing  headache. 

Chronic  alcoholic  tremor  has  been  confounded  with  shaTcing  palsy  (q.  v.), 
with  locomotor  ataxy,  and  softening  of  the  brain  ;  their  differential  diag- 
nosis will  be  considered  in  connection  with  the  history  of  these  diseases. 

Prognosis. — The  prognosis  is  good  if  the  patient  is  manageable.  Death 
may  occur  in  acute  alcoholic  coma,  and  from  acute  lobar  pneumonia  which 
so  often  complicates  it.  A  patient  in  delirium  tremens  may  suddenly  j)ass 
into  a  comatose  state,  which  will  soon  be  followed  by  death.  The  degenera- 
tive changes  which  take  place  in  the  vessels  and  viscera  in  chronic  alcohol- 
ism predispose  to  a  long  list  of  diseases  and  tend  to  shorten  life.  Insanity, 
impotence,  epilepsy,  melancholia,  and  organic  brain  diseases  are  its  fre- 
quent seqaelge. 

Treatment. — In  acute  mania,  delirium,  etc.,  w^ash  out  the  stomach  and 
give  a  simple  saline  purge.  Cold  affusions  and  galvanism  with  energetic 
friction  are  beneficial.  In  delirium  tremens  nothing  but  milk  must  be 
given  in  the  way  of  food.  Bromide  of  potash,  hydrate  of  chloral,  oj^ium, 
and  hyoscyamus  are  all  favorite  drugs  for  inducing  sleep.  Tartar  emetic 
sometimes  acts  in  this  way.^  Inhalation  of  chloroform  should  be  practiced 
with  great  care.  Sometimes  stimulants  are  necessary  if  the  vitaj  powers 
are  much  depressed.  In  chronic  alcoholismus  bromide  of  potash,  or  better, 
hydrate  of  chloral,  is  to  be  employed  for  the  insomnia.  For  the  craving 
for  alcohol,  opium  is  sometimes  given,  but  is  apt  often  to  engender  a  still 
worse  habit.  A  variety  in  the  diet,  pleasant  surroundings,  and  strong 
will-power  are  about  the  sole  means  of  combating  this  condition. 

1  Oinomania  is  a  condition  where  at  long  intervals  an  individual  has  paroxysms  of  alcoholic  excess,  be- 
tween which  he  neither  touches  nor  craves  alcohol.    This  form  is  truly  a  disease. 
a  Jones,  of  England,  advocates  digitalis. 


916 


CHRONIC    GENERAL   DISEASES. 


TRICHIlSrOSIS. 

Trichinosis  is  a  parasitic  disease,  classed  by  some  among  the  acute  in- 
fections diseases. 

Morbid  Anatomy. — Trichina  spiralis,  in  the  form  of  a  minute  worm,  meas- 
uring about  one  thirty-fifth  of  an  inch  in  length,  enters  the  human  system 
through  the  intestinal  tract  after  the  ingestion  of  trichinous  flesh.  The 
muscle  larvse  mature  two  days  after,  and  in  six  days  the  embryos  are  born. 
In  about  fourteen  days  the  migrating  progeny  reach  the  muscles.  Some 
believe  that  the  blood-vessels  are  the  channels  of  their  conveyance.  The 
most  prevalent  idea,  however,  is  that  they  pass  through  the  intestinal  walls 
and  peritoneal  cavity  and  then  enter  the  muscular  system.     Once  in  the 


IMW 


Fig.  186. 
Encapsulated  Trichinte  in  voluntary  muscle. 
X  300. 


Fig.  187. 
Trichinte  with  calcareous  deposits  and  de- 
generation of  the  capsules,     x  300. 


muscles,  ovoid  protective  capsules  are  thrown  around  the  entozoa,  each  of 
which  is  curled  up  spirally  like  a  hair  spring.  The  muscular  fibrillse  sub- 
sequently break  down  into  a  granular  debris,  interstitial  connective-tissue 
forms  in  abundance,  and  in  the  neighborhood  the  muscles  have  an  inflamed, 
gray-red  appearance. 

The  voluntary  muscles  are  those  usually  invaded.  The  ends  of  the 
muscle^where  it  becomes  tendinous — exhibit  the  greatest  number.  The 
diaphragm,  lumbar,  intercostal,  cervical,  and  laryngeal  muscles,  and  those 
of  the  eye  are  the  favorite  sites.  As  a  rule,  the  farther  from  the  trunk  the 
fewer  the  trichinae.  At  times  the  heart  has  been  infested  with  them.  The 
number  of  the  trichinae  in  the  muscles  is  greater  the  longer  the  disease  has 
lasted.*     Later  the  capsules  become  dense,  fibrous,  cheesy,  and  even  chalky. 

I  Oohnheim  states  that  the  muscles  have  no  ather  changes  exceut  those  met  with  in  acute  infectious 
diseases. 


TEICHINOSIS. 


917 


At  the  autopsy  of  one  who  has  died  of  trichinosis  during  the  first  week, 
only  the  signs  of  more  or  less  intense  intestinal  catarrh  are  found  ;  after 
the  fourth  or  fifth  week,  distinct  signs  of  interstitial  and  parenchymatous 
inflammation  of  the  muscles  are  found  as  fine  gra3''ish-red  striae.  Intestinal 
catarrh,  enlarged  mesenteric  glands,  peritonitis,  venous  thrombosis,  and 
hypostatic  congestion  of  the  lungs  are  also  quite  frequently  found.  En- 
cysted trichinae  retain  their  vitality  for  a  number  of  years. 

Etiology. — Trichinosis  in  the  human  being  results  almost  exclusively 
from  eating  trichinous  pork.  The  raw  flesh  is  most  dangerous  ;  the  more 
underdone  the  pork  the  greater  the  danger.  Pork  cooked  in  any  way  that 
does  not  kill  the  trichinae  is  dangerous.  Sausages,  ill-smoked  ham,  or 
quickly-broiled  ham,  or  any  form  of  pork  that  has  not  been  subjected  to  a 
moist  heat  of  ]  70°,  is  liable  to  induce  it.  Salting  meat  does  not  necessarily 
destroy  the  trichinae.  Each  trichina  may  give  birth  to  a  thousand  young ; 
about  one-half  a  pound  of  pork  containing  trichinae  could  rapidly  produce 
thirty  millions  of  trichinse.  * 

Symptoms. — The  symptoms  of  trichinosis  are  first  gastro-intestinal  and 
then  muscular  ;  associated  with  these  there  is  more  or  less  fever.  After  a 
varying  time  following  ingestion  of  trichinous  meat,  nausea,  vomiting, 
vertigo,  anorexia,  a  feeling  of  malaise,  and  a  slight  febrile  movement 
occur.  There  is  almost  always  diarrhoea,  the  passages  being  first  brownish, 
then  yellow  ;  after  a  short  time  there  are  wandering  pains  in  the  limbs, 
which  become  stiff  and  painful  to  the 
iouch,  and  the  muscles  are  swollen 
And.  rigid.  In  from  four  to  ten  days 
cedema  of  the  eyelids,  perhaps  of  the 
entire  face,  occurs.  The  temperature 
ranges  from  101°  to  106°  F.,  the 
pulse  from  110  to  120  ;  there  is  photo- 
phobia, and  movements  of  the  limbs 
or  of  the  eyes  are  accompanied  by  ex- 
cruciating pain.  The  pain  in  the 
limbs  becomes  so  great  that  the  patient 
cannot  sleep.  (Edema  of  the  lower 
extremities  is  common  ;  and  there 
may  be  general  anasarca.  Copious 
perspiration  with  sudamina  charac- 
terize the  fever  of  trichinosis.  The 
diarrhoea  becomes  exhaustive,  the 
limbs  are  paralyzed  and  the  patient 
lies  in  a  state  of  utter  helplessness. 

Abdominal     pains    are     sometimes 
present  and  the  muscles  of   the  ex- 
tremities may  become  strongly  flexed.      Deafness  and  aphonia  occur  when 
trichinosis  of  the  stapedius  muscle  or  of  the  muscles  of  phonation  respect- 


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Fig.  188. 
Temperature  Record  in  the  fourth  week  of  a  case 
of  Trichinosis.    Death  on  the  29th  day. 


»  Trichinae  have  been  found  in  rats,  mice,  dogs,  cats,  badgers,  etc.,  and  swine  get  them  by  eating  Van 
excrements  of  them;  auiuiulB  or  the  dead  animals  themselves,  rats  and  mice  especially. 


918  CHROIS"IC    GENERAL   DISEASES. 

ively  takes  place.  ^  When  recovery  is  to  occur  the  symptoms  all  gradually 
abate.  This  occurs  in  from  four  to  five  weeks  after  the  first  evidence  of 
its  commencement.  When  death  occurs  it  is  usually  during  the  fourth 
week,  and  it  may  or  may  not  be  preceded  by  delirium. 

Differential  Diagnois. — Trichinosis  may  be  confounded  with  typhoid 
fever,  myalgia,  Asiatic  cholera  and  inflammation  of  the  muscles.  The 
points  of  diagnosis  between  trichinosis  and  typhoid  fever  have  already  been 
considered. 

From  myalgia,  or  inflammation  of  muscles,  trichinosis  is  distinguished  by 
the  abdominal  pains,  the  diarrhoea,  febrile  movement,  and  the  history  of 
the  case. 

Cholera  is  distinguished  from  it  by  the  sub-normal  temperature,  absence 
of  sudamina  and  copious  perspiration,  and  by  the  presence  of  the  charac- 
teristic rice-water  discharges.  It  is  said  that  the  nematoid  can  be  found 
in  the  faeces.  In  all  cases  a  diagnosis  can  be  reached  by  excising  a  piece  of 
the  deltoid  muscle  and  examining  it  microscopically. 

Prognosis. — There  are  no  reliable  statistics  by  which  its  rate  of  mortality 
can  be  determined.  It  may  be  complicated  by  hydrothorax,  pneumonia, 
bronchitis,  haemoptysis,  gastritis,  enteritis,  peritonitis  and  anasarca. 

Treatment. — Preventive  treatment  consists  in  eating  no  pork  that  has  not 
been  so  prepared  as  to  kill  any  trichinae  that  might  exist.  The  first  indi- 
cation for  treatment  is  to  support  the  patient  by  a  nutritious  diet  and  mod- 
erate stimulus.  We  know  of  no  means  of  destroying  the  trichinae  after 
they  have  once  entered  the  muscles.  Very  early  in  the  disease  a  prompt 
emetic  or  a  brisk  purge  may  remove  the  trichinae  from  the  intestinal  tract. 
Calomel,  jalap,  scammony  and  colocynth  are  efficient  for  such  purpose. 
To  allay  the  fever  and  overcome  the  subsequent  anaemia  quinine  and  iron 
are  of  service.    The  treatment  is  mainly  symptomatic. 


SYPHILIS. 

Syphilis  is  a  specific  infectious  disease  produced  only  by  inoculation.  It 
presents  a  characteristic  acute,  initial  lesion,  and  multiform  chronic  mani- 
festations, which  follow  a  uniform  order  of  development,  and  are  of  two 
distinct  forms,  called  secondary  and  tertiary  lesions. 

Morbid  Anatomy. — The  pathological  changes  in  the  primary  and  second- 
ary stages  are  essentially  inflammatory.  About  the  point  of  inoculation 
there  is  hyperaemia  and  cell  infiltration,  followed  by  necrosis  or  ulceration, 
and  resulting  at  first  in  a  papule,  and  later  in  a  simple  excoriation  or  a 
shallow,  indolent  ulcer,  with  characteristic  induration  and  a  dirty-gray  base, 
which  eventually  leaves  a  discolored,  retracted  cicatrix.  This  ulcer  is  the 
typical  Hunterian  chancre.  For  its  many  deviations  due  to  adventitious 
circumstances  reference  must  be  made  to  surgical  works.  In  connection 
with  the  inflammatory  changes  of  the  secondary  stage  there  is  proliferation 

1  Cohnhelm  states  that  the  position  of  one  suffering  from  trichinosis  is  that  in  which  the  various 
groups  of  muscles  are  least  extended. 


SYPHILIS.  919 

of  connective-tissue  with  new  formations  which  soon  subside  or  merge  with 
the  tissue  in  which  thej  occur,  producing  ostoses,  or  in  vascular  organs  in- 
duration and  atrophy.  In  the  tertiary  stage  the  process  assumes  the  form 
of  specific  neoplastic  formations  termed  gummata,  which  may  be  circum- 
scribed and  isolated,  but  more  frequently  are  infiltrated  through  the  af- 
fected tissue.  They  may  appear  as  firm,  gray,  opaque  nodules,  or  as  soft, 
translucent  masses.  They  consist  histologically  of  a  cell-growth,  resembling 
granulation  tissue,  and,  unlike  the  earlier  manifestations,  show  little  tend- 
ency to  resolve,  but  evince  a  marked  tendency  to  undergo  caseous  and 
calcareous  changes  and  to  produce  necrotic  processes  in  the  infiltrated  tis- 
sue. 

In  the  skin,  mucous  membranes,  and  smaller  cartilages  and  bones,  this 
degenerative  process  results  in  fatty  degeneration,  ulceration,  and  slough- 
ing, and  may  result  in  widespread  destruction  of  tissue.  In  the  deeper 
organs  it  produces  more  or  less  circumscribed  tumors,  composed  of  ca- 
seous matter,  granular  detritus,  calcareous  deposits  and  fibroid  indura- 
tion. The  distinction  between  secondary  and  tertiary  lesions  is  often  more 
distinct  clinically  than  pathologically.  The  glandular  changes  which 
appear  soon  after  the  initial  lesion  are  permanent,  and  are  due  to  cellular 
infiltration  and  hyperplasia,  but  are  not  usually  attended  by  suppura- 
tion. 

Etiology. — There  is  no  doubt  as  to  the  specific  nature  of  syphilitic  poison, 
or  its  transmission  solely  by  inoculation,  which  may  be  mediate,  immediate, 
or  through  the  processes  of  conception.  The  poison  is  most  frequently 
communicated  during  sexual  intercourse,  but  inoculation  may  occur  from 
deposition  of  the  poison  upon  any  abrasion  of  the  surface  or  upon  delicate 
membranes,  as  those  covering  the  sexual  organs,  without  any  solution  of 
continuity.  Thus  infection  may  take  place  in  kissing,  or  from  the  use  of 
pipes,  drinking  vessels,  etc.,  upon  which  the  poison  has  been  deposited. 
Nursing  children  may  infect,  or  receive  the  poison  from  their  nurse. 
Physicians  not  infrequently  receive  it  accidentally  upon  the  fingers,  or  are 
the  agents  in  its  transmission  by  vaccination. 

Even  more  unfortunate  are  the  victims  of  syphilitic  parents.  The  poi- 
son in  the  mother  invariably  manifests  itself  in  the  child,  and  when  in  the 
father,  infects  the  offspring  and,  secondarily,  the  mother  through  the  foetal 
circulation.  The  syphilitic  poison  is  most  virulent  in  the  primary  sores  and 
glandular  affections,  but  is  present  in  the  blood  in  decreasing  quantity 
through  both  the  secondary  and  tertiary  stages.  Late  in  the  disease  it  is 
found  only  in  the  discharges  from  those  organs  which  are  involved  in  the 
specific  processes.  One  inoculation  of  syphilitic  poison,  with  rare  excep- 
tions, confers  protection  from  all  subsequent  poisoning. 

Symptoms. — Primary.  The  period  of  incubation  is  variable,  but  is  sel- 
dom less  than  ten  days  and  averages  about  twenty-five.  The  first  change 
is  the  appearance  of  a  dark-red  papule,  which  slowly  enlarges,  becomes  in- 
durated early,  is  not  painful,  and  may  even  escape  notice.  Although  it 
may  run  its  full  course  without  becoming  moist,  generally  the  apex  be- 
comes eroded,  leaving  a  moist  surface,  or  undergoes  ulceration.     The  true 


920  CHEOXIC    GENERAL   DISEASES. 

chancre  does  not  secrete  j)us  unless  it  becomes  inflamed,  but  remains  a  sim- 
ple excoriation,  either  moist  or  scabbed,  through  its  entire  course.  The  in- 
duration may  be  thin  and  superficial,  may  simply  underlie  the  excoriation, 
or  may  spread  extensively  into  adjacent  parts.  In  the  course  of  six  or  eight 
weeks  the  sore  begins  to  heal,  the  induration  subsides,  and  finally  there  is 
no  trace  left,  or  if  ulceration  has  been  present,  there  remains  a  white  or 
slightly  pigmented  cicatrix.  Soon  after  the  appearance  of  the  primary 
sore,  the  nearest  lymphatic  glands  indurate  and  enlarge  but  rarely  suppu- 
rate. Nor  do  they  resolve  with  the  healing  of  the  chancre,  but  remain  en- 
larged for  months  and  years,  and  are  eventually  joined  by  other  glands 
throughout  the  body. 

Secondary  syphilis  includes  the  earlier  and  generally  lighter  affections  of 
the  skin  and  mucous  membranes,  with  some  of  the  affections  of  the  organs 
and  nerves.  The  most  prominent  are  those  of  the  skin  which  usher  in  the 
eruptive  stage  of  syphilis.  They  appear  from  six  weeks  to  three  months 
after  inoculation,  and  in  nearly  one-half  the  cases  before  the  initial  lesion 
has  healed.  This  stage  is  often  attended,  at  its  invasion,  by  some  slight 
fever  and  constitutional  disturbance,  marked  by  weakness,  emaciation,  and 
wandering  pains  in  the  limbs  and  joints.  The  cutaneous  syphilides  assume 
nearly  all  the  types  of  skin  diseases,  and  present  in  this  multiplicity  of 
form  a  distinctive  characteristic.  The  earlier  eruptions  are  generally  the 
simpler  forms  of  erythema,  and  papules,  and  are  diffused  over  the  surface 
quite  uniformly.  Later,  there  appear  vesicles,  pustules,  tubercles,  and 
scaly  eruptions  which  are  more  apt  to  be  gathered  in  groups.  Not  infre- 
quently several  or  all  the  forms  may  be  present.  In  all  syphilides  there 
is  a  general  roundness  of  form,  an  absence  of  pain  and  itching,  and  a  pe- 
culiar livid  coppery  color  which  gradually  changes  in  cicatrices  to  a  glis- 
tening white. 

Secondary  syphilis  most  frequently  affects  the  mucous  membranes  of  the 
fauces  and  pharynx.  In  connection  with  the  earlier  symptoms  there  may 
be  only  a  diffuse  hypergemia  and  a  redness  with  or  without  ulceration  ;  but 
with  the  later  secondary  and  earlier  tertiary,  there  is  a  peculiar  dusky  red 
appearance,  the  result  of  chronic  congestion,  and  more  or  less  thickening 
and  induration  about  ulcers  and  mucous  patches.  This  condition  seldom 
causes  any  pain  or  discomfort,  and  the  ulcers  may  disappear  spontaneously. 
Mucous  patches  appear  most  abundantly  about  mucous  orifices,  as  the 
mouth  and  anus,  but  may  appear  on  the  skin.  They  are  round  or 
oval,  slightly  elevated  spots  of  varying  size,  with  a  moist  excoriated  sur- 
face, which  does  not  ulcerate  unless  irritated.  They  appear  with  the 
earliest  eruption  and  continue  with  decreasing  frequency  into  the  tertiary 
stage. 

The  secondary  affections  of  the  eye  assume  the  form  of  iritis  with  ex- 
tensive exudation,  and  retinitis,  which,  appearing  with  but  little  pain  or 
photophobia,  is  attended  by  extravasations  and  partial  or  complete  abolition 
of  function.  In  connection  with  the  general  tegumentary  inflammation 
the  hair-bulbs  are  involved,  and  the  hair  becomes  thin  or  is  lost  en- 
tirely. 


SYPHILIS.  921 

Tertiary. — Secondary  symptoms  usually  pass  away  after  a  few  months 
and  the  patient  may  never  suffer  further,  or,  more  frequently,  he  enjoys  a 
period  of  apparent  health  of  from  two  months  to  two  years,  in  some  cases 
extended  to  twenty  or  more  years.  In  other  instances  there  is  no  break,  but 
the  secondary  lesions  merge  into  those  of  the  tertiary  stage.  The  special 
characteristics  of  tertiary  lesions,  as  already  stated,  are  the  formation  of  new 
tissue — gummata — and  the  tendency  to  cause  degenerative  and  necrotic 
changes.  Fibroid  < change  and  induration  are  less  frequent  results.  They 
involve  deeper  parts,  and  are  not  symmetrical,  but  are  persistent  and  re- 
current. Tertiary  syphilis  is  rarely  attended  by  any  fever,  and  even  a  ca- 
chexia is  wanting  in  most  cases.  When  present  this  cachexia  is  indicated 
by  anaemia,  with  possibly  some  anasarca  and  general  depression,  both  physi- 
cal and  mental.  The  skiu  is  dry,  harsh,  and  dirty  looking,  the  face  thin, 
the  eye  dull,  and  the  general  appearance  that  of  decay.  In  the  skin, 
gummy  tubercles,  which  may  be  single  or  in  groups,  result  in  ecthyma, 
rupia,  and  extensive  ulcers,  which  leave  characteristic  cicatrices.  Sub- 
cutaneous gummata  may  soften,  break  through  the  skin,  and  form  deep 
ragged  cavities  which  heal  slowly.  Similar  processes  occur  in  mucous 
membranes,  more  particularly  of  the  mouth,  pharynx  and  nose,  and  may 
destroy  the  tonsils,  fauces,  and  soft  palate,  or  entirely  clear  out  the  nasal 
cavities.  The  resulting  cicatrices  produce  permanent  stricture  of  the  fauces 
or  oesophagus,  and  other  deformities. 

Syphilis  of  the  viscera  is  most  frequent  in  the  liver,  where  it  appears  as 
gummata  or  general  fibroid  induration.  All  the  organs  are  liable  to  sim- 
ilar deposits,  as  the  heart  and  arteries,  lungs — syphilitic  j)n€umonia — and 
bronchial  tubes,  or  any  abdominal  organ.  In  the  bones,  caries  and  necro- 
sis are  often  chronic  states,  and  diffuse  or  circumscribed  periostitis  with 
the  formation  of  painful,  tender  nodes  is  very  characteristic.  These 
nodes  do  not  often  suppurate,  but  are  quite  permanent.  Of  even  greater 
importance  are  the  lesions  of  the  nerves.  The  cranial  bones  and  cerebral 
membranes  are  the  seat  of  nodes  and  gummy  tumors  which  cause  convul- 
sions or  paralysis  and  disturbances  of  function,  as  epilejisy  and  insanity, 
by  direct  pressure  or  through  inflammatory  processes.  In  the  brain  sub- 
stance inflammatory  softening  and  induration  are  the  most  frequent  changes. 
In  the  eye  the  cornea,  iris,  and  retina  are  more  frequently  affected,  and 
the  changes  differ  in  degree  rather  than  in  form,  from  those  found  in  the 
secondary  stage. 

Inherited  Syphilis. — Syphilis  may  be  inherited  from  either  the  father 
or  the  mother.  If  from  the  father,  the  mother  will  not  escape  infection 
during  pregnancy  unless  he  is  in  the  tertiary  stage.  Syphilitic  mothers 
usually  abort  two  or  three  times,  then  produce  a  weak,  unhealthy  child 
that  dies  within  a  few  days.  Finally,  an  apparently  healthy  child  is  born. 
It  does  not  develop  properly,  however,  looks  old  and  withered,  and  in  a 
few  months  secondary  eruptions  make  their  appearance  with  excoriations, 
mucous  patches  and  ulcers  about  the  mouth,  nose,  anus  and  genitals.  At 
the  same  time  it  develops  the  characteristic  snuffles.  The  nose  discharges 
an  irritating  secretion  at  first,  producing  excoriations  on  the  lips.     Becom- 


922  CHRONIC    GENERAL   DISEASES. 

ing  closed  it  fills  with  mucus  and  pus  which  produce  ulceration  and  ne- 
crosis. Tertiary  symptoms  appear  early,  and  gummy  tumors  and  fibroid 
indurations  may  occur  in  the  yiscera  in  connection  with  the  secondary  erup- 
tions. Such  children  have  a  very  characteristic  appearance ;  they  are  thin 
and  poorly  nourished,  the  skin  is  pale,  coarse  and  wrinkled,  the  forehead 
and  cheek  prominent,  the  eyes  and  nose  sunken,  and  the  teeth  present  the 
peculiar  pegged  appearance.  Interstitial  keratitis  causes  defective  sight 
and  photophobia,  and  the  child,  with  some  deafness,  a  coarse,  harsh  voice, 
wrinkled  brows  and  apathetic  look,  presents  a  pitiable  sight. 

Differential  Diagnosis. — For  the  diagnosis  of  the  primary  lesions  reference 
should  be  made  to  surgical  works.  As  the  diagnosis  of  secondary  and  ter- 
tiary lesions  depends  so  largely  upon  their  location,  they  are  considered  in 
connection  with  the  diseases  of  the  various  organs.  In  inherited  syphilis 
the  coryza  and  snuffles,  the  cracks,  excoriations  and  fissures  about  mucous 
orifices,  with  mucous  patches,  are  the  early  characteristics.  Later  there  are 
the  scars  on  the  face  and  in  the  throat,  the  sunken  nose,  and  peculiar  teeth. 
In  many  cases,  however,  the  differentiation  can  be  made  only  by  the  results 
of  treatment. 

Prognosis. — As  a  rule  the  prognosis  is  favorable  before  destruction  of  tis- 
sue has  begun,  and  even  afterward  the  necrotic  process  may  be  arrested. 
It  varies  greatly,  however,  with  the  nature  of  the  lesions  and  their  situation. 
In  confirmed  drunkards,  and  when  the  disease  assumes  a  rapid  or  malignant 
form,  the  prognosis  is  grave.  In  inherited  syphilis  the  prognosis  varies 
with  the  date  of  the  appearance  of  symptoms.  If  the  eruption  is  present  at 
birth  or  occurs  early  the  child  seldom  lives.  The  longer  the  disease  remains 
latent,  the  more  favorable  the  prognosis. 

Treatment. — The  treatment  of  syphilis  is  primarily  specific,  and  confined 
to  the  use  of  two  drugs, — mercury  and  iodine.  Secondarily  it  is  hygienic 
and  tonic,  a  relation  which  for  a  time  is  reversed  in  some  cases.  Specific 
treatment  is  often  unavailing  when  used  alone,  but  becomes  brilliantly  suc- 
cessful when  assisted  by  fresh  air,  good  food,  exercise  and  rest,  with  oil, 
iron,  quinine  and  other  tonics. 

As  a  rule  mercurials  are  more  efficacious  in  the  earlier,  and  iodine  in 
the  later  manifestations.  Mercury  should  be  given  as  soon  as  a  diag- 
nosis of  chancre  is  established,  but  were  better  omitted  until  the  appear- 
ance of  secondary  symptoms  than  used  on  an  uncertain  diagnosis.  When 
treatment  is  begun  thus  early,  it  should  be  continued  for  at  least  a  year, 
and  followed  by  one  or  two  years  of  a  mixed  treatment  of  mercury  and 
iodine. 

When  treatment  is  begun  late  in  the  course  of  the  disease  either  iodides 
alone  or  a  mixed  treatment  will  most  speedily  remove  the  lesion,  after 
Avhich  the  patient  should  continue  treatment  for  a  year  or  more.  Gener- 
ally  it  is  well  to  continue  a  mild  mercurial  course  for  at  least  six  months 
after  all  lesions  have  disappeared.  The  present  tendency  is  toward  a  more 
extended  use  of  mercury  in  the  later  stages  of  the  disease.  The  methods 
of  administering  mercury  are  too  numerous  to  be  described  in  detail  :  the 
more  common,  aside  from  tliat  by  the  stomach,  are,  hypodermically,  by 


SYPHILIS.  923 


fumigation,  baths  and  inunction  ;  the  latter  being  the  most  desirable  for 
children  with  inherited  syphilis.  Iodine  may  be  used  in  its  combinations 
with  potash,  soda,  ammonia,  mercury,  iron,  etc.  The  doses  of  both 
mercury  and  iodine  must  be  determined  by  trial  for  each  case.  With 
mercury  they  should  fall  short  of  salivation,  but  with  iodine  should 
increase  to  the  limit  of  the  patient's  endurance,  or  until  the  lesions  yield  to 
treatment. 


SJi^CTION  Vl. 

DISEASES  OP  THE  NERVOUS  SYSTEM.  ' 
{Including  Diseases  of  the   Brain,  Spinal  Cord,  and  Functional  Weriaous  Diseases.) 

GEl^EEAL    SYMPTOMATOLOGY. 

The  symptomatology  of  nervous  diseases  presents  many  peculiarities  which 
render  their  diagnosis  especially  difficult.  Nearly  every  pathological  con- 
dition may  be  the  result  of  so  many  different  lesions  that  at  best  it  is 
indicative  of  the  seat  and  extent  of  the  lesion  only,  and  not  of  its  nature, 
and  often  only  determines  the  division  of  the  nervous  system  which  is 
affected.  Symptoms  are,  therefore,  entirely  negative  when  taken  singly, 
and  find  their  significance  only  in  the  order  and  manner  of  their  develop- 
ment, or  in  their  combinations  with  others  equally  valueless  per  se.  All 
symptoms  of  nervous  disease  appear  as  (1)  impairment  or  abolition,  (2)  ex- 
altation, and  (3)  perversion  of  function,  and  may  manifest  themselves 
through  the  motor,  sensory,  co-ordinating,  or  psychical  systems  by  symptoms 
which  will  vary  with  the  location,  nature,  and  extent  of  the  lesion.  I  shall 
first  consider  some  of  the  more  important  symptoms  in  their  general  rela- 
tions to  nerve  lesions. 

Motor  Paralysis. — Loss  of  motor  power,  or  voluntary  nervous  control 
of  muscular  movements,  may  exist  in  all  degrees,  from  the  slightest  weak- 
ening or  delaying  of  the  nervous  impulse  to  absolute  abolition  of  the  im- 
pulse or  its  complete  arrest  in  transit  to  the  muscles.  The  lighter  and 
intermediate  grades  are  termed  paresis,  while  paralysis  is  applied  to  ex- 
tensive or  entire  loss  of  motor  power.  The  nature  and  extent  of  the 
paralysis  is  evidenced  in  the  muscles,  so  that  the  muscular  condition  be- 
comes a  matter  of  primary  importance. 

(a)  Reflex  Action. — In  many  instances,  and  more  especially  in  spinal 
paralysis  from  circumscribed  lesions,  the  muscular  force,  as  indicated  by 
reflex  movements,  is  not  diminished.  Under  suitable  irritation  the  ap- 
parently powerless  muscles  execute  violent  movements  and  become  power- 
fully contracted.  These  reflex  movements  are  not  always  limited  to  the 
irritated  limb,  but  may  appear  in  other  paralyzed  muscles.  For  diagnostic 
purposes,  then,  reflex  action  indicates  unimpaired  nervous  connection  be- 
tween the  paralyzed  muscles  and  the  spinal  centres,  and  can  never  be 
present  when  the  paralysis  is  due  to  a  disseminated  destructive  lesion  of 
the  nuclei  of  origin  of  the  affected  nerves,  but  is  generally  most  distinct 
in  disease  interrupting  the  transmission  of  voluntary  motor  impulses.  A 
very  common  and  patent  form  of  reflex  action  is  known  as  tendon  reflex. 


GENERAL   SYMPTOMATOLOGY.  925 

If  in  health  the  tendon  of  any  muscle  be  struck  a  sharp,  quick  blow,  there 
will  immediately  follow  distinct  contraction  of  its  attached  muscles,  most 
marked,  of  course,  in  the  larger  muscles,  as  those  attached  to  the  patella 
or  tendo  Achillis.  Abolition  or  exaggeration  of  tendon  reflex  is  an  im- 
portant point  in  diagnosis.  Either  may  be  associated  with  decrease  or 
increase  of  reflex  action  from  irritation  of  the  skin.  A  third  form  of  re- 
flex action  is  called  ankle  clonus.  This  consists  in  a  clonic  tremor  of  the 
muscles,  particularly  of  the  leg,  occurring  whenever  the  muscle  is  stretched 
by  flexion  of  the  foot,  aud  continues  during  flexion.  In  severe  cases  it 
may  be  excited  by  putting  the  toe  to  the  floor,  and  then  often  involves  the 
entire  limb.  Abolition  of  reflex  action  maybe  due  to  degenerative  changes, 
either  in  the  nerve  trunk  or  spinal  centre,  but  exaggeration  is  generally  the 
result  of  central  irritative  lesions. 

(b)  Electrical  Irritability. — Electrical  contractility  of  paralyzed  muscles 
may  remain  normal,  be  increased,  or  impaired.  When  muscles  atrophy 
from  disease,  or  are  the  seat  of  degenerative  changes,  Faradic  contractility 
is  proportionately  decreased.  As  dependent  upon  nerve  changes  it  is  not 
only  generally  retained  in  both  cerebral  and  spinal  paralysis  due  to  inter- 
ruption of  nerve-currents,  but  is  frequently,  and  especially  in  thie  latter 
form,  increased.  When  disease  involves  central  nuclei  or  nerve-trunks, 
Faradic  contractility  is  often  rapidly  and  extensively  lost.  Such  muscles 
may  still  react,  however,  t0  the  slowly  interrupted  galvanic  current,  even 
after  they  fail  entirely  to  respond  to  the  Faradic.  Indeed,  galvanic  con- 
tractility may  increase  as  Faradic  decreases,  and  eventually  become  more 
marked  than  in  healthy  muscles. 

(c)  Muscular  Nutrition. — Muscular  nutrition  and  tonicity  generally  keep 
pace  with  contractility  ;  and  the  muscles  remain  firm  and  are  but  slightly 
reduced  in  bulk,  or  they  may  become  small  and  flabby,  or  in  some  cases 
contracted  and  rigid.  The  former  condition  prevails  when  disease  lies 
above  the  origin  of  the  implicated  nerve,  but  sudden  onset  of  the  disease 
or  implication  of  nuclei  or  nerve  trunks  results  in  flaccid  and  wasting 
muscles.  Rigidity  and  contraction  follow  irritative  lesions  or  complica- 
tions and  also  occur  in  paralysis  of  long  standing,  in  which  case  they 
are  mostly  due  to  secondary  descending  degeneration  of  the  cord. 

General  Paralysis.  — Lesions  resulting  in  general  paralysis  of  necessity 
involve  such  important  parts  as  to  be  followed  in  most  cases  by  immediate 
death.  General  paresis  occurs  in  connection  with  insanity  from  diffuse 
disease  of  the  cerebral  cortex.  It  implicates  all  the  voluntary  muscles,  not 
excepting  those  of  deglutition  and  phonation,  but  is  slight  in  degree,  sel- 
dom extending  beyond  weakness  and  sluggishness  of  movement. 

Bulbar  paralysis  is  perhaps  the  nearest  approach  to  general  paralysis. 
Disease  of  the  pons  or  medulla  generally  results  in  bilateral  paralysis,  and 
is  the  cause  of  the  mixed  and  crossed  paralyses  occasionally  met  with,  as 
paralysis  of  both  arms,  both  legs,  or  one  side  of  the  face  and  the  oppo- 
site side  of  the  body.  Motions  of  the  eye,  phonation,  deglutition  and  res- 
piration are  especially  liable  to  be  interfered  with,  and  death  is  seldom 
long  delayed. 


Cerebral  Causes. 


926  DISEASES   OF   THE   ]S"ERVOUS    SYSTEM. 

Hemiplegia  is  a  motor  paralysis  limited  to  a  lateral  half  of  the  body. 
It  is  generally  the  result  of  a  lesion  above  the  medulla,  and  most  fre- 
quently of  the  corpus  striatum,  but  may  result  from  injury  to  a  cerebral 
hemisphere  or  crus.  It  occurs  on  the  side  opposite  to  the  disease  or  in- 
jury. Its  most  frequent  cause  is  undoubtedly  apoplexy,  but  it  may  be 
due  to  other  cerebral  injuries  or  disease,  and  not  infrequently  is  functional. 
The  causes  of  hemiplegia  may  be  classified  as  follows  : 

'  Compression  from  bone,  blood,  pus,  or  inflamma- 
tory exudations. 
Tumors,  especially  carcinoma,  sarcoma,  gummata. 
Partial  ansemia  from  thrombosis,  embolism,   soft- 
ening, aneurism,  apoplexy. 
Encephalitis, — abscess. 
Atrophy  and  sclerosis. 
^  .     1  p  j  As  above,  or  any  disease  affecting  a  lateral  half  of 

■^  (      the  cord. 

-p,       , .       ,  p  j  Hysteria,    chorea,    epilepsy,    diphtheria,    malaria, 

(      poisons,  etc. 

Although  the  paralysis  is  of  central  origin,  the  muscles  are  seldom  af- 
fected uniformly,  and  ,it  has  been  noted  that  those  which  suffer  least  are 
such  as  act  in  conjunction  with  their  counterparts  on  the  non-paralyzed 
side.  The  muscles  of  the  arm  and  leg  are  chiefly  affected,  while  those  ol 
the  trunk  and  neck  often  escape  entirely,  so  that  the  body  and  head  remain 
erect  and  firm.  The  paralysis  is  generally  descending  in  its  onset,  and  as- 
cending in  its  recovery,  the  leg  being  last  involved  and  the  first  to  regain 
its  power.  Occasionally,  however,  the  leg  escapes  entirely,  or  it  may  suffer 
a  more  complete  paralysis  than  the  arm.  Of  the  cranial  nerves  the  third, 
fourth  and  sixth  seldom  suffer  unless  the  lesion  is  in  the  crus,  when  the 
third  will  probably  be  involved.  The  fifth,  also,  as  a  rule,  suffers  but 
little,  but  may  be  paralyzed  in  either  or  both  roots,  a  condition  indicated 
by  anaesthesia  of  the  face  and  cornea  and  paralysis  of  the  muscles  of  mas- 
tication on  the  affected  side.  The  facial,  on  the  other  hand,  seldom 
escapes  entirely  in  lesions  at  the  base.  The  face  becomes  blank  and  mo- 
tionless, the  mouth  is  drawn  toward  the  healthy  side,  and  the  j)aralyzed 
cheek  puffs  on  expiration.  The  muscles  of  the  tongue  may  escape  or  suf- 
fer with  the  others,  and  the  tongue  will  then  be  protruded  with  the  tip 
pointed  toward  the  affected  side.  When  hemiplegia  is  uncomplicated  its 
diagnosis  is  evident,  but  if  associated  with  coma  it  may  not  be  readily  ap- 
preciated. The  paralyzed  limbs,  however,  will  be  more  flaccid,  and  when 
raised  and  released  will  drop  more  heavily  and  limply  than  on  the  unaf- 
fected side.  If  the  face  is  implicated  the  peculiar  expression  and  retrac- 
tion of  one  angle  of  the  mouth  will  be  readily  appreciated.  In  the  differ- 
ential diagnosis  of  the  causes  of  hemiplegia  the  location,  nature,  and  ex- 
tent of  the  paralysis  will  be  of  value,  but  the  most  important  points  will 
be  found  in  the  history  of  the  case,  the  manner  of  invasion,  and  the  pe- 
culiar combination  of  other  symptoms. 


GENERAL   SYMPTOMATOLOGY.  937 

Paraplegia. — Bilateral  paralysis,  of  whatever,  extent  is  termed  paraple- 
gia, and  when  of  organic  origin  aif  ects  only  those  parts  of  the  body  supplied 
by  nerves  leaving  the  spinal  cord  at  or  below  the  seat  of  the  lesion.  Or- 
ganic paraplegia,  therefore,  is  commonly  of  spinal  origin,  and  in  extent 
varies  with  the  seat  of  the  lesion.'  If  this  is  located  in  the  dorsal  region 
the  lower  extremities  alone  are  affected  ;  the  paralysis  becomes  more  exten- 
sive the  higher  in  the  cord  it  has  its  seat ;  when  it  has  its  seat  in  the  cervical 
region  the  entire  body,  including  the  diaphragm,  may  be  paralyzed.  In  all 
forms,  however,  the  sphincters  are  liable  to  be  involved.  Generally  if  the 
disease  is  high  up  there  will  be  spasm  and  retention  ;  if  low  down,  paral- 
ysis and  incontinence.  Paralysis  may  be  of  all  grades  and  varieties,  ac- 
cording as  more  or  less  of  the  thickness  of  the  cord  is  involved.  There 
may  be  simply  slight  paresis,  decided  paralysis  with  sensation  unimpaired, 
or  complete  paralysis  of  both  motion  and  sensation.  Disease  of  the  cord 
has  a  special  tendency  to  be  unsymmetrical,  and  confined  to  particular 
tracts.  As  a  result  the  effects  are  very  varied.  When  the  changes  are 
confined  to  a  lateral  half,  motor  paralysis  affects  the  parts  below  on  that 
side,  but  owing  to  the  immediate  decussation  of  sensory  fibres  on  entering 
the  cord,  and  their  consequent  implication  with  motor  fibres  of  the  other 
side,  anaesthesia  is  found  on  the  opposite  side  of  the  body  below  the  lesion, 
with  possibly  a  distinct  line  of  anaesthesia  marking  the  upper  boundary 
of  motor  paralysis.  The  limitation  of  spinal  lesions  to  distinct  tracts  has 
given  rise  to  such  characteristic  combinations  of  symptoms  as  to  lead  to 
their  being  considered  as  special  diseases.^ 

Aside  from  the  foregoing  forms  of  paralysis  for  the  most  part  due  to  in- 
terruption of  the  connection  between  nerve-nuclei  or  trunks  and  the  higher 
centres,  paralysis  may  result  from  direct  injury  to,  or  destruction  of,  these 
nuclei  or  trunks.  In  such  cases  the  paralysis  is  confined  to  the  distribu- 
tion of  the  affected  nerves,  is  generally  more  complete  and  permanent  than 
in  other  forms,  and  is  attended  by  rapid  loss  of  Faradic  irritability  with 
wasting  of  the  muscular  tissue. 

Spasms,  Convulsions.  — In  determining  the  seat  and  nature  of  the  disease 
causing  spasms  the  same  anatomical  facts  are  to  be  considered  as  in  the 
diagnosis  of  paralysis.  It  is  probable  that  irritative  lesions  of  the  same 
centres  as  are  affected  in  paralysis  result  in  motor  disturbances  ;  hence  con- 
vulsions of  a  lateral  half  of  the  body  may  be  ascribed  to  irritation  of  the 
opposite  cerebral  hemisphere,  corpus  striatum  or  crus.  In  a  similar  man- 
ner spasms  confined  to  the  lower  portion  of  the  body  and  bilateral  are  to 
be  considered  of  spinal  origin,  while  general  convulsions  may  be  the  result 
of  general  cerebral  disturbance  or  of  a  general  affection  of  the  cerebro-spinal 

>  Etiology  : 

Brain \  Small  clot  in  the  pons. 

r  Compression  of  a  lateral  half  of  the  cord  from  bone  as  In  fracture,  caries,  dislocation, 

Spinal -j      spinal  bifida,  from  blood  (traumatic),  pus,  exudations,  tumors,  all  diseases  of  the  cord, 

1      shock  and  concussion. 
Functional  -{  Hysteria,  catalepsy,  rlieumatism,  syphilis,  poisons. 

Reflex -j  Diseases  of  geniro-urinary  organs,  diseases  of  intestines. 

'  See  locomotor  ataxia,  profjresdve  muscular  atrophy,  etc. 


9']Q  DISEASES   OF   THE   NERVOUS   SYSTEM. 

system.  Basing  the  diagnosis  upon  our  knowledge  of  the  motor  areas  of  the 
cerebral  cortex,  it  is  possible  in  many  cases  to  locate  the  lesion  quite  exactly 
by  careful  consideration  of  the  location  and  extent  of  the  convulsive  move- 
ments. Spasms  are  even  more  varied  in  their  distribution  than  paralysis, 
affecting  single  muscles,  muscular  groups,  a  single  limb,  half  the  body  or 
all  the  muscles,  not  excepting  those  of  respiration  and  deglutition,  and 
they  vary  in  degree  from  light  fibrillary  twitching  to  such  violent  cramps 
as  to  rupture  muscles  or  to  fracture  bones.  When  the  contractions  are 
persistent  they  are  termed  tonic,  but  when  rapidly  alternating  with  relaxa- 
tion are  called  clonic.  Convulsions  appear  as  symptomatic  of  both  organic 
and  functional  disease.  Tremulousness  of  the  muscles  often  accompanies 
paresis,  and  paralysis  is  frequently  followed  by  tonic  contractions.  Fibril- 
lary twitchings  are  common  in  debilitated  conditions,  in  general  paresis, 
the  typhoid  state,  paralysis  agitans,  etc. ;  while  the  severe  forms  are  illus- 
trated in  inflammatory  conditions  of  the  brain  and  cord,  epilepsy,  tetanus, 
strychnia  poisoning,  hydrophobia,  etc. 

Seiisory  Paralysis,  Anmstliesia. — Anaesthesia,  like  motor  paralysis,  may 
be  located  in  any  part  of  the  body,  may  be  of  all  degrees,  and  may  be  super- 
ficial or  extend  to  deep  parts.  When  slight  it  is  only  a  sense  of  numbness 
which  gives  the  impression  of  some  soft  substance  covering  and  protecting 
the  parts,  and  is  generally  attended  by  formication  or  burning  prickly  pains. 
In  complete  anaesthesia  the  patient  is  unconscious  of  the  severest  injury, 
and  bed-sores  may  denude  the  bones  without  his  being  aware  of  their  ex- 
istence. In  some  cases  sensations  of  heat  and  cold  are  still  appreciated, 
while  all  other  sensibility  is  lost.  Among  perverted  sensations  may  be 
placed  those  conditions  in  which  sensation  is  delayed,  and  the  patient  ap- 
preciates the  impression  only  after  the  lapse  of  some  seconds,  or  is  unable 
to  determine  its  nature.  In  many  cases  he  suffers  severe  neuralgic  pain  in 
the  anaesthetic  parts,  due  to  the  central  nervous  irritation.  Anaesthesia 
may  be  general  with  general  paresis  in  insanity,  but  rarely  so  in  other  con- 
ditions. It  more  commonly  appears  as  hemi-aneesthesia,  from  causes  sim- 
ilar to  those  of  hemiplegia,  but  is  less  frequent  than  the  latter.  It  most 
frequently  depends  upon  lesion  of  the  external  capsule  or  fibres  of  commu- 
nication between  the  optic  thalamus  and  hemisphere,  and  frequently  impli- 
cates some  Qf  the  nerves  of  special  sense.  Lesions  of  the  tegmentum  of  the 
crus  also  result  in  opposite  hemi-ansesthesia.  Spinal  anesthesia  is  also  far 
less  frequent  than  paraplegia,  but  when  present  is  almost  always  associated 
with  it.  The  condition  of  reflex  action  will  indicate  somewhat  its  nature. 
When  paraplegia  and  anaesthesia  are  the  result  of  destruction  of  nerve  nu- 
clei in  the  cord,  or  of  injury  to  the  nerve-trunks  supplying  the  paralyzed 
part,  reflex  activity  will  be  abolished.  When,  however,  the  paraplegia  is  of 
parts  below  a  spinal  lesion,  reflex  action  is  normal  or  often  increased.  As 
noted  before,  a  lesion  of  a  lateral  half  of  the  cord  may  give  a  joaraplegia 
compounded  of  motor  paralysis  on  the  side  of  the  lesion  and  sensory  ])aral- 
ysis  on  the  opposite  side. 

Hyperesthesia. — Hyperaesthesia,  either  general,  partial,  or  .of  the  nerves  ■ 
of  special  sense,  is  of  common  occurrence  in  nervous  disease,  since  it  may  be 


GEKERAL  SYMPTOMATOLOGY.  929 

the  result  of  the  most  trivial  disturbances.  It  is  present  in  the  congestive 
or  early  stages  of  inflammatory  conditions  of  the  brain  and  cord,  and  in 
functional  disturbances.  It  is  often  a  symptom  in  the  earlier  stages  of  fe- 
brile diseases  and  in  inflammation  of  the  skin*.  When  normal  sensation 
becomes  painful,  it  is  termed  dysaesthesia,  and  appears  as  gastralgia,  enteral- 
gia,  or,  in  the  nerves  of  special  sense,  as  sparks  and  flashes  of  light  or  even 
the  appearance  of  distinct  forms  of  men  and  animals,  ringing  or  violent  ex- 
plosive sounds,  and,  in  some  cases,  continuous  conversation,  or  as  disturb- 
ances of  taste  and  smell. 

Disorders  of  co-ordination  are  of  rare  occurrence  except  in  connection 
with  sclerosis  of  the  posterior  columns  of  the  cord.  Disease  of  the  cerebel- 
lum is  indicated  by  lack  of  co-ordination,  a  staggering  gait,  or  entire  ina- 
bility to  maintain  the  erect  position. 

Mental  Disturbances. — All  forms  of  cerebral  disease  are  attended  by 
more  or  less  perversion  of  the  mental  powers,  but  such  symptoms  are  sug- 
gestive only  of  the  general  nature  of  the  cerebral  changes,  and  but  remotely 
of  the  character  of  the  lesion.  Hypersemia  and  inflammatory  conditions 
generally  produce  at  first  exaltation  of  mental  processes  which  may  vary 
from  simple  excitement  to  the  wildest  delirium.  On  the  other  hand,  any 
lesion  which  causes  sudden  shock  to  nerve  centres  or  interferes  with  nutri- 
tion, either  by  simple  pressure  or  through  destruction  of  the  cerebral  tissue, 
is  generally  indicated  by  depression  or  abolition  of  mental  power.  Patients 
evince  the  most  varied  forms  of  mental  disturbance,  and  at  different  times 
suffer  in  their  emotions,  intelligence,  or  will.  They  may  be  happy, 
hilarious,  angry,  or  sober,  melancholy,  sullen  and  distressed.  In  intel- 
ligence they  may  appear  brilliant,  vivacious,  and  the  exaltation  may  extend 
to  delusions  and  hallucinations,  or  they  may  lose  all  reasoning  power  and 
memory  and  become  idiotic.  Delirium  of  meningeal  origin  is  generally 
active  or  even  maniacal,  but  becomes  low  and  muttering,  as  in  the  typhoid 
state,  when  the  lesions  implicate  the  cerebral  ganglia  and  result  in  general 
nervous  depression.  Like  all  other  symptoms  of  similar  origin  it  com- 
monly ends  in  coma,  with  abolition  of  sense,  sensation  and  voluntary 
motion.  Although  coma  is  the  usual  termination  of  cerebral  disease,  it  is 
dependent  upon  many  other  and  diverse  causes,  and  often  demands  a  dif- 
ferential diagnosis  as  to  its  origin.' 

Trophic  Clianges. — Many  forms  of  nervous  disease  are  attended  by  peculiar 
and  rapid  trophic  changes  throughout  the  body.  They  appear  in  the  skin, 
muscles,  joints,  bones,  and  viscera.  The  more  common  are  bed-sores  and 
inflammations  of  the  urinary  tract.  It  may  suffice  to  say  generally  that 
trophic  changes  are  associated  only  with  inflammatory  or  irritative  lesions, 
which  implicate  the  nerve  trunks  or  their  nuclei  of  origin  in  the  case  of 
motor  nerves,  but  in  the  case  of  sensory  nerves  may  be  located  in  the  gray 
matter  of  the  posterior  portion  of  the  cord.     Injury  of  motor  nerves  gener- 

1  Etiology  of  coma  : 
Cranial  i  Hypersemia,  Anemia,  OSdema,  Compression,  Tumors,  Thrombosis,  Embolism,  Apoplexy, 

/         Abscess,  Softenings,  Shock,  and  Concussion. 
Extra-cratial   J  Epilepsy,  Ursemia,  Ammonaemia,  Cholremia,  Poisons  of  drugs,  Narcotics  and  Ansesthet- 

(         ics,  Antispasmodics,  Alcohol,  Poisons  of  fevers.  Malaria.  Hysteria,  etc. 


930  DISEASES    OE   THE   NERVOUS    SYSTEM. 

ally  results  in  muscular  or  arthritic  changes,  while  cutaneous  changes  are 
dependent  upon  lesions  affecting  sensory  nerves. 


DISEASES  OF  THE 

BRAIN 

will  be  considered  under  the  following  heads 

: — 

I.   Cerebral  Hypercemia — active  or          V. 

passive.                                            VI. 

II.    Cerebral  Ancemia.                             VII. 

III.  lieningiti^.                                       VIII. 

IV.  Cerebral   Thrombosis  and  Em-       IX. 

holism.                                              X. 

Cerebral  Softening. 
Cerebral  Apoplexy. 
Abscess  of  the  Brain. 
Cerebral  Tumors. 
Sclerosis  of  the  Brain. 
Hypertrophy  of  the  Brain. 

CEEEBEAL   HYPEREMIA. 

{Congestion  of  the  Brain). 

Cerebral  hyperaemia  is  an  increase  in  the  quantity  of  the  blood  within  the 
capillaries  of  the  brain.  It  may  be  active  or  passive.  In  active  hyperge- 
mia  there  is  increased  current,  and  the  blood  is  arterial,  while  in  passive 
hypergemia  the  current  is  retarded,  and  there  is  an  excess  of  venous  blood. 

Morbid  Anatomy. — In  passive  hyperaemia,  the  veins  and  sinuses  are  en- 
gorged with  blood,  and,  when  long  continued,  the  dura  mater  appears 
distended,  and  sometimes  the  cerebral  convolutions  are  flattened,  with  a  de- 
cided  pinkish  color  in  the  gray  substance.  On  microscopical  examination, 
the  perivascular  lymph  spaces  are  seen  greatly  diminished,  or  possibly  ob- 
literated. In  the  former  case,  large  pigment  granules  are  scattered  outside 
the  vessels  along  their  line. 

On  section,  the  white  substance  is  seen  dotted  with  numerous  blood 
points,  and  the  cortex  is  grayish  red.  At  the  lower  portions  of  the  cere- 
bellum there  are  dark  red  patches.  In  active  hypermmia  the  small  arteries 
5,re  enlarged,  and  the  capillaries  of  the  meninges  are  distended.  This  may 
be  accompanied  or  followed  by  oedema  of  the  pia  mater  and  distention  of 
the  ventricular  cavities.^  The  condition  of  the  membrane  is  no  guide, 
•either  to  the  existence  or  degree  of  hypergemia,  and  transitory  active  or  pas- 
sive hyperaemia  often  leaves  no  trace  discoverable  at  the  autopsy.^ 

Etiology. — Active  hyperasmia  may  be  due  to  increase  in  the  blood  press- 
ure, from  excessive  action  of  the  heart,  from  contraction  of  the  surface 
capillaries  during  a  chill,  from  prolonged  mental  labor,  intense  emotion, 
digestive  disturbances,  acute  blood  poisoning,  increased  atmospheric  press- 
ure, and  gravitation  from  a  prolonged  recumbent  posture.  Local  arterial 
anaemia  in  other  parts  of  the  body,  such  as  arises  from  sudden  cold  to  the 
surface,  intense  muscular  exertion,  and  pressure  of  tumors  or  dropsical 
fluids  on  the  main  branches  of  the  aorta,  may  also  induce  active  hypergemia.^ 

1  Ecker  states  that  the  capillaries  and  small  vessels  are  sometimes  double  their  normal  calibre.  Niemeyer 
and  Nothnagel  state  that  atrophj'  of  the  brain  may  result  from  chronic  passive  hyperemia. 

2  Many  pathologists,  while  admitting  the  possibility  of  partial  congestion,  ascribe  to  post-mortem 
changes  what  others  denominate  local  congestion. 

'  Watson  states  that  men  have  been  arrested  as  drunk  on  cold  nights,  when  they  were  only  suffering 
from  active  cerebral  hyperaemia. 


CEREBKAL   HYPEREMIA.  931 

Paralysis  of  the  vaso-motor  nerves  of  unknown  origin,  or  severe  nervous 
shock,  and  poisons,  alcohol  and  certain  drugs,  especially  nitrite  of  amyl, 
will  give  rise  to  active  cerebral  hyperemia.  It  occurs  more  frequently  m 
hot  climates  than  in  cold,  and  is  said  to  follow  breathing  exceedingly  rar- 
efied air.     Insolation  is  probably  more  than  intense  active  hyperaemia. ' 

Passive  cerebral  hyperemia,  when  general,  is  the  result  of  obstructed 
venous  circulation,  itself  the  result  of  pressure  upon  the  jugular  or  vena 
cava  descendens.  Prolonged  fits  of  coughing,  playing  on  wind  instruments, 
and  prolonged  straining  at  stool  may  induce  it.  Any  cardiac  valvular  le- 
sion that  obstructs  the  blood  in  the  pulmonary  vessels,  or  any  disease  of  the 
lungs  which  offers  obstruction  to  the  onward  current,  will  lead  to  passive 
hyperaemia  of  the  brain.  Tricuspid  regurgitation  stands  iDre-eminent  among 
these  causes.  Partial  or  complete  stenosis  of  the  larynx  will  induce  it,  as 
in  croup  and  oedema  glottidis.  Thrombi  in  the  cerebral  sinuses  may  induce 
passive  hyperaemia;  and  it  sometimes  occurs  from  feebleness  of  the  incoming 
arterial  flow. 

Symptoms. — The  symptoms  of  cerebral  hyperaemia  may  be  grouped  in  two 
classes : — those  of  excitement  and  those  of  depression.  In  all  cases  these 
symptoms  are  increased  by  a  recumbent  posture,  by  a  forced  inspiration  and 
by  stimulants.  The  symptoms  of  excitement  are  a  diffuse  pain  and  throb- 
bing in  the  head,  accompanied  by  dizziness,  vertigo,  flashes  of  light,  ringing 
in  the  ears,  restlessness,  insomnia,  and  perhaps  delirium  and  convulsions. 
Photophobia  is  present ;  and  there  may  be  nausea  and  vomiting.  Sleep  is 
usually  broken  and  disturbed  from  the  onset.  The  gait  is  unsteady,  the  mind 
confused,  and  sometimes  the  speech  embarrassed.  In  active  hyperaemia  the 
pulse  is  accelerated,  full,  bounding,  and  hard,  and  the  carotids  and  tempo- 
rals pulsate  forcibly.  An  ophthalmoscojsic  examination  reveals  injection  of 
the  retinal  vessels,  and  the  conjunctivae  are  often  suffused.  In  most  cases 
there  are  both  motor  and  sensory  disturbances.  As  a  rule,  the  mental  state 
in  active  hyperemia  is  one  of  exaltation.  These  patients  are  irritable, 
peevish  and  highly  excitable.  They  are  apt  to  talk  a  great  deal.  When 
coma  occurs,  the  hyperaemia  is  described  as  apoplectic  ;  when  convulsions  or 
spasms  are  present,  it  is  called  epileptic  ;  and  when  there  is  delirium  we 
have  the  maniacal  form.  The  latter  is  mania  epliemera  or  impulsive  insan- 
ity."^    Paralytic  symptoms  are  rare  in  active  hyperaemia. 

The  symptoms  of  depression  are  dull  headache,  vertigo,  ringing  in  the 
ears,  with  confusion  of  mind  and  dulness  passing  into  somnolence,  stupor, 
or  complete  coma.  Illusions  and  hallucinations  are  uncommon/  Con- 
vulsions may  occur  in  children.  When  due  to  passive  hyperaemia,  as  is  not 
uncommon,  there  is  a  cyanotic  hue  to  the  face  and  neck,  the  jugulars  and 
venous  system  are  over-distended,  and  the  arterial  system  is  scantily  filled. 
The  pulse  varies  with  the  etiological  (cardiac)  lesion.     In  old  people,  after 

'  See  the  inleresting  experiments  of  S.  Mayer  and  Pribram  (Sitz.  der  Wien.  Akad.,  1873),  in  which  elec- 
trical or  mechanical  irritation  of  the  walls  of  the  stomach  produced  a  reflex  increase  of  the  vascular  press- 
ure and  considoruble  diminution  in  the  frequency  of  the  pulse. 

2  Trousseau  and  Nothnagol  both  claim  that  the  epileptic  and  apoplectiform  varieties  are  either  true  epi- 
lepsy or  are  due  to  actual  cerebral  hemorrhage. 

s  Griesinger  describes  a  peculiar /ear  of  places  that  seizes  patients  when  in  the  midst  of  a  crowd  or 
while  in  a  certain  place  or  street. 


933  DISEASES   OF   THE   NERVOUS   SYSTEM. 

depression  of  spirits,  or  a  long  period  of  taciturnity,  there  follows  wander- 
ing delirium,  usually  nocturnal,  talkativeness,  and  a  state  often  bordering 
on  hysteria.  The  mind  becomes  more  and  more  inactive,  and  sensation  as 
well  as  motion  is  diminished.  This  condition  is  followed  by  coma,  with 
stertorous  breathing  and  relaxation  of  the  sphincters.  This  coma,  which 
is  frequently  interrupted  by  local  or  general  convulsions,  generally  ends  in 
death. 

Differential  Diagnosis. — Cerebral  hyperaemia  may  be  mistaken  for  apo- 
plexy,  embolism,  urcemia,  acute  alcoholismus,  ejjilepsy,  and  cerebral  an- 
CBmia. 

In  cerebral  hemorrhage  the  onset  is  more  sudden  ;  the  coma  is  more  com- 
plete and  prolonged,  and  following  the  attack  there  is  always  hemiplegia. 

In  cerebral  embolism  the  onset  is  sudden  ;  the  face  is  pale,  the  head  cool, 
the  respirations  and  pulse-rate  are  rapid  and  irregular,  there  is  usually  evi- 
dence of  cardiac  valvular  disease,  aphasia  follows  the  attack,  and  the  symp- 
toms are  more  permanent  than  in  acute  hyperasmia. 

In  urcemia  the  coma  is  deeper  and  generally  preceded  by  convulsions. 
There  is  oedema  of  the  eyelids  or  of  the  lower  extremities,  and  the,  urine 
will  be  found  to  contain  albumen  and  casts. 

In  epilepsy  there  is  usually  an  aura,  and  the  patient  falls  as  if  from  a 
blow,  uttering  the  epileptic  cry.  In  the  fit,  which  is  of  short  duration,  the 
convulsions  are  first  tonic  and  then  clonic,  and  there  is  a  bloody  froth  about 
the  mouth. 

The  diagnosis  between  stomachic  and  cerebral  vertigo  will  be  found  under 
Diseases  of  the  Stomach. 

It  is  often  impossible  to  distinguish  between  acute  meningitis  and  cere- 
bral hypersemia  in  children,  except  from  the  results  of  treatment,  until  .the 
disease  is  well  advanced. 

In  cerebral  hypersemia  the  headache  is  generally  diffused  and  the  pupils 
are  contracted,  while  in  cerebral  ancemia  the  headache  is  vertical  and  the 
pupils  are  dilated.  In  hypersemia  there  are  loss  of  memory  and  hallucina- 
tions, in  anaemia  we  have  simply  incapacity  for  mental  work.  In  anaemia 
the  respirations  are  hurried,  the  pulse  is  quick,  feeble,  and  irritable,  there 
are  murmurs  at  the  base  of  the  heart  and  in  the  vessels  of  the  neck,  and 
the  face  is  pale  and  cold. 

Prognosis. — The  prognosis  depends  upon  the  cause  ;  as  a  rule,  therefore, 
passive  is  less  favorable  than  active  hypersemia.  The  maniacal  or  apo- 
plectiform variety  is  the  most,  the  convulsive  the  least,  dangerous.  The 
outlook  for  recovery  is  best  in  those  whose  habits  are  good,  who  can  ex- 
ercise mental  control  and  avoid  excitement,  and  in  those  between  twenty- 
five  and  fifty.  In  youth  and  old  age  the  prognosis  is  more  unfavorable  on 
account  of  the  condition  of  the  cerebral  vessels.  Accompanying  cardiac 
and  pulmonary  disease,  passive  hypersemia  is  a  symptom  of  secondary  im- 
portance. 

Treatment. — During  an  attack  of  cerebral  hyperaemia  from  whatever 
cause,  the  patient  must  be  kept  absolutely  quiet  in  bed  with  the  head 
raised,  and  the  diet  should  be  the  simplest  and  most  easily  digested,  and 


CEREBRAL   ANEMIA.  933 

taken  in  small  quantities  at  short  intervals.  In  active  hyperremia  cold 
to  the  head  and  heat  to  the  feet,  with  the  administration  of  a  brisk  purge, 
are  to  be  the  first  measures.  The  bromide  of  potassium  is  beneficial  in 
most  cases.  In  severe  active  hypereemia  blood-letting  is  permissible  in  the 
form  of  leeches  to  the  temples  or  nose.  The  constant  current  maybe  used 
to  stimulate  the  sympathetic  nerve,  and  thus  contract  the  cerebral  blood- 
vessels. Some  advise  zinc  in  combination  with  bromide  of  potassium. 
Ergot  and  antimony  have  been  used  with  some  success  in  active  hyperfemia. 
In  passive  hypersemia  stimulants  may  be  given  with  bromide  of  potash 
or  soda.  Digitalis  is  usually  indicated.  Sulphuric  ether,  inhaled  or  given 
internally,  often  produces  good  results.  In  coma  due  to  jjassive  cerebral 
hypersemia,  all  remedies  will  prove  ineffectual,  except  quinine,  which 
should  be  given  in  small  doses  at  short  intervals.  When  cessation  of  the 
menses  or  of  an  old  hemorrhoidal  flux  is  followed  by  cerebral  congestion, 
leeches  to  the  anus,  sitz-baths,  emmenagogues,  etc.,  should  be  given  in 
connection  with  the  other  remedies.  A  change  of  residence  with  rest 
from  mental  work  is  often  of  great  benefit. 

CEEEBEAL    ANEMIA. 

Cerebral  anaemia  is  a  condition  in  which  there  is  a  deficiency  in  the 
quantity  or  quality  of  the  blood  in  the  capillaries  of  the  brain. 

Morbid  Anatomy. — The  principal  change  in  cerebral  anaemia  is  pallor  of 
the  brain,  which  may  be  partial  or  general,  accompanied  by  serous  effusions 
into  the  meshes  of  the  pia  mater.  The  ventricles  are  often  distended  with 
fluid  and  the  veins  and  sinuses  are  engorged.'  In  some  cases  hypersemia  of 
the  meninges  coexists  with  cerebral  ansemia.  Partial  cerebral  anaemia  is  not 
often  demonstrable.  It  exists  about  neoplasia  and  adventitious  jDroducts  ; 
and  may  be  the  result  of  local  pressure,  or  partial  occlusion   of  an  artery. 

Etiology. — It  may  be  due  to  general  systemic  anaemia  from  excessive 
hemorrhages,  or  to  sudden  pulmonary  hepatization  and  congestion  in 
other  organs.  Exhausting  discharges,  prolonged  lactation,  etc.,  induce 
it.  Spurious  hydrocephalus  following  infantile  diarrhoea  is  a  condition  of 
cerebral  anaemia.  It  may  result  from  defective  blood  nutrition,  as  in 
chlorosis,  or  cardiac  weakness,  mitral  or  aortic  valvular  disease,  or  cardiac 
insufficiency  occurring  in  acute  febrile  diseases.  Fatty  heart  is  even  more 
potent  than  valvular  lesions  in  producing  it.  Any  mechanical  interference 
with  the  supply  of  blood  to  the  head,  as  pressure  on,  or  ligation  of,  the 
carotids,  may  induce  cerebral  anaemia.  The  arteries  that  form  the  circle 
of  Willis  are,  in  twenty  per  cent,  of  cases,  so  distributed  that  only  im- 
perfect communication  exists  between  their  two  lateral  halves.  Mental 
influences  through  vaso-motor  spasm  may  produce  it ;  thus  fright,  joy,  or 
anger  will,  in  many,  produce  syncope  dr.e  to  cerebral  anaemia. 

Cerebral  anaemia  sometimes  follows  the  application  of  strong  electrical 
currents  to  the  spinal  region  and  irritation  of  the  peripheral  nerves.  It  is 
claimed  that  zinc  oxide,  the  bromides,  tobacco,  calomel,  and  tartar  emetic, 

'  Golgi  claims  that  there  is  enlargement  of  the  perivascular  lymph-spaces. 


934  DISEASES   OF   THE    NERVOUS   SYSTEM. 

if  long  continued,  will  cause  cerebral  anaemia.  Partial  cerebral  anaemia  is 
always  due  to  local  obstructions,  which  may  result  from  narrowing  of  the 
vessels  from  disease  of  their  walls,  from  spasm  of  their  muscular  coats, 
from  embolism  or  thrombosis,  and  from  pressure  of  tumors,  blood,  bone 
or  inflammatory  products. 

Symptoms. — The  symptoms  of  cerebral  anaemia  may  appear  suddenly  or 
slowly.  In  the  former  case  they  are  the  ordinary  phenomena  of  a  fainting 
fit ;  the  individual  becomes  dizzy,  nauseated,  and  the  sight  is  obscured  ; 
there  is  ringing  in  the  ears,  the  pupils  dilate,  the  gait  is  unsteady,  cold 
perspiration  covers  the  surface,  the  pulse  becomes  feeble,  rapid,  and  thready, 
and  the  respirations  hurried ;  and  the  patient  may  fall  to  the  ground  with 
slight  spasmodic  twitchings.  Such  a  condition  is  common  from  reflex 
causes.  If  due  to  extensive  hemorrhage  the  loss  of  sight  in  those  that  re- 
cover may  be  permanent. 

When  cerebral  angemia  comes  on  slowly  it  is  attended  by  headache, 
drowsiness,  vertigo,  muscse  volitantes,  tinnitus  aurium,  sometimes  attacks  of 
total  blindness,  inability  to  perform  work,  insomnia,  extreme  sensitiveness 
to  light  and  noise,  and  at  times  delirium  and  hallucinations.  Notwith- 
standing the  maniacal  character  of  the  delirium,  melancholia  is  often  its 
predominant  feature.  Though  usually  of  brief  duration,  it  may  end  in  per- 
manent insanity.  In  most  cases  the  pupils  are  sluggish  and  dilated,  the 
retina  is  anaemic,  and  the  headache  is  confined  to  a  small  circumscribed 
spot.  The  recumbent  posture  induces  insomnia,  and  the  erect  position 
often  causes  a  sense  of  general  muscular  weakness  and  faintness.  The  face 
is  pale  and  cold.  In  the  cerebral  anaemia  of  children — spurious  hydro- 
cephalus— restlessness,  jactitation,  grinding  of  the  teeth,  and  muscular 
twitchings  are  followed  by  symptoms  of  collapse  and  coma. 

Diiferential  Diagnosis. — The  points  of  differential  diagnosis  may  be  found 
under  the  heads  of  Tubercular  Meningitis  and  Cerebral  Hyperaemia. 

Prognosis. — The  prognosis  in  cerebral  anaemia  will  be  determined  in  most 
cases  by  its  causes.  Where  acute  anaemia  results  from  hemorrhage,  death 
may  result,  although  the  hemorrhage  has  been  arrested.  The  prognosis  is 
more  favorable  when  there  is  no  organic  disease  of  the  heart  or  vessels.  The 
more  speedily  the  cause  can  be  removed  the  better  the  prognosis.  In  the 
so-called  spurious  hydrocephalus  the  prognosis  is  favorable,  if  met  by 
prompt  and  suitable  treatment. 

Treatment. — In  acute  anaemia  with  syncope  the  head  must  be  lowered  at 
once  and  the  patient  may  even  be  inverted,  cold  water  may  be  dashed  over 
the  face,  the  vapor  of  ammonia  inhaled,  and  bandages  applied  from  the 
feet  upwards.  As  soon  as  consciousness  is  regained,  champagne,  ether, 
ammonia,  coffee,  or  other  cardiac  stimulants  maybe  administered.  If  these 
measures  fail  transfusion  should  be  resorted  to.  Alcohol  is  to  be  given 
very  cautiously  in  cerebral  anaemia  ;  and  exercise  of  either  brain  or  body 
must  be  carefully  undertaken.  Bromides  are  never  to  be  given.^  For 
chronic  anaemia  the  treatment  can  only  be  determined  by  causal  indica- 
tions. 


1  Nothnagel  advises  small  doses  of  morphine  for  the  excitement  that  precedes  anaemic  delirimn. 


MENIlfGITIS. — ACUTE   MEKIKGITIS.  935 


MENINGITIS. 

The  membranes  covering  the  brain  are  the  pia  and  dura  mater  ;  the  pia 
mater  is  a  delicate  and  exceedingly  vascular  membrane  which  is  intimately 
adherent  to  the  brain,  sending  jDrolongations  into  the  sulci  and  fissures  ; 
its  connective-tissue  is  very  extensive.  The  external  layer  of  the  pia  mater 
is  the  structure  formerly  called  the  arachnoid.  The  meshes  of  the  pia 
mater-were  formerly  denominated  the  subarachnoid  space.'  The  dura  mater 
acts  as  the  periosteum  of  the  cranial  bones  ;  it  is  firm,  not  very  vascular, 
and  encloses  venous  sinuses  between  its  folds.  Its  inner  surface  is  covered 
with  a  layer  of  endothelial  cells. 

Inflammation  may  have  its  seat  in  the  dura  mater,  the  pia  mater,  or  both 
may  be  involved.  Inflammation  of  the  pia  mater  is  usually  called  menin- 
gitis. The  term  pachymeningitis  is  applied  to  inflammation  of  the  dura 
mater. 

When  inflammation  of  the  pia  mater  is  attended  by  rapid  changes  in  the 
membrane  and  by  the  eJSusion  of  sero-fibrin  and  pus,  with  varying  quanti- 
ties of  red  blood  globules,  it  is  called  acute  meningitis. 

So-called  sub-acute  meningitis  is  a  mild  tyj)e  of  acute,  in  which  extensive 
serous  effusions  are  the  chief,  and  at  times  almost  the  sole,  event,  although 
small  quantities  of  lymph,  white  and  red  blood  cells,  and  fibrin  are  usually 
present. 

Inflammation  of  the  pia  mater,  when  chronic,  results  in  thickening, 
opacity,  and  adhesions.  It  might  be  called  interstitial  meningitis,  while 
the  acute  and  sub-acute  belong  to  the  class  of  exudative  inflammations. 

The  dura  mater  has  an  external  and  an  internal  layer,  the  external  is  in- 
timately connected  with  the  inner  surface  of  the  calvarium.  Inflammation 
of  this  layer  is  c,sWe(i  pachymeningitis  externa,  and  is  marked  by  thickening, 
opacity  and  localized  adhesions  of  the  dura  with  the  skull. 

Pachymeningitis  interna  is  an  inflammation  of  the  inner  surface  of  the 
dura  mater,  and  may  be  acute  or  chronic  ;  it  is  usually  localized.  Chronic 
pachymeningitis  interna  often  results  in  the  formation  of  flat,  oval,  lami- 
nated sacs  containing  blood  which  lie  between  the  dura  and  pia  mater, 
and  is  called  hcematoma  of  the  dura. 

ACUTE  MENINGITIS. 

Acute  meningitis  is  also  callerl  simple  meningitis  of  the  convexity  (from 
its  usual  site),  cerebral  fever,  and  arachnitis.  When  the  unqualified  word 
meningitis  is  used,  acute,  non-sjoecific  inflammation  of  the  j)ia  mater  is 
understood. 

Morbid  Anatomy. — The  inflammatory  process  may  be  established  in  any 
portion  of  the  pia  mater  ;  but  it  usually  involves  the  hemispheres.  Only 
in  rare  cases  is  it  confined  to  the  base  of  the  brain.  There  is  always  more 
or  less  thickening  and  redness  of  the  membrane,  and  it  loses  its  glistening 

1  Ilandb.  d.  Hist.— Strieker. 


936 


DISEASES    OP   THE   NEEVOUS   SYSTEM. 


appearance.  Around  the  vessels  where  the  connective- tissue  is  most  abun- 
dant, there  is  first  a  slight  serous  effusion,  which  is  quickly  followed  by 
cellular  infiltration.  An  opaque  zone  of  exudation  surrounds  the  vessels. 
In  mild  cases  the  exudation  is  limited  to  the  perivascular  lymph  spaces. 


Fig.  189. 

Acntc  Meningitis. 

Portion  of  the  under  surface  of  the  Brain,  including  the  middle  lobe  of  the  Cerebrum  and  the 

Cerebelluni. 

TTie  opaque  exudation  is  seen  upon  the  cerebral  meninges  completely  covering  the  pons  and  surrounding  the 
medulla.     The  basilar  artery  is  dimly  seen  through  the  exudation. 

The  character  of  the  exudation  varies  ;  it  may  be  serous  or  sero-purulent, 
and  occupy  the  deeper  meshes  of  the  pia  mater,  or  a  thick  puro-fibrinous 
exudation  may  cover  the  convexity  of  the  brain  as  a  firm  membrane  or  a 
creamy  diffluent  mass.'  This  layer  of  fibro-pus  or  false  membrane  is 
thickest  and  most  abundant  in  the  fissure  of  Sylvius  and  the  sulci  and 
along  the  vessels,  which  are  visible  as  red,  inosculating  lines  in  a  yellow- 
green  or  distinctly  green  mass.  On  raising  this  layer  the  brain  beneath  is 
found  studded  with  minute  hemorrhages  from  the  ruptured  vessels  con- 
necting the  pia  and  gray  substance.  The  wJiite  substance  may  also  show, 
on  section,  numerous  puncta  vasculosa.  The  convolutions  are  flattened, 
the  sulci  deepened,  and  the  ventricular  cavities  will  contain  very  little,  if 
any,  fluid.^  "When  the  cerebellar  pia  mater  is  involved,  as  in  young  subjects,^ 
the  roots  of  the  cranial  nerves  about  the  medulla  are  sheathed  in  the  exuda- 
tion, and  there  is  inflammatory  infiltration  of  the  neighboring  plexuses. 

Etiology.— Meningitis  of  the  convexity  is  most  frequent  in  early  adult 
life  and  in  young  children.  It  is  more  common  in  males  than  in  females. 
Acute  alcoholismus  and  prolonged  and  intense  mental  anxiety  and  grief  are 
among  its  predisposing  causes.  Injuries  of  the  cranial  bones,  as  fractures, 
severe  blows,  or  punctured  wounds  are  the  most  frequent  exciting  causes. 

1  Klob  is  of  the  opinion  that  the  pus  is  furnished  in  great  measure  from  the  arachnoidean  epithelia. 

2  Huguenin  states  that  in  meningitis  of  unknown  origin  the  pia  mater  is  often  so  adherent  that  it  tears 
Bway  portions  of  the  brain  substance  when  it  is  removed. 

'  Beduar. 


ACUTE   MElsriNGITTS. 


937 


Disease  of  the  cranial  bones  and  suppurative  inflammation  of  the  middle 
ear  may  induce  meningitis,  and  inflammation  of  the  dura  mater  is  often 
complicated  by  simple  meningitis.  Diabetes  and  irritation  caused  by  cere- 
bral tumors,  or  supj)uration  in  the  eyeball,  and  large  carbuncles  about  the 
cranium  have  caused  it. 

Meningitis  occurs  as  a  complication  in  certain  diseases — as  measles,  small- 
pox, scarlet  fever,  ulcerative  endocarditis,  Bright's  disease,  acute  croupous 
pneumonia,  typhus,  typhoid  fever,  diphtheria,  pyaemia  and  rheumatism. 
Acute  alcoholism  is  said  to  induce  meningitis  in  children.'  Long-continued 
exposure  to  intense  heat  of  the  sun  under  conditions  favorable  to  the  de- 
velopment of  miasmatic  contagious  diseases  may  result  in  meningitis. 
Finally,  meningitis  is  sometimes  idiopathic. 

Symptoms. — The  symptoms  of  meningitis  may  be  divided  into  the  tbree 
stages  of  headache,  delirium,  and  coma.  Premonitory  symptoms,  such  as 
general  malaise,  wandering  pains  in  the  head  and  limbs,  irritability,  in- 
somnia and  a  sense  of  imjoending  trouble,  are  all  indefinite  "ijrodromata." 
It  may  be  ushered  in  by  a  distinct  chill  or  by  repeated  rigors. 

Usually  the  first  prominent  symptom  is  intense  and  persistent  headache, 
localized  in  the  frontal,  temporal,  or  occipital  region,  which  increases  in 
severity  from  hour  to  hour.  In  severe  cases  the  headache  is  diffuse,  al- 
though it  may  extend  obliquely  across  the  head,  or  shoot  from  temple  to 
temple.  Accompanjnng  the  headache 
there  is  vertigo,  intense  photophobia, 
loud  ringings  in  the  ears,  nausea,  and 
projectile  vomiiing.  There  is  cuta- 
neous hyperaesthesia,  and  convulsive 
movements  of  certain  groups  of  mus- 
cles. The  upper  and  lower  extremi- 
ties, and  the  posterior  cervical  mus- 
cles suffer  most.  The  face  is  rarely 
flushed,  but  has  a  pale,  anxious  ex- 
pression. The  conjunctiva  are  in- 
jected, and  the  pupils  are  contracted 
and  respond  slowly  to  light.  The 
degree  of  contraction  of  the  pupil  varies 
considerably  in  different  patients  dur- 
ing the  twenty-four  hours.  It  may 
only  be  contracted  on  the  same  side 
as  the  meningeal  inflammation. 
Aphasia  has  been  noticed  as  occurring 
in  a  few  cases  ;  loss  of  co-ordinating 
power  is  a  marked  symptom,  so  that 
the  individual  has  an  unsteady,  tot- 
tering gait.  The  temperature,  which  rises  rapidly,  reaches  102°  or  103°  F., 
rarely  higher  ;  it  may  have  a  morning  remission  and  evening  exacerbation. 

"  Ramskill  states  that  in  some  inscances  when  impetigo  and  eczemn  about  the  face  and  head  suddenly 
disappear,  the  symptoms  of  acute  meningitis  of  the  convexity  are  developed. 


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771.  e.  7 

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Fi(i.  190. 

Temperature  Record  in  a  case  of  Acute 

Meningitis. 


938  DISEASES   OF  THE   NEEVOUS   SYSTEM. 

In  those  cases  which  are  rapidly  fatal  there  is  continuous  high  tempera- 
ture. The  pulse  is  firm,  hard,  wiry,  and  small,  varying  in  frequency  with 
the  temperature  range.  The  bowels  are  constipated  and  the  abdomen  is 
retracted.  In  old  people  the  stage  of  headache  may  pass  unnoticed,  and 
the  delirium  first  attract  attention.  In  children  general  convulsions  may 
be  the  initiatory  symptom,  with  marked  strabismus  from  its  very  onset. 
If  constipation  is  not  present  the  discharges  are  scanty  and  offensive.  In 
this  class  of  cases  the  first  stage  is  always  preceded  by  peevishness  and  irrita- 
bility, which  lasts  from  a  few  hours  to  two  or  three  days. 

In  adults  the  stage  of  delirium  is  ushered  in  by  an  increase  in  restless- 
ness, jactitation,  irritability,  and  mental  confusion.  It  is  sometimes  wild, 
simulating  acute  mania  ;  at  first  it  may  be  present  only  at  night,  coming  on 
with  the  evening  rise  in  temperature.  In  the  aged  the  delirium  is  typhoid 
in  character,  or  marked  by  incessant  talking.  Sometimes  the  aged  are  only 
lethargic  and  stupid.  In  adults  muscular  twitchings  of  the  extremities 
and  face  are  present  in  this  stage  ;  the  eyeballs  roll  about  vaguely,  the 
flexor  muscles  are  often  powerfully  contracted  in  one  or  both  limbs,  and 
there  may  be  opisthotonos  or  even  hemiplegia.  Paresis  of  the  thoracic  and 
faucial  muscles  causes  dyspnoea,  irregular  respiration,  and  dysphagia.  In 
metastatic  meningitis  delirium  may  be  the  first  symptom,  and  simulate 
delirium  tremens,  or  the  patient  may  be  absolutely  mute.  The  result,  if 
death  does  not  occur,  is  sometimes  permanent  insanity.'  As  this  stage  ad- 
vances the  temperature  rises  to  104°  F.,  the  pulse  becomes  more  frequent 
and  irregular ;  the  abdomen  is  retracted,  the  vomiting  continues  projectile, 
and  the  respirations  become  sighing  in  character.  During  this  stage  the 
pupils  are  uneven — one  may  be  of  normal  size  while  the  other  is  quite 
small ;  when  the  delirium  is  subsiding  they  dilate  and  contract  by  turns, 
or  oscillate.  The  tdchs  cerebrate  may  appear,  and  herpetic  eruptions  are 
not  infrequent.     This  stage  lasts  from  one  to  three  days. 

The  stage  of  coma  comes  on  gradually.  The  delirium  subsides,  and  is 
followed  by  a  tendency  to  stupor,  lethargy,  and  deep  sleep.  Headache, 
jactitation,  and  hyperasstliesia  disappear.  The  pulse  becomes  slow,  irregu- 
lar, and  intermittent.  The  pupils  are  markedly  dilated,  the  breathing  is 
superficial  and  irregular.  The  patient  is  insensible  to  all  impressions  ;  he 
rolls  his  head  and  grinds  his  teeth,  j)icks  stupidly  at  the  bedclothes,  and 
the  face  becomes  alternately  white  and  red.  Gradually  the  coma  becomes 
complete,  and  the  urine  and  fgeces  are  retained,  or  the  latter  are  passed  in- 
voluntarily. Drawing  off  the  urine  may  temporarily  rouse  the  patient 
from  the  coma.  The  head  is  drawn  to  one  side,  and  as  the  circulation 
is  retarded  the  extremities  and  face  are  often  of  a  purple  hue.  Subsultus 
tendinum  is  marked.  The  pulse  runs  up  to  160  to  170,  or  until  it  cannot 
be  counted  at  the  wrist ;  the  Cheyne-8tolces  respiration  of  ascending  and 
descending  rhythm  becomes  established.  The  expirations  are  puffing. 
The  body  is  bathed  in  cold  sweat,  and  death  results  from  central  paralysis, 
causing  asphyxia,  or  heart-failure  and  pulmonary  oedema.  The  temperature 
may  rise  very  high  or  fall  to  a  subnormal  just  before  death. 

1  Vigla,  Actes  de  la  Soc.  Med.  des  Hop.  de  Paris. 


ACUTE    MENINGITIS.  939 

Differential  Diagnosis. — Acute  meningitis  may  be  confounded  with  acute 
urcBmia,  typhus  fever,  variola,  and  delirium  tremens. 

In  urcemia  the  face  will  be  turgid,  and  there  will  be  puffiness  al>out  the 
eyelids ;  in  meningitis  the  face  is  pale  and  anxious,  and  there  is  no  oede  Jia. 
In  ursemia  the  urine  will  contain  albumen  and  blood  or  exudative  casts ;  in 
meningitis  only  a  small  amount  of  albumen  is  present  and  no  casts.  Con- 
vulsions, preceding  the  coma,  are  far  more  common  m  uraemia  than  in 
meningitis.  The  pulse,  temperature,  and  the  subjective  symjotoms  of 
meningitis  are  absent  in  acute  uraemia.  In  some  cases  only  a  microscopic 
examination  of  the  urine  will  enable  one  to  make  a  differential  diagnosis. 

In  typhus  fever,  although  the  cerebral  symptoms  closely  resemble  those 
of  meningitis,  the  temperature  range  is  higher,  often  reaching  106°  to 
107°  F.  The  pulse  is  more  rapid  and  compressible  in  typhus  than  in 
meningitis.  In  typhus  the  countenance  has  a  dull,  leaden,  or  mahogany 
hue  ;  in  meningitis  it  is  pale  and  anxious.  Surface  sensibility  is  blunted 
in  typhus,  and  is  exaggerated  in  meningitis.  Vomiting  is  infrequent  in 
typhus,  in  meningitis  it  is  persistent  and  projectile  in  character.  The 
characteristic  typhus  eruption  appears  on  or  about  the  fifth  day ;  there  is 
no  characteristic  eruption  in  meningitis.  In  typhus  the  pupils  are  equal, 
in  meningitis  they  are  unequal. 

In  small-pox  the  face  is  flushed,  the  pulse  is  full  and  bounding,  there  is 
intense  pain  in  the  back  and  loins,  the  vomiting  is  retching  in  character, 
and  at  the  end  of  the  third  day  the  characteristic  eruption  occurs  along 
the  roots  of  the  hair.  These  symptoms  are  all  absent  in  meningitis.  In 
many  cases,  however,  it  is  necessary  to  await  the  appearance  of  the  eruption 
before  a  diagnosis  can  be  made. 

In  delirium  tremens  there  is  a  busy  delirium,  the  patient  imagines 
persons  and  animals  about  him,  and  is  wild  in  his  gestures  and  utterances  ; 
in  meningitis  the  delirium  is  incoherent  and  milder,  but  marked  by  a  de- 
sire to  get  out  of  bed.  The  surface  is  bathed  in  a  profuse,  clammy  sweat 
in  delirium  tremens ;  it  is  hot  and  dry  in  meningitis.  In  delirium  tre- 
mens the  temperature,  pulse-rate  and  pupils  are  normal ;  there  is  no  head- 
ache. 

Prognosis. — The  prognosis  in  acute  meningitis  is  very  unfavorable  ;  severe 
cases  terminate  fatally,  mild  cases  may  recover.  The  duration  varies  from 
two  days  to  four  weeks  ;  fatal  cases  rarely  last  more  than  eight  days.  If 
recovery  takes  place  convalescence  may  not  be  fully  established  before  the 
third  week.  The  average  duration  of  the  disease  is  about  eight  days. 
Strabismus,  hiccough,  and  local  paralyses  are  very  unfavorable  symptoms. 
The  prognosis  is  better  in  children  than  in  adults. 

Treatment. — The  most  important  local  measures  at  the  onset  of  the  dis- 
ease are  local  blood-letting  and  the  application  of  cold  to  the  head. 
Leeches  may  be  applied  to  the  nuchal  region  or  temples.  The  best  method 
of  applying  cold  is  by  means  of  the  ice-bag  or  coiled  tube,  and  that  it  may 
be  thoroughly  applied  the  head  should  be  shaved.  The  patient  must  be 
placed  in  a  large,  quiet,  darkened  room,  with  the  head  elevated  and  all 
obstruction  to  the  return  circulation  removed.     The  bowels  must  be  freely 


940  DISEASES   OF   THE    NERVOUS    SYSTEM. 

acted  upon  by  croton  oil,  and  some  drastic  purge  and  saline  diuretic  are 
indicated  if  the  urinary  secretion  is  scanty. 

In  the  stage  of  coma  blisters  to  the  back  of  the  neck  are  of  service.  To 
relieve  the  great  restlessness  which  often  precedes  the  stage  of  delirium, 
hydrate  of  chloral  and  opium  may  be  given.  Iodide  of  potash  and  mer- 
cury are  strongly  recommended  in  all  stages  of  this  disease,  but  I  have 
never  obtained  any  positive  beneficial  effects  from  their  use.  Strong  broths 
and  alcoholic  stimulants,  if  indicated,  may  be  administered  throughout  the 
whole  course  of  the  disease.  The  condition  of  the  bladder  and  the  bowels 
must  be  carefully  looked  after  during  the  stage  of  coma,  and  especially  in 
the  meningitis  of  old  age. 

SUBACUTE    MEJSrn^GITIS. 

Subacute  meningitis  differs  from  acute  in  that  it  is  always  secondary,  is 
of  longer  duration,  and  is  attended  by  less  active  symptoms. 

Morbid  Anatomy. — Upon  the  convexity  of  the  brain  there  is  found  a  sero- 
fibrinous exudation,  containing  few  pus  globules,  and  fibrin  only  in  small 
quantities.  The  effusion  will  occupy  the  meshes  of  the  pia  and  the  ven- 
tricular cavities.  As  a  result  of  the  effusion  the  convolutions  are  flattened 
and  the  sulci  are  deepened.  Flocculi  of  lymph  will  be  found  most  abun- 
dantly along  the  line  of  the  vessels  of  the  convexity,  and  the  vessels  of  the 
pia  mater  will  be  more  or  less  distended.  The  pia  mater  will  be  lifted 
from  the /Surface  of  the  brain,  will  lose  its  glistening  appearance,  and  in  old 
cases  will  be  slightly  opaque. 

Etiology. — This  form  of  meningitis  may  occur  during  the  course  of  any 
exhausting  disease,  as  chronic  diarrhoea,  cancer,  chronic  Bright's  disease, 
typhoid  fever,  etc. 

Symptoms. — Being  subacute  and  always  secondary,  its  early  symptoms  are 
obscure.  The  stage  of  headache  is  wanting  or  lasts  only  a  few  hours,  and 
is  never  severe.  The  delirium,  which  is  often  preceded  by  extreme  jactita- 
tion, comes  on  gradually  and  is  always  quiet  in  character,  and  is  character- 
ized by  an  attempt  on  the  part  of  the  patient  to  get  out  of  bed  and  walk 
around  the  room ;  the  patient  in  walking  staggers  and  is  apt  to  fall  for- 
ward. The  stage  of  delirium  may  last  only  a  few  hours.  In  most  cases 
headache  and  delirium  are  rapidly  followed  by  coma.  Thus,  if  a  patient 
with  chronic  Bright's  disease,  after  a  short  delirium,  passes  slowly  into  a 
state  of  coma,  there  is  reason  to  suspect  the  development  of  this  form  of 
meningitis. 

When  the  active  delirium  of  typhus  fever  becomes  muttering  in  charac- 
ter, when  the  pupils  dilate  and  the  pulse  becomes  slow  and  irregular,  sub- 
acute meningitis  may  be  suspected.  As  the  coma  begins  the  respirations 
become  sighing  and  puffing  in  character,  and  the  urine  collects  in  the  blad- 
der. As  it  deepens,  the  pulse,  which  has  been  slow,  is  accelerated  and  in- 
termits ;  the  expirations  are  short  puffs,  and  the  interval  between  expira- 
tion and  inspiration  becomes  lengthened.  The  typhoid  state  is  rapidly 
developed,  deglutition  becomes  difficult,  there  is  blueness  of  the  finger- 


CHRONIC    MENINGITIS.  941 

nails  with  cyanosis,  and  the  coma  ends  in  death,  or  is  slowly  recovered  from 
and  followed  by  a  long  convalescence. 

Differential  Diagnosis. — The  history  of  the  case  will  aid  very  much  in  its 
diagnosis.  Coma  being  its  prominent  symptom,  the  differential  diagnosis 
is  from  other  forms  of  coma. 

From  coma  of  acute  meningitis,  of  tumors,  compression,  concussion,  or 
cerebral  softening,  the  previous  history  is  sufficient  to  distinguish  it. 

From  coma  of  poison  and  narcotics  it  is  differentiated  by  examination  of 
the  secretions  and  excretions  and  by  the  state  of  the  pupil ;  thus,  in  lead 
poisoning  the  line  on  the  gums,  in  alcoholic  coma  an  examination  of  the 
urine,  and  in  ojoium  coma  the  pin-head  pupils  will  at  once  decide. 

Hysteria,  eiailepsy,  and  catalepsy  are  attended  with  such  distinctive  signs 
that  they  cannot  be  mistaken  for  sab-acute  meningitis. 

Prognosis. — The  prognosis  of  sub-acute  meningitis  is  determined  by  the 
disease  with  which  it  occurs.  When  it  occurs  with  Bright's  disease  it  is 
usually  fatal,  but  when  complicating  tyj)hus  and  other  fevers  it  is  fre- 
quently recovered  from. 

Treatment. — The  chief  indication  is  to  remove  the  cause.  In  Bright's 
disease,  elimination  of  urea,  which  is  causing  the  meningitis,  should  be 
attempted.  In  typhus  fever  free  ventilation,  stimulants,  and  concen- 
trated nutrition  will  remove  the  cause  so  far  as  possible.  In  most  instances 
blisters  applied  to  the  neck  will  be  followed  by  marked  improvement, 
and  not  infrequently  by  recovery. 

CHEOlSriC    MENESTGITIS. 

Chronic  meningitis  is  an  interstitial  inflammation  of  the  pia  mater, 
which  causes  thickening  and  opacity  of  the  membrane.  It  may  be  lim- 
ited to  the  convexity. 

Morbid  Anatomy. — The  pia  mater  is  thickened,  callous,  and  opaque,  and 
maybe  infiltrated  with  serum,  pus,  and  new  connective-tissue  cells.'  There 
is  thickening  of  the  walls  of  the  blood-vessels  of  the  pia,  and  of  their 
branches  which  enter  the  brain  substance.  These  last  adhere  to  the  sur- 
rounding brain  substance,  so  that  it  is  torn  when  the  pia  mater  is  lifted 
from  the  brain.'  Attendant  upon  all  forms  of  chronic  meningitis  there  is 
more  or  less  interstitial  inflammation  of  a  very  low  grade  of  the  hrain- 
sudstance  (diffuse  interstitial  encephalitis),  although  meningitis  chronica 
is  not  ordinarily  diffuse,  but  limited  in  extent.  When  the  pia  and  dura 
raater  are  bound  together,  pachymeningitis  has  preceded  the  development 
of  adhesions.  The  ventricles  usually  contain  more  or  less  fluid.  The 
development  along  the  f  alx  of  glandulm  pacchionii  is  due  as  much  to  senil- 
ity as  to  chronic  meningitis. '  Atrophy  of  the  cortex  results  from  long- 
continued  chronic  meningitis. 


1  Ramskill  states  osseous  plates  have  been  found  embedded  in  the  thickened  membrane. 

«Some  authors  describe  a  degenerative  change  in  the  vessels  resulting  from  previous  peri-  or  endarter- 
itis, which  is  said  to  resemble  colloid  metamorphosis.    This  change  is  rare. 

a  Foster  states  that  he  has  seen  cheesy  degeneration  of  the  exudation  lying  in  the  sulci,  and  that  a  cyst- 
wall  of  connective-tissue  has  formed. 


942  DISEASES    OF   THE   NEEVOUS   SYSTEM, 

Etiology. — Chronic  meningitis  is  a  disease  of  adult  life,  especially  after 
fifty  years  of  age.  It  is  often  idiopathic,  and  is  met  with  among  the  poor 
and  badly  nourished.  It  is  very  frequently  a  complication  of  chronic 
alcoholismus,  syphilis/  rheumatism,  gout,  and  chronic  Bright's  disease 
(small  granular  kidney.)  It  is  sometimes  of  traumatic  origin,  and  is  fre- 
quently found  in  the  general  paralysis  of  the  insane.^ 

Symptoms.  — The  symptoms  of  chronic  meningitis  are  always  obscure.  In 
some  cases  there  are  no  symptoms ;  patients  die  of  other  diseases  and 
meningitis  is  found  at  the  autopsy.  In  others  there  are  well-marked 
symptoms.  The  patient  grows  stupid,  dull  and  apathetic,  the  mental 
faculties  are  blunted,  and  there  is  headache  and  a  constant  desire  to  sleep, 
or  the  patient  may  become  morose  and  fretful.  In  the  old  the  headache 
comes  in  paroxysms,  and  is  attended  by  marked  flushing  of  the  face,  fre- 
quent pulse  and  high  arterial  tension,  occasionally  attended  by  delirium. 
In  nearly  all  cases  vomiting  becomes  a  prominent  symptom,  producing 
great  exhaustion.  Muscular  weakness  attends  the  decline  in  mental  pow- 
ers ;  the  legs  tremble  in  walking,  control  of  the  sphincters  is  lost,  and  the 
urine  and  faeces  may  be  passed  involuntarily.  In  many  cases,  chiefly  the 
aged,  there  is  paralysis  of  the  bladder.  The  appetite  is  good,  but  diges- 
tion is  slow  and  the  bowels  are  constipated.  The  speech  is  thick,  or  the 
power  to  articulate  certain  words  is  lost.  Vertigo,  tinnitus  aurium,  and 
muscse  volitantes  are  present,  with  localized  numbness  or  hyperaesthesia. 
The  very  aged  often  lie  in  a  stupor,  exhibiting  no  mental  or  physical  signs 
of  life  except  to  breathe  and  take  food. 

There  is  no  typical  temperature  range.  Indeed,  in  many  cases  there  is 
no  pyrexia  during  the  whole  period  of  the  disease,  in  others  there  will  be  a 
chill  and  fever  resembling  in  its  variations  that  of  malaria.  In  some  forms 
of  chronic  meningitis  hemiplegia  occurs,  both  with  and  without  facial  pa- 
ralysis. When  the  trigeminus  is  involved  the  eyeball  may  slough.^  Ptosis, 
strabismus,  and  variations  in  the  size  of  the  pupils  indicate  that  the  third 
nerve  is  involved.  These  irregular  symptoms  may  continue  with  increasing 
severity  for  months  or  years.  Toward  the  end  convulsions  may  occur,  and 
death  takes  place  in  deep  coma.* 

Differential  Diagnosis. — The  diagnosis  of  chronic  meningitis  is  always  dif- 
ficult.    It  may  be  mistaken  for  cerebral  tumors  or  softening. 

With  tumors,  the  headache  is  more  intense  and  circumscribed,  paralysis 
of  nerves  of  special  sense  or  of.  certain  sets  of  nerves  is  common,  and  the 
signs  of  general  decline  in  mental  and  physical  power  are  less  marked. 
Chronic  meningitis  appears  in  its  whole  symptomatology  to  be  of  a  more 
general  nature,  while  tumors  produce  local  symptoms;  speech  and  intellect 
are  usually  unimpaired.  When  neoplasias  excite  chronic  meningitis  in  their 
vicinity  the  diagnosis  is  often  impossible. 

1  Virchow  states  that  when  constitutional  syphilis  exists  in  the  human  body,  its  localization  depends 
greatly  upon  previous  states  of  the  system. 

2  Calmeil. 

»  See  Effect  of  cutting  fifth  cranial  nerve,  in  M.  Poster's  Physiology,  p.  381  to  382. 

*  Many  attribute  the  symptoms  of  chronic  meningitis  occurring  in  the  insane,  epileptic,  and  imbeciles  to 
a  cortical  encephalitis  frequently  found  at  tlie  autopsy,  with  the  changes  of  meningitis. 


TUBERCULAE   MENINGITIS.  943 

Softening  of  the  drain  is  also  often  associated  with  chronic  meningitis. 
In  softening  there  may  be  a  history  of  a  previous  apoplectic  seizure  ;  mus- 
cular contractions  are  common,  and  the  headache  is  not  so  severe  as  in 
chronic  meningitis.  In  chronic  meningitis  there  is  more  mental  excitement 
than  in  cerebral  softening,  and  the  hemiplegia  is  more  complete  after  apo- 
plectic seizures. 

Prognosis. — The  prognosis  is  bad;  the  disease  is  a  progressive  one.  Only 
in  cases  of  a  syphilitic  origin  can  we  offer  any  hope  of  recovery.  Many  be- 
come permanently  insane,  and  some  die  from  inanition.  Death  may  also 
result  from  exhaustion,  from  cerebral  pressure,  and  from  complicating  dis- 
eases, as  pneumonia,  etc. 

Treatment. — The  patient  is  to  be  kept  quiet  mentally,  and  the  diet  must 
be  fluid  and  nutritious  ;  stimulants  being  only  administered  to  sustain  vi- 
tality. The  bichloride  of  mercury  and  iodide  of  potassium,  in  small  doses, 
are  the  remedial  agents  most  frequently  employed.  Blisters  may  be  applied 
to  the  back  of  the  neck,  or  a  seton  introduced  there.  The  bowels  need 
careful  attention.  The  urine,  if  not  passed  freely,  should  be  drawn  and 
the  bladder  washed  out. 

TUBEECULAR   MENESTGITIS. 

{Acute  hydrocephalus.) 

Tubercular  meningitis '  is  an  inflammation  of  the  basal  pia  mater, 
caused  or  attended  by  an  eruption  of  gray,  miliary  tubercles,  and  occur- 
ring most  frequently  in  children. 

Morbid  Anatomy.  — The  dura  mater  is  rarely  involved.  The  pia  mater  in 
some  cases  is  congested,  in  others  pale,  and  it  may  be  infiltrated  with 
serum,  fibrin,  and  pus.  The  vessels  along  the  Sylvian  fissure  and  the  an- 
terior peduncles  of  the  cerebellum  are  studded,  especially  at  their  bifurca- 
tions, with  miliary  tubercles,  which  lie  in  the  perivascular  lymph-spaces. 
The  lymph-spaces  may  become  filled,  and  a  covering  be  thus  formed  over 
the  vessel ;  or  the  miliary  granules  dot  the  vessel  like  a  string  of  beads. 
As  they  develop  they  compress  and  finally  occlude  the  vessels.  These  gran- 
ules are  sometimes  met  with  in  small  numbers  on  the  convexity  and  along 
the  longitudinal  fissure,  but  are  always  more  abundant  at,  if  not  confined 
to,  the  base,  from  which  they  may  extend  to  the  pia  mater  of  the  cervical 
cord.  Even  at  the  base  they  may  be  few  and  limited,  or  so  abundant  and 
extensive  as  to  obstruct  the  circulation  and  impair  the  walls  of  the  vessels, 
causing  multiple  hemorrhages  and  red  softening. 

The  inflammatory  exudation  at  the  base  is  a  turbid,  serous  effusion,  or 
more  commonly  a  thick,  yellow,  semi-plastic  layer  which  extends  from 
the  fossa  8ylvii,  where  it  is  most  abundant,  to  the  inferior  surface  of  the 
cerebellum.  When  the  pia  mater  of  the  convexity  is  involved  it  may  show 
no  evidences  of  exudative  inflammation,  but  present  a  bright,  rosy  hue. 
The  ventricles  are  distended  by  a  serous  fluid,  usually  turbid  from  admix- 

'  Is  alt^o  called  by  the  Germans  basilar  meningitis ;  and  by  the  English  acute  hydrocephalus.    The  die 
ease  was  properly  named  tubercular  meningitis  by  the  French. 


944  DISEASES   0¥  THE   NERVOUS   SYSTEM. 

ture  of  cellular  elements,  which  flattens  the  convolutions  and  causes  cede- 
matous  softening.  The  membrane  of  the  ventricles  is  thick  and  opaque. 
In  cases  running  an  acute  course,  the  only  lesion  except  the  tubercles  may 


Fig.  191. 

Tubercular  Meningitis. 

Region  of  the  Sylvian  Jismre  showing  at  A,  A,  miliary  tubercles  along  the  line  of  the  blood-vessels. 

be  a  large  serous  effusion  into  the  ventricles.  In  most  cases  tubercular 
meningitis  is  associated  with  general  tuberculosis. 

Etiology. — Tubercular  meningitis  is  rare  before  the  first  and  after  the 
fifth  year.  It  occurs  almost  exclusively  in  children  of  a  scrofulous  diathe- 
sis, either  inherited  or  acquired.  In  such  children  the  tuberculous  process 
is  latent,  and  any  debilitating  disease  may  excite  it,  such  as  diarrhoea,  the 
exanthemata,  especially  measles,  whooping-cough,  otorrhoea,  and  skin  and 
scalp  diseases  of  a  chronic  nature,  dentition,  insufiicient  or  improper 
food,  and  injuries  to  the  head,  more  particularly  at  the  base  of  the 
brain. 

Symptoms. — The  symptoms  of  tubercular  meningitis  are  due  not  so  much 
to  the  tubercular  developments,  as  to  the  exudative  products  of  the  inflam- 
matory process,  as  the  pia  may  be  studded  with  tubercles  both  at  the  con- 
vexity and  base  without  the  slightest  symptomatic  indications  of  their  pres- 
ence. Its  advent  is  generally  very  insidious  ;  if  convulsions  usher  it  in,  its 
course  is  rapid. 

The  premonitory  stage  is  marked  by  changes  in  the  nutritive  and  diges- 
tive processes  ;  the  appetite  is  diminished  and  capricious  ;  the  breath  is 
offensive,  the  tongue  coated,  constipation  and  diarrhoea  alternate.  The 
child  becomes  dull,  languid,  apathetic,  and  desires  quiet ;  its  sleep  is 
restless  and  troubled.  The  face  assumes  a  dull,  anxious  appearance,  and 
when  at  play  the  child  will  stop  suddenly  and  rest  its  head  on  its  hands  or 


TUBERCULAR   MENINGITIS. 


945 


the  floor.  During  the  progress  of  these  symptoms  a  cachexia  is  developed 
and  there  is  progressive  emaciation,  which  in  connection  with  the  etiology 
gives  rise  to  the  suspicion  that  the  disease  is  developing.  These  prodro- 
mata  may  last  from  a  few  days  to  a  month,  and  will  often  attract  the 
attention  of  strangers  before  they  are  observed  by  the  parents.  In  most 
instances  there  is  a  slight  evening  rise  in  the  temperature  and  a  short 
hacking  cough  at  intervals.     The  symptoms  may  be  divided  into  three 


The  first  is  the  irritative  stage  or  period  of  invasion.  In  this  period  the 
little  patients  dislike  to  be  disturbed ;  light  and  noise  annoy  them  ;  they 
answer  questions  intelligently,  but  unwillingly  and  slowly.  The  expression 
of  the  countenance  is  anxious.  '  The  cheeks  will  be  alternately  flushed  and 
pale.  Headache,  which  is  often  severe,  is  paroxysmal  and  seldom  constant. 
It  is  usually  frontal  and  may  be  accompanied  by  dizziness.  In  some  cases 
the  intermissions  are  short  and  the  pain  is  diffused.  The  sufferer  will  moan 
and  clasj)  the  head  with  his  hands.  In  young  children  pressure  on  the  fon- 
tanelles  increases  the  pain.  There  is  mild  delirium  alternating  with  dis- 
turbed and  fitful  sleep,  from  which  the  child  starts  with  a  piercing  Tiydro- 
ceplialic  cry.  They  grind  their  teeth,  roll  their  eyeballs,  and  the  facial 
muscles  are  contorted.  The  hands  will  be  clenched  and  the  thumbs  flexed 
on  the  palms.  Muscular  tremors  pass  over  the  face  and  body  in  quick  suc- 
cession. The  abdomen  is  retracted  and  hard,  due  to  contraction  of  the 
intestines  from  central  irritation.  Projectile  vomiting  occurs  at  varying 
intervals,  independent  of  the  ingestion  of 
food,  and  resists  all  treatment.  The  bowels 
are  constipated.  The  tongue  is  dry,  covered 
with  a  white  coating,  and  the  tip  is  red. 
The  pupils  are  contracted,  there  is  photo- 
phobia and  possibly  strabismus  ;  the  con- 
junctivae are  injected  and  the  brows  con- 
tracted. On  drawing  the  finger  firmly  over 
the  skin,  a  red  line,  after  a  moment,  will 
follow  the  removal  of  the  pressure.  The 
evening  temperature  is  a  degree  or  two 
higher  than  that  of  the  morning,  but  rarely 
rises  above  103°  F.  Sometimes,  in  cases 
where  convulsions  usher  in  the  disease,  the 
temperature  will  reach  104°  or  105°  F.  The 
exacerbations  and  remissions  are  always 
irregular.  The  pulse  is  at  first  full,  com- 
pressible and  regular,  or  it  maybe  normal  in 
character.  After  the  first  twenty -four  hours 
it  shows  a  marked  tendency  to  become  accelerated  and  slightly  irregular 
upon  muscular  exertion  or  excitement.  The  respirations  at  times  are  rapid 
and  irregular,  at  others  slow  and  regular,  during  sleep  perfectly  natural.  At 
first  drowsiness  alternates  with  periods  of  excitement,  but  gradually  becomes 
more  persistent,  and  the  child  is  disposed  to  sleep  constantly  unless  aroused. 


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Fig.  193. 
Temperature  Record  in  a  case  of  Tuber- 
cular Meningitis.    The  disease  was  ush- 
ered in  by  convulsions,  and  terminated 
in  death  on  the  ninth  day. 


946  DISEASES    OE   THE    KERVOUS    SYSTEM. 

After  a  few  days,  a  week  in  most  cases,  these  signs  of  cerebral  irri- 
tation give  place  to  evidences  of  depression  which  attend  the  second 
stage.  The  pupils  are  unequal  and  respond  slowly  to  light.  The  photo- 
phobia and  irritability  disappear.  The  muscles  at  the  back  of  the 
neck  become  rigid ;  the  head  is  retracted  and  rolled  slowly  from  side  to 
side  ;  sometimes  distinct  opisthotonos  occurs.  This  state  is  irregularly 
interrupted  by  sudden  spasms  with  the  hydrocephalic  cry,  or  by  parox- 
ysms of  delirium.  The  pulse  becomes  slow,  irregular,  and  intermit- 
tent ;  the  irregularity  is  very  distinctive.  It  may  be  doubled  in  frequency 
on  slight  excitement.  There  are  partial  or  general  convulsions ;  ptosis, 
strabismus,  loss  of  sight,  anesthesia,  local  paralysis  or  complete  hemiplegia 
may  occur.  There  is  constipation  and  retention  of  urine  or  involuntary 
passages.  The  projectile  vomiting  ceases.  Deglutition  may  become  dijBB- 
cult,  and  the  unparalyzed  hand  will  grasp  at  the  mouth  and  throat  to  re- 
move supposed  obstructions.  The  respirations  are  irregular  and  sighing, 
and  Cheyne-Stokes'  respiration  is  common.  As  a  rule  complete  anorexia 
exists  ;  the  tongue  and  mouth  are  covered  with  sordes ;  and  the  passages 
are  unnatural  and  offensive,  often  having  a  slimy,  greenish  appearance. 
The  urine  is  diminished  in  quantity,  of  high  specific  gravity,  dark  colored, 
and  contains  chlorides,  phosphates  and  albumen  in  varying  proportions. 
Facial  convulsions  are  not  infrequent.  In  young  children,  the  temperature 
may  be  subnormal  during  this  stage,  even  when  convulsion  follows  convul- 
sion in  quick  succession.  The  ophthalmoscope  reveals  varicosities'  of  the 
retinal  veins,  points  of  hemorrhage,  serous  peri-papillary  infiltration,  and 
white  miliary  granulations  on  the  retina  and  choroid.  Optic  neuritis  is 
sometimes  present.  It  is  said  that  ocular  disturbances  will  be  present  in 
this  disease  only  when  the  cliiasm.  is  involved.^  They  are  not  present  in 
tubercular  meningitis  of  the  convexity. 

At  this  stage  of  the  disease  apparent  recovery  is  of  common  occurrence. 
The  child  sits  up  in  bed,  is  free  from  pain  or  delirium,  eats  with  avidity, 
and  will  play  as  though  completely  convalescent.  This  is  deceptive  ;  for 
.after  a  few  hours  he  lapses  into  a  deeper  stupor  than  before. 

The  last  stage  is  indicated  by  a  change  in  the  pulse  and  by  deepening 
coma.  The  pulse  runs  up  to  150  or  170  per  mmute,  is  feeble,  small  and 
irregular.  The  pupils  are  widely  dilated ;  the  fontanelles  in  the  very 
young  may  become  prominent ;  the  paralyses — which  may  have  been  tran- 
sient— are  now  permanent,  and  convulsions  occur  during  the  development  of 
the  coma.  The  breathing  is  sighing  or  snoring  in  character.  Dysphagia 
is  marked.  The  contents  of  the  bladder  and  rectum  are  passed  involunta- 
rily ;  the  body  is  covered  with  a  clammy  sweat,  and  one  side  may  be  hot,  the 
other  cold.  The  patient  lies,  when  convulsive  movements  are  absent,  on 
his  back,  the  head  drawn  to  one  side  or  still  rolled  from  side  to  side.  One 
side  of  the  mouth,  and  one  nostril,  show  that  paralysis  has  occurred.  Soon 
only  reflex  movements  can  be  excited.  Contractions  about  the  jaw  and 
neck  are  frequently  observed.  The  abdomen  becomes  tympanitic,  subsul- 
tus  tendinum  is  marked  ;  the  capillary  circulation  is  more  and  more  inter- 

1  Cohnheim  and  Bouchut.  2  jjnvon  MediccUe,  1867,  GalezowskL 


TUBERCULAR   MEN-INGITIS.  947 

fered  with,  respirations  become  less  distinct,  and  death  may  occur  quietly 
in  deep  coma,  or  from  asphyxia  at  the  height  of  a  severe  convulsion. 
During  these  last  hours  the  temperature  may  reach  106°  F.,  is  of  varying 
intensity,  and  is  rarely  subnormal.  In  some  severe  cases  the  stage  of  coma 
is  reached  in  a  few  hours,  and  death  occurs  within  forty-eight  hours  ;  again 
there  may  be  no  actual  coma  throughout.  I  have  occasionally  seen  cases 
begin  with  paralyses  (facial  hemijalegia,  etc.,  etc.),  and  with  aphasia. 

Differential  Diagnosis. — Tubercular  meningitis  may  be  mistaken  for  acute 
meningitis,  gastro-enteritis,  acute  Brigltfs  disease,  spurious  hydrocephalus 
and  infantile  remittent  fever. 

Acute  meningitis  has  none  of  the  prodroraata  that  in  over  80  per  cent. 
of  the  cases  precede  tubercular  meningitis ;  it  is  sudden  in  its  onset  and 
rapid  in  its  progress  ;  the  temperature  is  higher  and  has  none  of  the  exacer- 
bations and  remissions  that  cause  the  tubercular  form  to  simulate  infantile 
remittent  fever.  The  ocular  symptoms  and  the  boat  shaped  abdomen 
are  more  prominent  in  the  tubercular  than  in  other  forms  of  meningitis. 
The  hydrocephalic  cry,  and  the  irregular,  slow  development  are  character- 
istic of  the  tuberculous  variety. 

Gastro-enteritis  is  accompanied  by  diarrhoea,  abdominal  pain  and  tender- 
ness. But  headache,  contracted  jDupils,  photophobia,  the  slow,  irregular 
pulse,  reflex  movements  during  sleep,  projectile  vomiting,  and  the  hydro- 
cephalic cry  of  acute  hydrocephalus  are  wanting. 

In  Brighfs  disease  the  oedema,  the  characteristic  facial  expression,  and 
the  absence  of  prodromes,  taken  in  connection  with  the  presence  of  albu- 
men and  casts  in  the  urine,  will  establish  the  diagnosis. 

A  comatose  state  following  cholera  infantum,  called  spurious  hydroceph- 
alus, will  be  recognized  by  a  feeble,  rapid  pulse,  a  low  (even  sub-normal) 
temperature,  a  dilated  pupil,  a  distended  abdomen,  and  the  absence  of  the 
characteristic  nervous  phenomena  of  meningitis  ;  the  fontanelle  is  depressed 
in  spurious  hydrocephalus,  elevated  and  strongly  pulsating  in  tubercular 
meningitis. 

Infantile  remittent  is  attended  by  a  high  temperature  that  remits  with 
regularity ;  the  exacerbations  and  remissions  of  tubercular  meningitis  are 
irregular,  and  the  fever  is  rarely  over  103°  F.  In  infantile  remittent  the 
vomiting  is  retching  in  character,  diarrhoea  is  jDrominent  and  the  discharges 
pea-soup  in  character,  the  abdomen  is  distended  and  tender ;  there  is  great 
thirst,  rapid  pulse,  and  normal  pupils.  The  photophobia,  irregular  pulse, 
hydrocephalic  cry,  and  the  grinding  of  the  teeth  so  common  in  acute 
hydrocephalus  are  absent.  The  severe  cerebral  symptoms  that  often  attend 
the  invasion  of  acute  pneumonia,  pleurisy,  bronchitis,  or  the  exanthematous 
fevers  in  children  are  to  be  distinguished  by  a  physical  exploration  of  the 
chest  or  by  the  appearance  of  the  eruptions  and  the  high  fever  and  pulse-rate. 

Prognosis. — Tubercular  meningitis  is  one  of  the  most  fatal  diseases  of 
childhood.  Many  authors  state  that  it  is  always  fatal  after  its  character- 
istic symptoms  are  developed.  The  duration  varies  from  five  days  to  four 
weeks  ;  from  sixteen  to  twenty-one  days  after  the  initial  symptoms  death 
may  be  expected.     If  ushered  in  by  convulsions  its  duration  is  short. 


948  DISEASES    OF   THE    NERYOUS   SYSTEM. 

Treatment. — It  is  unnecessary  to  refer  to  all  the  different  measures  which 
have  been  resorted  to  for  the  cure  of  this  disease,  for  they  have  all  failed. 
Prophylaxis  alone  is  effective.  A  child  whose  antecedents  lead  us  to  fear 
the  advent  of  acute  hydrocephalus  should  be  given  a  healthy  wet-nurse 
from  its  birth,  and  the  greatest  care  exercised  as  to  its  hygiene  and  diet  for 
the  first  few  years  of  life.  Children  who  exhibit  the  premonitory  symp- 
toms, and  in  whom  its  development  is  feared,  should  be  given  cod-liver 
oil,  kept  out  of  doors  as  much  as  possible,  and  placed  under  the  most 
favorable  hygienic  conditions  possible  ;  a  frequent  change  of  surroundings 
and  of  climate  is  important. 

The  treatment  after  the  disease  is  established  is  almost  entirely  symp- 
tomatic. The  bowels  are  to  be  kept  open,  and  absolute  quiet  enjoined. 
Ice-bags  may  be  placed  on  the  head  ;  but  depletion  of  all  kinds  is  contra- 
indicated.  Iodide  of  potassium  (pushed  to  toxic  effects),'  the  mercury 
salts,  and  soda  phosphate  have  been  advocated,  but  their  utility  is  ques- 
tionable. I  have  obtained  the  greatest  benefit  from  opium  and  bromide  of 
potash  during  the  stage  of  excitement,  to  relieve  the  restlessness  and  jac- 
titation. I  have  never  found  that  any  of  the  plans  of  treatment  proposed 
for  this  disease  have  any  power  to  arrest  its  progress. 

Tubercular  meningitis  in  the  adult  is  of  rare  occurrence,  and  is  found 
only  in  connection  with  general  tuberculosis.  The  pathological  changes 
are  the  same  as  those  found  in  children,  and  its  etiology  is  identical  with 
that  of  general  tubercuiosis.  When  latent,  it  may  be  excited  by  severe 
mental  emotions  or  over-work.  Symptom atically,  it  differs  from  infantile 
hydrocephalus  in  degree  rather  than  kind,  the  symptoms  being  perhaps  less 
violent.  In  all  other  respects  the  description .  just  given  will  apply  in  all 
points  to  the  same  disease  in  adults. 

CHEOKIC    HYDEOCEPHALUS. 

Chronic  hydrocephalus  is  a  cerebral  dropsy  from  some  cause  not  well 
understood.  It  is  divided  into  external  hydrocephalus,  in  which  the  serous 
effusion  is  in  the  meshes  of  the  pia  mater,  and  internal  hydrocephalus, 
where  the  accumulation  of  fluid  is  in  the  ventricular  cavities.  When  both 
coexist,  it  is  called  mixed  hydrocephalus.  Chronic  hydrocephalus  may  be 
intra-uterine  or  extra-uterine. 

Morbid  Anatomy. — The  essential  lesion  of  chronic  hydrocephalus  is  a 
serous  effusion  either  into  the  ventricles  or  upon  the  surface  of  the  brain. 
The  fluid  consists  chiefly  of  water,  containing  albumen,  sodium  chloride, 
traces  of  lime  and  potash  salts,  epithelial  and  blood  cells,  rarely  scanty 
lymph-flocculi  and  urea.^  The  ventricles  may  contain  from  twenty  to 
thirty  pounds  of  fluid. ^  The  upper  wall  of  the  lateral  ventricles  may  be 
ruptured  ;  the  brain  substance  is  either  softened  or  abnormally  tough  and 
resistant.  The  brain  will  be  enlarged,  and  the  convolutions  flattened.  In 
congenital  hydrocephalus  the  bones  of  the  skull  are  thin,  the  fontanelles 

1  Niemeyer. 

2  BrighPs  Reports,  vol.  i.,  p.  433. 

8  Trousseau  ( Clin.  Med.)  mentions  a  case  in  which  the  amount  was  fifty  pounds. 


CHEOKIC    HTDKOCEPHALUS.  949 

and  sutures  are  enlarged  ;  or,  if  united,  numerous  ossa  triquetra  are  found 
between  them  ;  and  the  supra-orbital,  temporal,  and  occipital  regions  are 
distinctly  depressed.  The  head  may  measure  from  eighteen  to  forty  inches 
in  circumference.  The  large  ganglia  at  the  base  are  pressed  downward  ; 
the  yarious  septa  and  commissures  are  thinned  or  ruptured  ;  and  finally, 
there  may  be  left  only  a  thin  layer  of  brain  matter  together  with  the 
thalami  and  corpora  striata.  The  optic  chiasm  is  flattened,  and  the  pons 
and  cerebellum  are  compressed.  When  the  lateral  ventricles  are  distended 
and  the  ependyma  thickened  and  granular,  the  term  chronic  or  granular 
ependymitis  is  given  ;  in  this  condition  there  may  be  new  tissue  formation, 
and  bands  of  cicatricial  tissue  join  the  walls  of  the  ventricles. 

Hydrocephalus  ex  vacuo  is  the  result  of  defective  development  of,  or 
atrophic  degenerative  changes  in,  the  brain  ;  the  space  thus  left  is  filled 
hy  a  serous,  sometimes  slightly  bloody  fluid,  seldom  in  great  quantity 
(hydrocephalus  senilis).  The  membranes  (in  the  very  young)  are  seen 
studded  with  ossific  granules.  If  the  bones  should  unite,  there  is  subse- 
quent thickening,  and  the  head  is  either  unsymmetrical,  or  nearly  globu- 
lar.' It  is  not  uncommon  to  find  evidences  in  the  membranes  of  acute  or 
sub-acute  inflammatory  processes. 

Etiology. — Hydrocephalus  may  be  congenital  or  acquired.  When  ac- 
quired it  usually  appears  before  dentition.  A  few  cases  occurring  in  old 
people  are  mentioned  by  Watson  "^  and  Golis,  and  Dean  Swift  is  said  to 
have  died  of  it  in  the  seventy-eighth  year  of  his  age  ;  atrophy  or  imperfect 
development  of  the  brain  causes  it  ;  and  it  may  arise  from  chronic  passive 
hyperemia,  weakness  of  the  vascular  walls,  from  compression  of  the  veins, 
occlusion  of  one  or  both  lateral  sinuses,  or  the  presence  of  tubercular 
masses  in  the  brain-substance.  Eickets  and  syphilis  in  children,  and 
dementia  and  alcoholismus  in  adults,  are  regarded  as  causes.  It  is  met 
with  in  tubercular  and  scrofulous  subjects,  and  it  is  said  to  have  followed 
measles  and  scarlet  fever.'  Inflammatory  changes  in  the  ventricles  and 
ependyma  are  accompanied  by  hydrocephalus.  One  hydrocephalic  child 
renders  it  probable  that  subsequent  children  will  be  hydrocephalic* 

Symptoms. — The  symptoms  vary  with  the  rapidity  of  its  development. 
If  intra-uterine,  hydrocephalus  develops  rapidly  ;  the  head  becomes  so 
large  that  its  delivery  can  only  be  accomplished  by  operative  procedure. 
If  such  children  are  born  alive  they  die  within  a  few  days.  In  those  cases 
where  the  disease  is  slight,  the  child  at  birth  appears  healthy,  but  after  a 
few  weeks  the  head  begins  to  enlarge  ;  the  sutures  do  not  close,  and  the 
fontanelles  are  persistent ;  the  forehead  bulges  so  that  it  overhangs  the 
face,  which  is  pale,  small  and  weazened,  giving  a  dwarfish  expression  to 
the  child.  The  limbs  do  not  develop  ;  the  abdomen  is  distended  and  tym- 
panitic, and  the  skin  dry  and  scaly.     Fluctuation  *  may  sometimes  be  ob- 

1  Barthez  and  Rilliet  state  that  in  a  few  cases  of  congenital  hydroceplialus  the  bones  were  normal. 
"^  Practice  of  Phynic  :  Sir  Thomas  Watson. 
»  Tanner's  Practice. 

*  Hoppe,  Niemej'er  and  others  regard  hydrocephalus  arising  from  nutritive  changes  in  the  capillary 
Walls  as  analogous  to  "  skin  inflammations  that  produce  blebs," 

*  Sir  T,  Watson  ;  Dr.  Bright. 


950  DISEASES    OF   THE   ^^TEEVOUS    SYSTEM. 

tained  between  the  anterior  and  posterior  fontanelles.  Often  the  child  is 
unable  to  hold  its  head  erect  even  for  a  few  moments ;  the  pupils  are 
dilated  and  the  eyes  protruded.  There  are  periods  of  apparent  improve- 
ment, but  after  a  year  of  gradual  decline  death  occurs  in  convulsions,  from 
starvation  or  intercurrent  disease. 

In  another  class  of  milder  cases  the  mental  faculties  are  normal,  but 
nutrition  is  imperfect ;  the  limbs  are  small  and  the  muscles  flabby.  The 
children  are  irritable,  and  at  times  have  fever,  nausea  and  vomiting. 
After  an  unusually  severe  attack  of  fever  they  may  gain  flesh  and  seem 
much  improved,  but  the  head  still  increases  in  size.  After  a  variable  time 
of  improvement  they  again  become  worse,  lose  strength,  and  all  the  active 
cerebral  symptoms  return.  When  they  attempt  to  walk  they  totter,  stum- 
ble and  fall.  Spasms,  epileptiform  convulsions  and  paralysis  of  certain 
groups  of  muscles  follow,  and  they  become  idiotic.  Such  children  do  not 
die  from  hydrocephalus  but  from  intercurrent  disease.  Some  of  these  cases 
live  for  four  or  five  years,  having  periods  when  they  seem  to  be  recover- 
ing. When  anaemia  and  asthenia  cause  death  the  usual  duration  is  a 
year. 

A  few  rare  cases  are  recoi-ded  where  hydrocephalic  subjects  have  lived 
five,  ten,  and  even  thirty  years. 

Differential  Diagnosis. — Congenital,  or  intra-uterine  hydrocephalus  cannot 
well  be  mistaken  for  any  other  malady. 

Cranial  rachitis  does  not  cause  the  mental,  or  even  the  physical,  derange- 
ments induced  by  hydrocephalus  ;  but  it  induces  an  nnsymmetrical  en- 
largement of  the  bones. 

Prognosis. — The  prognosis  is  always  unfavorable.  The  average  duration 
is  one  year.  Death  may  result  from  any  of  the  complications,  from  simple 
asthenia  and  anemia,  from  meningitis,  ependymitis,  apoplexy,  rupture  of 
the  fluid  through  the  brain  substance  into  the  epicranial  aponeurosis,'  or 
from  general  paralysis.  The  only  condition  of  recovery  is  a  cessation  of 
increase  in  the  fluid  and  closing  up  of  sutures  ;  the  cases  of  absorption  of 
fluid  and  return  of  mental  power  are  doubtful.  ^ 

Treatment. — There  is  very  little  to  be  done  for  this  disease.  The  treat- 
ment which  has  been  employed  may  be  divided  into  external  or  mechanical, 
and  internal  or  medicinal.  Mercurial  inunctions  and  strapping  the  head 
with  adhesive  plasters  have  been  advised,  but  are  of  doubtful  utility.  Sud- 
den compression  of  the  head  may  cause  death.  Pale,  flabby  children  bear 
it  best. 

Tapping  can  be  advocated  only  in  external  hydrocephalus  and  where  no 
inflammatory  or  organic  changes  coexist.  The  anterior  fontanelle  is  the 
proper  point  to  insert  the  aspirating  needle  ;  only  a  few  ounces  should  be 
drawn  at  a  time,  the  child  being  carefully  watched  during  and  after  the 
operation.  Subsequently  the  head  should  be  lightly  bandaged.  Langen- 
beck  passes  behind  the  upper  lid  through  the  superior  wall  of  the  orbit  and 

1  Rokitansky's  case. 

*  Otto  states,  however,  "  that  new  cerebral  matter  may  be  deposited  in  place  of  re-absorbed  fluid."— 
Rokitansky's  Pathological  Anatomy. 


PACHYMENINGITIS   EXTERNA.  951 

enters  the  anterior  horn  of  the  lateral  ventricle.     But  inflammatory  action 
is  apt  to  be  excited  by  any  such  procedure. 

Internally  cod-liver  oil  and  the  syrup  of  the  iodide  of  iron  and  potash 
should  be  given  throughout  the  disease  Calomel  (gr.  ^^-l)  daily  has 
been  recommended,  until  purging  becomes  severe.  The  food,  the  hygienic 
surroundings  and  the  clotliing  should  also  receive  careful  attention. 
Change  of  air  is  also  highly  beneficial.  If  rickets  coexist  phosphatic  salts 
are  indicated. 

PACHYMEN^ESTGITIS    EXTERNA. 

Pachymeningitis  is  an  inflammation  of  the  dura  mater  which  may  be 
acute,  chronic,  or  syphilitic.  The  inflammation  may  involve  either  the 
external,  internal,  or  both  layers  of  the  dura  mater.  When  the  external 
layer  is  primarily  involved,  it  is  called  external  pachymeningitis  ;  when  the 
internal  layer  is  the  primary  seat  of  the  inflammatory  process,  it  is  called 
pachymeningitis  interna.  External  pachymeningitis  is  almost  always  a 
secondary  inflammation. 

Morbid  Anatomy. — In  the  non-suppurative  form  of  pachymeningitis  ex- 
terna the  dura  is  injected,  softer  than  normal,  and  covered  with  ecchymo- 
tic  spots.  New  connective-tissue  formations  occur,  which  lead  to  thicken- 
ing and  induration  of  the  dura  and  adhesions  between  it  and  the  cranial 
bones.  Numerous  pigment  granules  stud  the  thickened  membrane.  Os- 
teophytes form  and  the  appearance  closely  resembles  periostitis  with  exos- 
tosis. In  many  cases  bony  flakes  can  be  detached  from  the  tough,  pale, 
leathery  dara  mater. 

In  purulent  pachymeningitis  externa  suppurative  processes  are  early 
established  and  the  external  layer  is  softened,  disintegrated,  thinned,  and 
rendered  very  friable.  A  thick  layer  of  new  connective-tissue  separates 
the  pus  from  the  i7iternal  layer  of  the  dura  mater.  These  purulent  collec- 
tions are  usually  of  traumatic  origin  and  circumscribed,  as  inflammation  of 
the  dura  is  rarely  diffuse,  and  the  pus  detaches  the  dura  from  the  bone  and 
may  lead  to  necrosis.  When  the  sinuses  are  involved  in  pachymeningitis 
their  walls  undergo  thickening,  the  intima  is  roughened,  and  thrombi  form 
at  the  seat  of  the  lesion,  which  may  break  down  and  be  absorbed  or  give 
rise  to  emboli  or  pulmonary  infarctions. 

In  old  age  it  is  physiological  for  the  dura  to  be  thick,  leathery,  cartilagi- 
nous and  of  a  dull  white  color.     The  sheaths  of  the  arteries  are  thickened. 

Etiology. — Idiopathic  pachymeningitis  externa  is  of  doubtful  occurrence. 
Secondary  pachymeningitis  may  result  from  injuries  to,  and  caries  of  the 
cranial  bones  or  upper  cervical  vertebrae.  Hemorrhage  of  traumatic  ori- 
gin may  separate  the  dura  from  the  bone  and  be  followed  by  inflammation. 
Chronic  internal  otitis  and  suppurative  inflammation  of  the  orbit  may  lead 
to  it.  An  external  periostitis  maybe  followed  by  external  pachymeningitis 
without  apparent  intervening  bone-changes.  Inflammation  in  the  venous' 
sinuses,  especially  the  transverse  and  petrous,  may  lead  to  it,  especially 
when  the  thrombus  formed  undergoes  suppurative  changes. 


953  DISEASES   or   THE   IS-ERVOUS    SYSTEM. 

Symptoms. — The  symptoms  of  pachymeningitis  are  generally  very  ob- 
Bcnre.  After  an  injury  of  the  skull  or  a  chronic  otorrhoea,  we  may  sus- 
pect external  pachymeningitis  when  there  is  somnolence,  headache,  dizzi- 
ness, photophobia  followed  by  delirium,  and  perhaps  conyulsions  and 
coma.  In  cases  attended  by  thrombosis  of  a  sinus  there  will  be  hectic 
fever  and  rigors  and  symptoms  simulating  an  attack  of  intermittent  fever. 
When  metastatic  abscesses  develop  in  the  joints  and  internal  organs,  the 
headache  will  be  severe  and  localized,  and  possibly  attended  by  nausea  and 
vomiting.  If  there  is  cerebral  pressure,  the  pulse  becomes  slow  and  irregu- 
lar, rarely /regwew^  and  feeble ;  the  pupils  are  unequal;  the  headache, 
apathy,  and  somnolence  increase  and  are  attended  by  facial  paralysis.  Just 
before  death  the  pulse  slows  and  coma  is  developed.  Circumscribed  pain- 
ful oedema  behind  the  ear*  and  less  fulness  of  the  jugular  of  that  side  are 
indicative  of  thrombosis  in  the  transverse  sinus. ^ 

Differential  Diagnosis. — In  one  who  has  received  an  injury  of  the  skull, 
with  possibly  fracture  of  the  base,  if  the  signs  of  cerebral  compression  per- 
sist, pachymeningitis  externa  may  be  suspected.  With  caries  of  the  cranial 
bones  or  otitis  interna,  the  diagnosis  can  be  made  from  the  complicating 
cerebral  symptoms.  But  in  chronic  cases  the  symptoms  are  often  so  obscure 
that  a  positive  diagnosis  is  impossible. 

Prognosis. — Recovery  is  possible  and  depends  largely  upon  the  cause. 
Alcoholic  pachymeningitis  is  almost  invariably  fatal.  That  due  to  otorrhoea 
may  end  favorably  if  the  pus  is  evacuated  either  spontaneously  or  by  opera- 
tion. The  great  danger  is  in  extension  of  the  inflammation  to  the  internal 
layer  of  the  dura  mater  and  to  the  pia  mater. 

Treatment. — The  treatment  is  mainly  surgical.  Trephining  may  some- 
times save  life.  Rest,  a  mild  diet,  a  free  evacuation  of  the  bowels,  cold  to 
the  head  and  warmth  to  the  extremities  are  the  principal  means  of  treat- 
ment. Disease  of  the  ear  demands  immediate  attention.  I  recall  a  case 
where,  after  a  deep  coma  of  five  days'  duration,  recovery  unexpectedly  oc- 
curred after  a  copious  discharge  of  pus  from  the  ear.  Should  symptoms  of 
suppuration  be  well  marked,  alcoholic  stimulants,  quinine,  and  opium  are 
indicated  and  the  question  of  surgical  interference  will  present  itself. 

PACHYMENINGITIS    BSTTERNA. 

Pachymeningitis  interna  may  be  acute  or  chronic.  ^ 

Morbid  Anatomy. — In  acute  pachymeningitis  interna  the  inner  surface  of 
the  dura  mater  is  intensely  hypersemic  and  covered  with  a  layer  of  iibrin 
and  pus  which  may  be  circumscribed  or  diffused.  The  substance  of  the 
membrane  may  be  thickened  by  new  connective-tissue  developments  ;  but 
the  larger  part  of  the  inflammatory  exudation  is  upon  its  free  surface.  This 
form  of  pachymeningitis  is  apt  to  be  complicated  by  inflammation  of  the 
pia  mater.  In  chronic  pachymeningitis  interna  the  dura  is  covered  with  a 
layer  of  organized  tissue.     This  thin,  filmy  new  membrane  is  very  rich  in 

^  Oriesinger  calls  this  phlegmasia  alba  dolens  en  miniature.  2  Gerborett. 

^  Vircbow  was  the  first  to  interpret  and  classily  the  changes  which  take  place  in  this  inflammation. 


PACHYMENINGITIS    INTEENA. 


953 


large  capillaries  with  tkiii  walls.  It  is  composed  mainly  of  cells,  having 
very  little  basement  substance,  and  is  usually  most  abundant  at  ^-he  con- 
vexity of  the  brain. 

Some  pathologists  claim  that  before  these  changes  occur,  a  thin  layer  of 
compact  jfibrin,  which  can  readily  be  stripped  off,  occupies  the  site  where 


Fig.  193. 

Pachymeningitis  Interna. 

Vertical  Section  of  the  Skull  and  Cerebral  Meninges. 
^    SsctzoTh  of  tJhB  skull 
B.  Dura  mater  thicTcened  and  connected  intimately  with  C,  the  first  layer  of  the  inflammatory  deposit. 

D.  Deposit  of  pigrnent. 

E.  Svperftcial  layer  of  exudation  containing  an  hematoma  F,  caused  by  rupture  of  the  capillaries  m  trie 

highly  vascular  tissue. 
O.  A  second  and  superposed  hmmatoma  appearing  in  a  new  layer  of  exudation,     x  250. 

subsequently  a  hsematoma  is  developed.  The  capillaries  in  the  new  tissue 
are  easily  ruptured  and  hemorrhages  are  liable  to  occur,  forming  hsema- 
tomata,  ranging  in  size  from  small  clots  to  large  blood  sacs  covering 
the  whole  convexity.'  After  a  time  the  v^^alls  of  the  new  vessels  become 
thicker.  In  rare  instances  the  blood  extravasates  in  small  amounts  and 
is  absorbed,  and  only  a  thin,  transparent  well-defined  membrane  marks  the 
spot  where  the  pachymeningitis  existed. 

The  hsematoma  may  become  encysted  (Virchow's  hygroma  of  the  dura 
mater),  or  its  contents  may  undergo  caseous  and  calcareous  changes.^  In 
some  cases  the  blood  has  either  dissected  between  the  layers  of  the  wall 
of  the  hagmatoma,  or  else,  after  one  hemorrhage,  a  new  layer  of  pseudo- 
membrane  forms,  and  a  second  extravasation  is  followed  by  a  second  tis- 

'  In  oppopition  to  the  above  description,  Huguenin  states  that  a  thick  (one-twelfth  inch)  layer  of  fibrin 
forms  on  an  intact  dura.  This,  he  says,  is  rarely  demonstrable  ;  the  new,  yellow-stained  membranes,  in 
which  are  colorless  masses  (?  white  blood  corpuscles)  of  protoplasm,  form  later. 

"^  Rokitaneky  and  Forster. 


954  DISEASES    OE    THE    NERVOUS    SYSTEM. 

sue  formation.  The  ventricular  cavities  are  sometimes  filled  with  a  sero- 
sanguinolent  fluid. 

Etiology. — Both  acute  and  chronic  pachymeningitis  interna  are  usually 
secondary,  but  in  rare  instances  are  of.  idiopathic  origin.  The  acute  form 
may  be  secondary  to  pachymeningitis  externa,  pyaemia,  Bright's  disease, 
or  the  acute  infectious  diseases.  Chronic  pachymeningitis  interna  is  a 
disease  of  advanced  life,  rare  before  forty,  and  most  frequent  between  sixty 
and  eighty.  Chronic  alcoholismus  is  its  most  frequent  cause.  Atrophy 
of  the  brain,  hydrocephalus,  cerebral  tumors,  and  general  paralysis  and 
dementia  are  often  followed  by  pachymeningitis  interna.  In  progressive 
pernicious  anaemia,  hematoma  appears  in  thirty-three  per  cent,  of  all 
cases.'  Leucocytheemia,  the  hemorrhagic  diathesis,  scorbutus,  and  splenic 
anaemia  are  blood  states  especially  liable  to  be  accompanied  by  pachymen- 
ingitis. Valvular  diseases  of  the  heart  impairing  venous  return  and  athe- 
roma are  important  factors  in  its  causation. 

Symptoms. — The  symptoms  vary  with  its  extent  and  the  amount  of  the 
new  tissue  formation.  When  the  disease  is  slight,  there  are  no  symptoms  ; 
when  extensive,  most  of  the  symptoms  are  due  to  cerebral  pressure.  At 
first  there  is  constant  headache,  dizziness,  vertigo,  tinnitus  aurium,  mus- 
cse  volitantes,  photophobia,  constipation,  anorexia  and  insomnia,  with 
slight  febrile  movements.  The  intellect  is  impaired,  memory  fails,  and 
sometimes  there  will  be  a  temporary  loss  of  consciousness  and  partial  loss 
of  sjieech.  The  symptoms  of  slight  extravasation  simulate  very  closely 
those  of  a  small  cerebral  apoplexy.  The  pupils  will  be  contracted,  one 
more  than  the  other.  There  may  be  slight  wandering,  and  when  the  attack 
is  partially  recovered  from  the  mental  and  bodily  conditions  are  palpably 
impaired.  The  temperature  may  be  slightly  raised  and  attended  by  irreg- 
ular exacerbations  and  remissions.  The  pulse  is  slow,  becoming  irregular 
upon  excitement. 

Paralysis  comes  on  gradually,  as  one  hemorrhage  follows  another.  Be- 
tween the  attacks  localized  headache  is  the  prominent  symptom.  Some- 
times slight  epileptiform  convulsions  occur,  followed  by  temporary  loss  of 
consciousness.^  If  the  hemorrhage  in  the  new  tissue  is  rapid  and  exten- 
sive, patients  may  die  suddenly  from  cerebral  compression  ;  or  one  slight 
hemorrhage  which  gives  rise  to  few  symptoms  may  be  followed  by  a  second 
more  extensive  bleeding,  attended  by  the  ordinary  symptoms  of  apoplexy. 
Recovery  after  slight  hemorrhage  not  infrequently  occurs  :  but  the  patient 
afterward  will  be  troubled  with  more  or  less  constant  headache,  insomnia, 
and  perhaps  by  localized  paralysis.  Moderate-sized  htematomata  have 
been  found  at  autopsies,  where,  during  life,  no  signs  existed. 

During  the  course  of  acute  and  chronic  pachymeningitis  the  venous 
sinuses  may  become  involved  in  the  inflammatory  process,  causing  thrombi 
which  give  rise  to  pulmonary  or  other  infarctions,  attended  by  the  usual 
symptoms  :  rigors,  followed  by  a  temperature  of  103°  or  104°  F,,  with  ir- 

1  Huguenln. 

*  Pon  states  that  pachymeningitis  interna  begins,  often,  with  the  symptoms  of  the  general  paralysis 
of  the  insane  upon  one  side  of  the  body. 


PACHVMKJSIKGITIS    SYPHILITICA.  955 

regular  yariations.  The  pulse  at  first  is  rapid,  but  after  a  few  days  it 
becomes  slow.  As  the  case  approaches  a  fatal  termination  the  pulse  runs 
up  to  120  or  140,  and  is  small  and  feeble.  The  patient  becomes  delirious 
and  rapidly  passes  into  coma,  preceded  or  followed  by  convulsions. 

DiiFerential  Diagnosis. — The  diagnosis  of  pachymeningitis  interna  is 
always  difficult ;  it  may  be  confounded  with  acute  meningitis  of  the  con- 
vexity with  which  it  is  frequently  associated,  with  chronic  vieningitis,  and 
softening  of  the  irain.  The  diagnosis  of  a  haematoma  is  based  on  the  fol- 
lowing conditions,  viz. :  continued,  vertical,  localized  headache,  contracted 
pupils,  strabismus  or  ptosis,  very  slight  fever,  slow  pulse,  a  history  of  one 
or  more  apoplectic  seizures,  or  of  periods  of  loss  of  consciousness  followed 
by  dysphagia,  facial  paralysis  or  hemiplegia.  The  diagnosis  is  always 
problematical,  complicating,  as  it  does,  so  many  cerebral  affections,  and 
its  symptoms  are  masked  and  indefinite. 

Prognosis. — The  prognosis  is  bad,  although  the  course  of  the  disease  is 
usually  slow.  The  cerebral  symptoms  often  intermit.  Some  die  from  the 
extension  of  the  inflammation  ;  others  from  rapid  and  extensive  blood  ex- 
travasation ;  some  become  insane  or  demented  ;  the  larger  number  die  from 
intercurrent  disease.  When  the  venous  sinuses  are  involved  patients  may 
die  from  the  effects  of  the  inflammation  or  from  infarctions.  The  disease 
lasts,  in  most  cases,  from  one  to  three  weeks,  yet  one  day  and  one  year  are 
given  in  a  few  recorded  cases  as  the  limits  of  this  affection. 

Treatment. — There  is  no  cure  for  pachymeningitis  interna  :  all  that  can 
be  done  is  to  treat  symptoms.  Absolute  rest  in  a  cool,  quiet  room  is  to  be 
enjoined.  Irritative  or  inflammatory  symptoms  demand  cold  to  the  head, 
mild  counter-irritation,  and  heat  to  the  extremities.  The  bowels  are  to  be- 
kept  freely  opened,  and,  at  the  onset,  a  brisk  purge  may  be  given.  As  the 
disease  progresses  stimulants  and  a  highly  nutritious  diet  are  the  best 
means  to  combat  the  affection  ;  and  anodynes  may  be  necessary  to  induce 
sleep  and  relieve  headache.  Ergot  is  indicated  on  the  ground  of  its 
physiological  action  on  the  vascular  system,  to  prevent  or  diminish  future 
hemorrhages.  Eamskill  advocates  iodide  of  potash  as  the  chief  remedy,  but 
this  and  mercury  are  rarely  employed  at  the  present  day. 

PACHYMENINGITIS    SYPHILITICA. 

Pachymeningitis  syphilitica  is  a  form  of  meningitis  which  is  met  with  in 
the  advanced  stage  of  syphilis. 

Morbid  Anatomy. — Its  lesions  differ  from  the  other  forms  of  meningitis, 
in  that  the  inflammatory  product  is  circumscribed  in  the  form  of  gum- 
matous tumors,  which  are  composed  of  small  round,  oval,  and  pyriform 
cells  with  basement  substance.  Tiiese  gummatous  masses  may  degenerate 
and  become  cheesy,  or  be  converted  into  a  purulent-looking  fluid  consisting 
of  serum,  degenerated  cells,  and  granular  matter.  They  may  be  developed 
either  on  the  external  or  internal  surface  of  the  dura  mater,  and  are  usually 
multiple.  Accompanying  this  form  of  meningitis,  gummatous  masses  may 
develop  in  the  substance  of  the  cranial  bones  and  cause  more  or  less  de- 


956  DISEASES   OF   THE   IITERVOFS   SYSTEM. 

struction  of  them,  or  it  may  be  complicated  by  inflammation  of  the  pia 
mater,  and  then  gummy  masses  may  develop  beneath  the  pia  mater. 

Symptoms. — As  in  the  other  varieties  of  pachymeningitis,  persistent  local- 
ized headache  is  the  most  constant  and  prominent  symptom  ;  convulsions 
and  temporary  loss  of  consciousness  not  infrequently  accompany  the 
headache.  The  intellect  is  impaired,  and  the  patient  lapses  into  a  dull, 
stupid,  apathetic  condition.  They  may  be  wildly  delirious.  In  some  in- 
stances there  is  loss  of  sight  and  hearing.  If  the  gummatous  masses  attain 
a  large  size,  facial  paralysis  and  hemiplegia  may  occur.  I  have  known  a 
patient  with  syphilitic  pachymeningitis  to  become  hemiplegic,  pass  into  a 
state  of  complete  unconsciousness,  with  stertorous  breathing,  relaxed 
sphincters,  and  dilated  pupils,  remain  in  this  condition  for  ten  days,  and 
finally  completely  recover. 

Differential  Diagnosis. — The  diagnosis  rests  entirely  on  the  syphilitic  his- 
tory in  one  who  has  any  of  the  external  manifestations  of  syphilis  asso- 
ciated with  the  cerebral  symptoms  of  pachymeningitis. 

Prognosis. — The  natural  termination  of  this  disease  is  in  death.  If  these 
patients  are  subjected  to  proper  treatment  before  the  gummatous  masses' 
have  become  too  large  or  are  too  far  advanced  in  degenerative  changes,  re- 
covery is  almost  certain.  Eecovery,  however,  in  these  cases  is  rarely  per- 
manent, for  after  the  treatment  has  been  abandoned,  the  disease  is  apt  to 
return.  In  one  who  is  addicted  to  the  use  of  alcohol  the  prognosis  is  very 
unfavorable. 

Treatment. — The  treatment  is  that  of  advanced  sypliilis.  Mercury  and 
iodide  of  potassium,  either  together  or  alternately,  are  the  means  to  be  re- 
lied upon.  The  mercury  is  best  employed  by  inunctions  and  baths.  My 
rule  is  to  apply  each  day  a  drachm  of  strong  mercurial  ointment  in  the  ax- 
illa and  flexures  of  the  joints  until  its  specific  effects  are  produced.  Iodide 
of  potassium  must  always  be  given  in  large  doses  ;  from  thirty  to  sixty  grains 
may  be  given  in  from  four  to  six  ounces  of  water,  three  or  four  times  daily 
until  the  desired  effect  is  reached,  which  is  the  disappearance  of  the  cerebral 
symptoms.  Tonics  and  cod-liver  oil  are  always  indicated,  and  of  service 
between  the  periods  of  the  administration  of  the  mercurials  and  the  iodide. 
Under  no  circumstances  should  this  class  of  patients  be  allowed  to  use  stim- 
ulants habitually  in  any  form. 

CEREBEAL    THROMBOSIS   AND    EMBOLISM. 

The  cerebral  arteries  may  be  obstructed  by  emboli  or  thrombi,  the  cere- 
bral veins  and  sinuses  by  thrombi  only.  The  changes  in,  and  effects  pro- 
duced by  a  plug  in  the  cerebral  vessels,  whether  embolic  or  thrombotic  in 
its  origin,  are  identical  with  similar  changes  in  other  parts  of  the  body. 
The  walls  of  a  cerebral  artery  which  is  the  seat  of  thrombosis  are  usually 
thickened.  The  thrombosis  may  be  the  result  of  slowing  of  the  blood  cur- 
I'ent  from  any  cause.  The  results  and  symptoms  of  cerebral  thrombosis  are 
essentially  the  same  as  those  of  cerebral  embolism. 

Cerebral  emboli  may  be  bilateral ;  several  may  coexist ;  and  they  have 


CEREBRAL   THROMBOSIS   AND    EMBOLISM.  957 

been  found  in  all  of  the  cerebral  arteries.  The  left  middle  cerebral  is  their 
most  frequent  seat  (forty-six  in  one  hundred  cases) ;  next  the  internal  ca- 
rotid, the  basilar,  and  vertebral.  Ninety  per  cent,  are  in  vessels  that  sup- 
ply the  ganglia  at  the  base.  The  artery  of  the  corpus  callosum  is  rarely 
implicated.'  Embolism  in  the  cortex  is  rarely  attended  by  serious  results, 
on  account  of  the  free  anastomoses  between  the  cerebral  capillaries  and 
those  of  the  pia  matei". 

When  the  left  middle  cerebral  artery  is  plugged,  it  being  a  terminal  ar- 
tery with  no  anastomoses,  well-marked  symptoms  occur  and  destructive 
lesions  follow.  This  artery  has  the  most  direct  communication  of  any  of 
the  cerebral  arteries  with  the  left  ventricular  cavity.  This  anatomical  fact 
readily  explains  the  frequent  occurrence  of  embolism  in  it.  The  result  of 
cerebral  embolism  or  thrombosis  is  to  deprive  the  portion  of  the  brain  sup- 
plied by  the  obstructed  vessel  of  its  nutrition,  in  consequence  of  which  it 
degenerates  and  softens.  Softening  of  the  brain  is  the  usual  result  of  embo- 
lism ;  the  name  embolic  softening  has  been  applied  to  it,  to  distinguish  it 
from  inflammatory  softening.^  Niemeyer  describes  the  initial  result  of  em- 
bolism and  thrombosis  as  partial  anaemia  of  the  brain,'  and  states  that  the 
subsequent  softening  is  analogous  to  gangrene  in  the  extremities  induced 
by  obstruction  or  obliteration  of  the  vessels.  But  the  difference  is,  that 
within  the  skull  the"  absence  of  exposure  to  air  precludes  decomposition. 

If  a  large  cerebral  vessel,  or  a  large  number  are  obstructed  suddenly,  it 
may  cause  sudden  death,  and  there  will  be  no  time  for  cerebral  softening. 
Many  writers  include  in  the  signs  of  cerebral  embolism  those  of  the  first 
stage  of  softening. 

Symptoms. — The  symptoms  produced  by  the  plugging  of  cerebral  vessels, 
either  by  emboli  or  thrombi,  are  sudden  in  their  advent.  When  an  artery 
of  considerable  size  is  obstructed  there  is  temporary  loss  of  consciousness, 
the  patient  passing  rapidly  into  coma,  from  which  he  gradually  recovers 
•with  complete  hemiplegia.  If  only  a  small  branch  of  a  cerebral  artei'y  is 
plugged  there  may  be  only  a  slight  and  transient  loss  of  consciousness  or 
confusion  of  mind,  or  there  may  be  nothing  to  indicate  its  occurrence 
except  sudden  loss  of  speech.  During  the  period  of  loss  of  consciousness, 
if  it  occur,  the  face  is  pale  and  cold. 

Aphasia  is  common,  but  not  a  constant  attendant.  It  may  be  complete 
or  partial,  the  patient  may  be  able  to  use  only  one  or  two  words,  as  ''no" 
or  '"table,"  and  employs  them  to  answer  all  questions.  Again,  his  vocab- 
ulary may  consist  of  a  number  of  words,  but  he  cannot  use  them  aright ; 
he  calls  for  his  boots  when  he  intends  to  call  for  bread. 

Aphasia  may  be  of  two  kinds,  amnesic  or  ataxic.  Amnesic  aphasia  is 
where  the  memory  of  words  is  lost,  though  the  capability  of  uttering  them 
may  exist.     Ataxic  aphasia  is  where  the  muscles  and  parts  that  produce 

1  It  is  interesting  to  note  that  the  vertebral  was  oftenest  involved  in  the  large  number  of  cases  seen  by 
Nothnagel. 

2  Nothing  can  be  definitely  stated  concerning  embolism  and  thrombosi-:  of  the  capillaries  from  pigment 
(in  malaria),  leucocytes  (in  leukaemia),  and  from  fatty  granules  or  salts.  They  are  more  pathological  curi- 
oaities  than  well-defined  diseases. 

'  The  only  other  form  of  partial  cerebral  anicmia  is  from  collateral  oedema  about  spots  of  extravasa- 
tion. 


958  DISEASES   OF  THE  JSTEEVOUS   SYSTEM. 

articulate  speech  cannot  be  co-ordinated  ;  the  patient  knows  just  the  word 
he  wants  to  speak  but  he  cannot  utter  it.  The  ataxic  form  is  commonly 
associated  with  hemiplegia  of  the  right  side.'  In  ataxic  aphasia  a  patient 
can  read,  write^  and  listen  intelligently  to  the  speech  of  others.  In  amne- 
sic he  only  reads  and  understands  what  others  say.  After  repeated  attacks 
of  embolism  a  patient  may  have  both  amnesic  and  ataxic  aphasia. 

Within  twenty-four  hours  after  the  occurrence  of  a  cerebral  embolism 
there  may  be  conyulsive  movements  in  the  muscles  which  are  afterward  to 
be  paralyzed  ;  epileptiform  convulsions  frequently  occur.  If  the  patient 
pass  into  coma  he  may  continue  in  a  comatose  state  and  die  within  a  few 
days ;  or  he  may  recover  from  the  coma  with  permanent  hemiplegia 
and  aphasia.  There  may  be  temporary  improvement  in  the  hemiplegia, 
but  after  the  degenerative  changes  take  place  in  the  brain  the  hemi- 
plegia becomes  permanent.  In  most  of  the  cases  where  the  hemiplegia  is 
permanent  the  paralyzed  muscles  become  contracted.  When  the  hemi- 
plegia and  aphasia  are  partial,  and  there  has  been  no  loss  of  consciousness, 
complete  recovery  generally  takes  place.  A  cerebral  embolism  may  be  so 
slight  that  there  may  be  aphasia  for  a  few  days,  and  then  the  patient  will 
completely  recover  without  any  other  symptom. 

Hemiopia  and  unilateral  amaurosis  with  alternate  hemiplegia  are  symp- 
toms of  cerebral  embolism  ;  they  are  due  to  extravasations  into  the  optic 
nerve  and  to  embolism  of  the  arteria  centralis  retinae  on  the  corresponding 
side.  Embolic  amaurosis  may  precede  cerebral  embolism  for  a  few  days. 
The  ophthalmoscope  shows  pallor  of  the  papilla  and  absence  of  pulsation 
in  the  retinal  arteries.  Even  when  the  middle  cerebral  is  alone  occluded 
collateral  fluxion  may  cause  arterial  and  venous  hyj)er8emia  of  the  reti- 
nal vessels  and  congestion  of  the  optic  disc.  If  the  patient  does  not  begin 
to  improve  in  twenty-four  or  forty-eight  hours  after  embolism  occurs,  a 
fatal  issue  may  be  expected.  In  such  cases  the  temperature  rises  to  104° 
E.,  remains  at  that  point  for  a  couple  of  days,  and  then  rapidly  declines.' 
There  are  often  evidences  of  embolism  in  other  j)arts  of  the  body,  as  the 
spleen,  kidneys,  extremities,  etc.,  etc.,  which  will  aid  in  the  diagnosis. 

Bilateral  embolism  usually  results  from  separate  attacks.  These  cases 
are  marked  by  epileptiform  convulsions,  temporary  aphasia,  l>emiplegia,  or 
rarely  double  hemiplegia,  accelerated  and  irregular — perhaps  difficult — res- 
piration, unilateral  anaesthesia  of  the  conjunctiva,  and  normal  sensibilty 
of  the  cornea. 

Differential  Diagnosis. — Cerebral  embolism  and  thrombosis  often  cannot 
be  positively  distinguished  from  cerehral  hemorrhage.  The  symptoms  in 
some  cases  are  the  same.  If  the  hemiplegia  is  upon  the  right  side  and 
there  is  aphasia  the  probabilities  are  in  favor  of  embolism.  If  there  is 
no  aphasia,  and  the  loss  of  consciousness  is  prolonged  and  the  facial  paraly- 
sis is  marked,  cerebral  apoplexy  has  occurred.  If  the  paralysis  is  rapidly 
recovered  from,  it  indicates  embolism  and  not  apoplexy. 

Cerehral  thromhi  form  in  old  age  without  cardiac  or  pulmonary  disease, 

>  Ogle  states  that  in  left-lianded  individuals  the  centre  for  language  is  in  the  right  island  of  Eeil. 
*  Boumeville. 


CEEEBEAL  SOFTENTTTG.  959 

on  account  of  rigid,  calcified  and  atheromatous  arteries ;  the  paralysis  is 
less  marked,  and  aphasia  is  usually  incomplete.  If  the  j^aralysis  improves 
after  a  day  or  two  and  then  gets  worse,  it  indicates  embolism. 

Prognosis. — The  prognosis  will  depend  upon  the  size  of  the  artery  plug- 
ged ;  complete  recovery  is  always  possible,  partial  recovery  is  not  inf  i-equent. 
Still,  cerebral  embolism  and  thrombosis  are  serious  conditions,  on  account 
of  the  danger  that  they  will  lead  to  cerebral  softening.  The  prognosis  is 
usually  better  in  those  cases  where  the  hemiplegia  is  partial  than  when  it  is 
comjolete.  In  cases  wliere  the  symptoms  at  first  are  mild,  but  gradually 
grow  worse,  the  prognosis  is  unfavorable.  It  is  impossible  to  determine  the 
extent  and  duration  of  the  paralysis  which  sometimes  continues  after  its 
occurrence.  Chronic  visceral  diseases,  senility,  and  debility  or  anasmia  ren- 
der the  prognosis  unfavorable.  The  occurrence  of  coma  is  very  unfavorable. 
Even  after  rapid  disappearance  of  the  paralysis  and  aphasia  there  is  great 
danger  of  another  attack. 

Treatment. — The  plan  of  treatment  in  cerebral  embolism  and  thrombosis 
is  a  tonic  and  stimulant  one.  No  depletory  or  revulsive  measures  are 
ever  admissible.  The  action  of  the  heart,  and  the  constitutional  appear- 
ance of  the  patient  must  determine  whether  alcoholic  stimulation  is  to  be 
resorted  to  or  not.  In  cases  of  coexistent  cerebral  hyperaemia,  local  de- 
pletion may  be  of  service.  The  hemiplegia  is  to  be  treated  the  same  as  in 
cerebral  apoplexy.  Iron,  cod-liver  oil,  and  a  tonic  plan  of  treatment 
should  follow  the  disappearance  of  the  paralysis. 

CEREBEAL    SOFTEKING. 

Embolism  and  thrombosis  are  undoubtedly  the  most  frequent  causes  of 
cerebral  softening.  But  I  shall  adopt  the  view  that  there  are  several 
varieties  of  very  different  causation  and  anatomical  changes,  and  shall 
follow  the  usual  classification  of  red,  yelloio,  and  loliite  softening,  although 
this  division  is  somewhat  arbitrary  and  unsatisfactory. 

Morbid  Anatomy. — Red  softening  is  marked  by  punctate  redness  or  by 
numerous  minute  capillary  apoplectic  foci,  with  fatty  degeneration  of  the 
nerve  cells  and  fibres.  The  pultaceous  spot  is  deep  red,  shading  off  into 
the  neighboring  brain-tissue  with  no  distinct  limit.  There  may  be  several 
of  these  red  foci ;  as  many  as  twenty  have  been  found  in  different  stages 
of  discoloration  and  softening.  In  all  cases  the  centres  show  most  marked 
changes.  There  is  more  or  less  oedematous  swelling  of  the  adjacent  brain- 
tissue,  so  that  upon  cutting  into  it  the  softened  spot  will  rise  above  the  plane 
of  the  section.  The  vessels  are  enlarged,  often  from  proliferation  of  the  en- 
dothelium, forming  masses  of  varying  sizes,  frequently  within  the  vascular 
lymph-sheaths,  making  a  white  rim  visible  on  cross-section.  There  is  pro- 
liferation of  the  cellular  elements  of  the  neuroglia,  and  the  nerve-elements 
simultaneously  undergo  fatty  changes.  Few  pathologists  claim  that  any  in- 
flammatory exudation  accompanies  these  changes.  There  is  a  debris  in  and 
about  the  focus,  consisting  of  fat  granules,  altered  blood  corpuscles,  and  free 
nuclei,  a  few  pigment-granules,  shreds  of  brain-tissue,  and  large  granular 


960 


DISEASES    OF   THE   NERVOUS    SYSTEM. 


corpuscles.  ^    The  nerve  fibres  become  macerated,  and  their  white  substance 
is  coagulated  and  broken  up  into  large  masses.   There  is  varicose  hypertrophy 

of  the  axis-cylinders. 
This  condition  is  called, 
by  Hayem,  the  cloudy 
swelling  of  VircJioio. 
A  spot  of  red  soften- 
ing may  become  dry 
and  shrunken,  or  cica- 
trization may  occur. 
The  phenomena  of  ab- 
sorjotion  consist  in  fatty 
degeneration  and  casea- 
tion, or  the  formation 
of  a  cyst  by  a  process 
analogous  to  that  de- 
scribed under  the  head 
of  Apoplexy. 

Yellow  softening  is 
usually  the  result  of 
partial  cerebral  ansemia 
'from  obstruction  of  the 
cerebral  vessels.  It  may 
occur  in  any  portion  of 
the  brain,  but  most  fre- 
quently has  its  seat  in 
the  middle  or  posterior 
lobes,  and  in  the  cortex 
or  corpus  striatum.  Stasis  is  accompanied  by  all  the  changes  described 
as  occurring  with  an  infarction  which  is  followed  by  fatty  degeneration, 
and  it  may  proceed  very  slowly  or  with  great  rapidity  should  hemorrhage 
fail  to  occur.  The  coagulated  blood  in  the  vessels  undergoes  a  retrogres- 
sive change,  the  fibrin  becoming  granular.  Fatty  and  granular  matter 
in  large  quantities  surrounds  the  infarction,  which  becomes  dry  and  slowly 
contracts.  Corpora  amylacea,  blood-pigment,  and  crystals  from  the  al- 
tered fatty  material  are  found.  A  soft,  yellow-white  mass — often  of  a  sul- 
phur color — is  thus  formed,  varying  in  size  from  a  hazel-nut  to  an  orange. 
The  consistence  is  variable,  but  in  typical  cases  it  is  a  gelatinous,  moist, 
and  tremulous  pulp.  A  stream  of  water  will  readily  wash  out  the  focus  of 
softening.  These  degenerative  changes  proceed  until  the  focus  of  softening 
becomes  changed  into  a  mass  of  reticulated  fibres,  in  whose  meshes  is  a 
milky  fluid.  The  vessels  in  the  wall  of  this  cyst  are  covered  by  fat  granules, 
and  are  empty  or  contain  a  yellowish  clot ;  but  their  lymph-sheaths  are 
irregularly  dilated  with  pigment,  fatty,  granular  and  detached  endothelial 

^  Gluge's  corpuscles  are  large  spherical  cells,  filled  with  fat ;  they  are  abundant,  dark  by  transmitted 
and  bright  by  reflected  light.  The  origin  of  Gluge's  corpuscle,  so  prominent  in  yellow  softening,  is  as 
various  as  that  of  pus-cells. 


Fig.  194. 

Cerebral  Softening.  Elements  from  an  Apoplectic  Focus  in  Eed 
Softening. 

A.  Shreds  of  }wrve  fibres. 

B.  Altered  blood  corpuscles. 

C.  Fat  spherules. 

B.  Masses  of  myeline- 

E.  Free  nuclei frmn  neuroglia. 


X  300. 


CEREBRAL   SOFTENING. 


961 


cells.  In  this  form  of  softening  there  is  usually  a  faint  line  of  demarcation 
between  the  focus  and  healthy  brain-tissue.  The  color  of  yellow  softening 
is  due  to  fatty  changes  and  a  deposit  of  blood-pigment.  These  foci  may 
cicatrize  similarly  to  apo- 
plectic foci,  or  result  in 
the  formation  of  a  cyst. 
This  process  may  follow 
either  an  obstructive  or 
hemorrhagic  infarction. 
Eed  softening  may  also 
terminate  in  yellow  soften- 
ing.' 

White  or  atrophic  soft- 
ening is  the  form  met 
with  so  frequently  in  old 
age."  It  is  white  or  re- 
sembles healthy  brain- 
tissue;  the  process  is  a  slow 
one.  Hemorrhage  or  hy- 
persemia  is  rarely  present. 
It  is  usually  met  with 
in  the  white  matter  of  the 
hemispheres,  and  the  de- 
gree of  change  may  be  • 
BO  slight  as  to  render  its 
detection  difficult,  or  it 
may  be  soft  and  diffluent 
The  specific  gravity  of  the  softened  mass  is  less  than  normal  brain  sub- 
stance. White  softening  is  never  distinctly  limited,  but  shades  off  into  the 
adjacent  tissue.  In  chronic  softening  of  the  convolutions  their  form  ia 
preserved,  but  they  are  markedly  atrophied ;  over  them  the  pia  mater  is 
more  or  less  oedematous,  and  fills  up  to  a  certain  degree  the  space  caused 
by  the  atrophy.  Should  the  vessels  in  or  near  a  white  softened  patch  be 
examined,  they  will  usually  be  found  atheromatous  or  the  seat  of  end- 
arteritis. Thus  it  is  evident  that  the  color  has  no  relation  to  the  patho- 
logical changes.  Red  softening  may  come  from  embolism  ;  yellow,  directly 
from  thrombosis,  embolism,  or  be  a  second  stage  of  red  ;  white  may  be 
primary,  or  secondary  to  yellow.  In  every  case  the  cause  is  the  primary 
pathological  feature — the  color  is  secondary. 

Etiology.— Embolism  and  thrombosis  are  most  frequently  the  causes  of 
cerebral  softening,  especially  in  old  age.  It  is  essentially  a  disease  of  old 
age,  for  nearly  all  the  predisposing  causes  of  thrombosis  are  met  with  in 
advanced  life.     Thrombotic  softening  between  thirty  and  fifty  is  rare.    But 


Fig.  195. 

Cerebral  Softening.    Small  Blood-vessel  from  a  Focns  of 
Yellow  Softening. 

A  A.  Lumen  of  the  vessel  contairdng  the  remains  of  a  clot. 
BBB.  Irregmarly  dilated  lymph-sheath  containing  granulo- 
fatty  viatter  and  detached  e.ndothelia.     x  300. 


'  Rokitansky  flescribed  yellow  softening  as  occurring  in  well-developed  spots.  The  fluid  is  acid  in  re- 
action from  liberation  of  fatty  and  phosphoric  acids.  He  further  says  the  same  kind  of  softening  occurs 
about  adventitious  product-^  in  the  brain,  tumors,  clots,  etc.,  etc. — Path.  Anatomy. 

2  Durand-Pardel  and  Lancereaux  both  describe  mw,oWis.s«wie«i:  Wawc  as  the  last  stage  of  red  softening. 
Charcot  speaks  of  Us  frequency  in  old  people  with  cancer.— jlfa^.  des  Vieillards. 
61 


962  DISEASES    OF   THE   NERVOUS    SYSTEM. 

eirbolic  softening  may  occur  at  any  period  of  life  where  the  predisposing 
causes  of  emboli  exist.  Syphilis  and  chronic  alcoholismus  must  be  ranked 
next  to  embolism  and  age  as  causes.  It  has  been  shown  that  syphilitic 
disease  of  the  arteries  leads  to  softening.  Although  the  embolus  that  in- 
duces cerebral  softening  is  usually  cardiac  in  origin,  it  may  spring  from  an 
aneurismal  clot,  from  thrombosis  in  the  large  arterial  trunks,  or  originate 
in  gangrenous  or  carcinomatous  foci  in  the  lungs.  Cerebral  hemorrhage 
is  a  frequent  cause  of  softening,  and  it  may  follow  blows  on  the  head  or  ex- 
posure to  intense  cold  or  heat  (sun-stroke). 

It  is  well  established  that  any  new  growth  in  the  brain  is  accompanied 
by  a  zone  of  peripheral  yellow  softening.  Fevers,  the  exanthematous 
especially,  ulcerative  endocarditis,  necrotic  and  ulcerative  diseases  in  the 
lungs  and  bronchi  and  osteo-myelitis  have  led  to  softening,  but  are  more 
frequently  the  cause  of  abscess.  '  Glanders,  puerperal  diseases,  and  the 
toxic  action  of  mercury  and  lead  are  regarded  by  some  as  causes.^ 

Symptoms. — Inflammatory  red  softening  is  usually  attended  by  well 
marked  febrile  symptoms  ;  the  temperature  may  reach  102°  or  103°  F. 
The  pulse  is  accelerated  at  first,  but  afterward  it  becomes  slowed.  The 
face  is  flushed  and  the  pupils  irregular.  There  is  intense  and  persistent 
cephalalgia,  accompanied  by  dizziness,  vertigo,  and  somnolence,  and  fol- 
lowed by  confusion  of  mind,  delirium,  convulsions  and  stupor  or  coma. 
The  gait  is  tottering  and  speech  embarrassed.  At  first  there  is  hyperses- 
thesia,  formication,  itching,  and  neuralgic  pains.  Latex — with  the  paral- 
ysis— there  is  anaesthesia.  Vomiting  is  often  severe  and  obstinate.  Mus- 
cular twitchings,  contractions,  clonic  convulsions,  and  hemiplegic  symp- 
toms are  present  and  precede  coma.  Aphasia  may  accompany  these  symp- 
toms. If  meningitis  complicate  the  softening,  its  diagnosis  is  difiicult. 
The  softening  may  take  place  rapidly  and  be  accompanied  by  hemorrhage. 
In  such  a  case  apoplectic  symptoms  will  be  prominent.  Sudden  and  deep 
coma,  however,  may  occur  in  acute  softening  without  hemorrhage.  Death 
may  result  in  from  two  to  eight  days  ;  or,  recovery  may  rarely  occur  with 
more  or  less  permanent  paralysis. 

White  softening  is  oftenest  met  with  in  old  age,  and  is  usually  preceded 
by  despondency,  physical  weakness,  loss  of  memory,  and  inability  for  pro- 
longed mental  labor. ^  It  may  come  on  with  acute  symptoms,  or  insid- 
iously. Even  when  sudden  in  its  development  prodromata  may  have,  ex- 
isted very  like  those  of  apoplexy.  Diminution  in  the  motor  |)ower  is  often 
an  important  precursor  of  softening.  When  such  premonitions  occur,  the 
symptoms  either  gradually  increase  or  advance  by  sudden  exacerbations, 
with  intervals  of  apparent  improvement.  The  affected  side  becomes 
feeble,  the  hands,  feet  and  fingers  are  moved  awkwardly,  there  is  an  un- 
steady tottering  gait,  and  finally  complete  paralysis.  Death  may  result 
from  implication  of  the  respiratory  centres. 

Many  cases  are  ushered  in  by  the  symptoms  of  cerebral  thromiosis  or 

1  Reynolds  and  Bastian  state  that  red  softening  may  be  caused  by  "  prolonged  mental  exertion  or  ex- 
citement." 

2  M.  Rosenthal,  Dis.  of  Nervous  System,  vol.  1. 

'  Durand-Fardel  lay  stress  upon  monotony  of  word  or  gesture  as  a  valuable  diagnostic  sign. 


CEREBRAL   SOFTENING.  963 

embolism,  and  subsequently,  as  softening  slowly  progresses,  its  characteris- 
tic symptoms  are  developed.  In  tlie  aged,  prodromata  may  not  be  promi- 
nent, and  with  momentary  or  without  loss  of  consciousness  the  joatient 
becomes  suddenly  paralyzed  and  aphasic.  This  resembles  an  apoplectic 
seizure,  and  is  accompanied  by  headache  and  vertigo.  The  features  are 
symmetrical  until  attempts  at  exj^ression  are  made.  Again,  conviiUions 
may  occur  instead  of  an  apoplectiform  seizure,  or  delirium  may  be  promi- 
nent with  muscular  rigidity,  spasmodic  twitchings,  dysphagia,  and  suffu- 
sion of  the  eye.  Stupor  and  paralysis  seem  to  alternate.  The  urine  and 
fasces  are  passed  involuntarily,  and  the  patient  dies  from  exhaustion.  Bed- 
sores are  apt  to  form  about  the  buttocks. 

In  all  forms  of  softening  there  is  more  or  less  complete  hemiplegia  at- 
tended either  by  ansesthesia  or  hypersesthesia.  When  convulsions  occur 
they  are  followed  by  increasing  stupor  and  paralysis.  If  the  paralysis 
begins  at  the  fingers  or  toes  and  extends  toward  the  trunk  (creeping 
palsy),  it  is  the  chief  symptom  aside  from  the  failure  of  mind  and  mem- 
ory. After  a  time  these  patients  have  to  be  fed  and  watched  like  children  ; 
after  eating  they  sleep  until  they  are  aroused  again,  and  they  often  in  their 
actions  and  in  their  mental  capacity  appear  like  very  young  children. 

Differential  Diagnosis. — Eed  softening  may  be  mistaken  for  acute  men- 
ingitis. Acute  meningitis  is,  however,  attended  by  a  higher  temperature,  a 
peculiar  pulse,  more  intense  headache  and  vomiting,  and  is  marked  by  dis- 
tinct stages — headache,  delirium  and  coma.' 

Yellow  and  white  softening  may  be  confounded  with  chronic  meningitis 
a,nd  cerebral  tumor. 

In  softening  there  is  usually  a  history  of  cardiac  valvular  disease  or  of 
senile  atheroma.  There  is  well-defined  local  pain  in  cerebral  tumor, 
while  the  headache  in  softening  is  dull  and  diffused.  Speech  and  intel- 
lect are  less  affected  in  tumors;  they  are  both  markedly  implicated  in 
softening.  Permanent  facial  paralysis  is  usually  present  with  cerebral  tu- 
mors, and  absent  in  softening.  The  limbs  are  principally  involved  in  soft- 
ening. Epileptiform  convulsions  occur  far  more  frequently  with  tumors. 
The  symptoms  of  softening  are  usually  steadily  progressive ;  while  those 
of  tumors  are  irregular  and  of  longer  duration. 

The  diagnosis  between  the  varieties  of  softening  can  only  be  made  by 
the  previous  history  of  the  patient. 

Prognosis. — Acute  red  softening  may  lead  to  abscess,  or  be  a  rapidly 
fatal  complication  of  a  pre-existing  cerebral  disease  ;  death  is  rarely  de- 
layed beyond  the  tenth  day.  Chronic  softening  is  a  slowly  fatal  disease. 
Death  may  be  due  to  the  softening,  to  meningitis,  asphyxia,  pulmonary 
complications,  diarrhoea,  acute  bed-sores,  hemorrhage  into  the  softened 
spot,  or  to  exhaustion  and  anaemia. 

Treatment. — In  all  varieties  of  cerebral  softening  the  most  important 
thing  to  be  accomplished  is  to  improve  nutrition.  In  the  acute  variety  the 
patient  must  be  kept  quietly  in  bed  ;  cold  may  be  applied  to  the  head,  and 
mild  revulsives  to  the  extremities. 

In  threatened  chronic  softening — in  the  aged  especially — attention  is  to 


964 


DISEASES   OF   THE   NERVOUS   SYSTEM. 


be  paid  to  the  diet.  The  food  must  be  simple,  supporting,  and  very  easy 
of  digestion ;  the  best  article  of  diet  is  milk.  Excitement,  active  and 
prolonged  mental  or  physical  exertion  must  be  carefully  guarded  against, 
and  the  bowels  gently  moved  each  day.  Zinc,  phosphorus,  and  strychnia 
may  be  given  in  combination  with  iron  and  quinine.  The  constant  current 
alternating  with  the  Faradic  should  be  employed  on  the  paralyzed  limbs. 
For  the  relief  of  insomnia  and  the  nervous  phenomena  cannabis  indica 
combined  with  the  bromides  and  chloral  may  be  given.  Bed-sores  demand 
prompt  treatment,  for  they  frequently  hasten  the  fatal  issue.  Alcoholic 
stimulants  are  indicated  in  the  feeble  and  aged. ' 


CEEEBEAL    APOPLEXY. 


The  term  cerebral  apoplexy,  although  often  applied  to  a  somewhat  uni- 
form combination  of  symptoms  of  varied  causation,  will  be  confined  to  non- 
traumatic hemorrhage  into  the  cerebral  substance  or  meninges  and  the  re- 
sulting symptomatic  conditions. 


Fig.  196. 

Cerebral  Apoplexy. 

Horizontal  Section  of  the  Cerebrum  through  a  Clot  in  the  Left  Optic  Tract. 

A,  A.  Clots  from  hemorrhaqe. 

B,  B.  Area  of  tissue  stained  with  blood  pigment.    Lebert. 

Morbid  Anatomy. — Cerebral  hemorrhages  are  of  all  sizes,  from  minute 
capillary  extravasations^  to  large  clots  containing  several  ounces  of  blood, 

1  Cautery,  blisters,  etc.,  have  often  been  tried.  In  none  of  the  cases  did  benefit  ensue  ;  in  some,  actual 
increase  in  the  severity  of  the  symptoms  followed.  Dr.  Reynolds  regards  cod-liver  oil  as  "  the  most  valu- 
able agent  in  the  treatment  of  chronic  cerebral  softening."  Reynolds'  System,  art.  Softening,  by  Reynolds 
and  Bastian. 

*  Capillary  apoplexy  of  Cruveilhier. 


CEREBEAL   APOPLEXY.  965 

the  so-called  hemorrhagic  foci.  Preceding  the  hemorrhage  the  ruptured 
vessel  is  the  seat  of  miliary  aneurisms  due'  to  arterio-capillary  fibrosis,  which 
commences  in  the  perivascular  lymph-spaces,  and  extends  to  the  tunica  in- 
tima.  Globular,  saculated,  or  fusiform  dilatations  are  developed  in  vary- 
ing numbers,  which  are  generally  microscopic  in  size,  but  may  be  as  large 
as  a  pin-head,  and  through  their  ruptured  walls  hemorrhage  occurs.  Mi- 
nute extravasations,  however,  play  an  important  part  in  the  development 
of  apoplexy.  Such  foci  are  sometimes  the  result  of  venous  thrombosis,  and 
are  probably  soon  absorbed,  or  they  may  accompany  cerebral  softening,  as 
well  as  occur  in  the  neighborhood  of  large  aj^oplectic  spots.  More  rarely 
an  aggregation  of  these  pin-head  extravasations  forms  an  apoplectic  focus. 
In  capillary  hemorrhage,  the  lymph-sheath  may  remain  intact,  or  be  filled 
and  more  or  less  distended  with  blood.  Fatty  degeneration  of  the  walls  of 
the  central  vessel  usually  follows.  In  the  other  form  (hemorrhagic  focus), 
there  is  found,  on  autopsy,  a  clot,  varying  in  size  from  a  pea  to  a  hen's 
Gg^,  imbedded  in  the  cerebral  substance,  which  is  irregularly  spherical  in 
the  hemispheres,  but  in  the  motor  tracts  it  is  elliptical  or  irregular.  In 
some  cases  an  entire  hemisphere  is  ploughed  ujd  by  a  large  irregular  hem- 
orrhage, which  when  near  the  cortex  may  break  through  the  brain  sub- 
stance, dissecting  up  or  even  rupturing  the  pia  mater. 

The  most  frequent  locations  of  these  extravasations  are  the  intraven- 
tricular nucleus  of  the  corpus  striatum,  the  extraventricular  nucleus,  optic 
thalamus,  cerebellum,  and  pons— in  the  order  named.  The  corpus  stria- 
tum is  sometimes  pushed  up  and  surrounded  by  the  extravasation  ;  this  is 
made  out  most  distinctly  by  looking  into  the  ventricles.  The  ventricles 
themselves  may  also  be  filled  by  a  hemorrhage,  or  their  septa  torn  and  blood 
escape  upon  the  surface  of  the  brain.  In  the  aged,  apoplectic  foci  are  not 
infrequently  found  between  the  membranes,  in  the  meshes  of  the  pia,  or 
even  superficially.  When  extravasations  are  extensive  the  cerebral  convo- 
lutions are  flattened,  the  sulci  more  or  less  obliterated,  the  dura  is  tense, 
and  sometimes  there  is  visible  bulging  when  the  hemorrhages  are  super- 
ficial. The  adjacent  pia  mater  and  uninjured  brain  substance  are  anaemic 
from  pressure. 

A  recent  clot  is  a  soft,  grumous  mass,  composed  of  coagulated  blood  and 
brain  substance  in  varying  proportions,  at  whose  centre  is  the  opening  into 
the  ruptured  vessel.^  It  has  a  ragged  wall  of  cerebral  pulp,  more  or  less 
deeply  stained,  and  covered  with  fibrinous  material,  the  result  of  the  hem- 
orrhage. Surrounding  this  is  a  zone  of  discolored  oedematous  brain  sub- 
stance, studded,  in  many  cases,  with  capillary  hemorrhages. 

When  the  apoplectic  stroke  is  not  immediately  fatal,  the  following  changes 
may  take  place  in  the  clot :  (1)  the  fluid  parts  may  be  absorbed,  leaving  the 
solid  elements  to  undergo  secondary  changes  ;  (2)  the  clot  and  the  lacerated 
cerebral  tissue  surrounding  it  may  undergo  fatty  metamorphosis  and  be 
absorbed  ;  (3)  inflammation  may  occur  in  the  surrounding  brain  substance. 

1  Charcot  et  Bouchard  ;  Kouvelles  recherches  sur  V hemorrliaiie  cerebrate.    Arch,  de  Phys. 

2  Rokifansky  states  that  in  one  form  of  apoplectic  clot  the  fibrin  collects  near  the  centre,  and  in  another 
toward  the  periphery  of  the  mass.    Path.  Anatumy. 


966  DISEASES   OF   THE   NEEVOUS   SYSTEM. 

The  subsequent  changes  which  follow  the  absorption  of  the  fluid  portion  of 
the  clot  are  a  granular  and  fatty  degeneration  of  its  solid  constituents.  It  may 
then  go  on  to  caseation  and  subsequent  calcareous  change,  or  it  may  become 
encysted  by  the  development  of  new  connective-tissue  from  the  neuroglia", 
forming  a  firm,  smooth,  pigmented  cyst  wall, 'in  which  granular  and  fatty 
corpuscles  are  mingled  with  hsematoidin  crystals.  The  contents  of  this 
cyst  are  at  first  a  milky  or  dark  chocolate  fluid,  according  to  the  amount  of 
red  globules  present,  which  later  becomes  thick  and  creamy,  and  finally 
forms  a  firm,  hard  caseous  mass,  or  if  entirely  absorbed  there  remains  a  firm, 
or  friable,  pigmented  cicatrix.  Around  spots  of  capillary  hemorrhage,  the 
brain  is  softened  and  stained  ;  the  medullary  substance  of  the  nerve  fibref 
is  broken  up  and  intermingled  with  pigment  granules  and  red  and  white 
blood  corpuscles. 

Whether  a  cyst  must  have  existed  previous  to  the  formation  of  a  cicatrix 
is  a  question  still  in  dispute.  It  requires  from  six  months  to  two  years  fo^ 
the  cyst  to  be  absorbed  and  cicatrix  to  form.  There  may  be  a  number  ol 
these  in  the  same  brain,  corresponding  to  the  number  of  apoplexies.^  G-ran- 
ules  and  crystals  of  hsematoidin  are  found  between  the  adjacent  nerve  ele- 
ments and  in  the  perivascular  lymph-spaces,  when  the  deep  layers  of  the 
cortex  are  involved.  The  nerves  connected  with  the  motor  tracts  undergo 
degeneration,  and  connective-tissue  increase  takes  place  between  the 
atrophied  nerve  fibres.  These  degenerative  changes  after  a  time  extend 
into  the  spinal  cord,  and  general  atrophy  of  the  brain  may  follow.^ 

Etiology. — Apoplexy  is  rare  before  forty  years  of  age  ;  and  after  this  the 
tendency  steadily  increases.  Thus  age  is  the  most  powerful  predisposing 
cause.  When  it  is  stated  that  after  seventy  the  tendency  ceases,  the  small 
number  of  those  who  live  after  seventy  is  not  taken  into  account. 

It  is  now  generally  believed  that  miliary  aneurism  is  the  antecedent  state 
of  every  vessel  that  spontaneously  ruptures  within  the  cranial  cavity.  Peri- 
arteritis is  thus  a  powerful  predisposing  factor,  causing  arterio-sclerosis. 
Fatty,  atheromatous,  and  fibroid  degenerations  of  the  walls  of  the  vessels 
also  predispose  to  apoplexy.  Hence  the  importance  of  gout,  rheumatism, 
syphilis,  chronic  Bright's,  and  chronic  alcoholismus  as  predisposing  causes. 
Aortic  insufficiency,  pulmonary  emphysema,  and  left  ventricular  hyper- 
trophy are  important  etiological  factors.* 

I  have  already  spoken  of  the  liability  to  hemorrhage  in  leukasmia  and 
progressive  pernicious  anaemia.  Scorbutus,  typhus,  pyaemia,  malignant 
jaundice  and  chlorosis  are  conditions  in  which  the  blood  does  not  afford 
adequate  nutrition  to  the  vascular  walls,  and  they  are  then  easily  ruptured. 
Men  are  more  liable  to  apoplexy  than  women,  on  account  of  their  active 
mode  of  life  and  greater  liability  to  excitement.  Apoplexy  occurs  more  in 
winter  than  in  summer.  The  so-called  plethoric  habit  which  causes  so 
much  anxiety  has  little  significance,  for  the  emaciated  valetudinarian  is 

'  Forster  states  that  a  connective-tissue  wall  is  not  always  found,  even  when  death  does  not  occur.  Path, 
Anatomy. 
"^  Cruveilhier  states  that  he  found  fifteen  in  one  brain.    They  cause  thickening  of  the  brain. 

*  Diseases  of  Old  Age  ;  Charcot  and  Loomis,  N.  Y.    Wm.  Wood  &  Co.,  1881. 

*  Simple  ventricular  hypertrophy  is  a  physiological  condition  in  old  age.  . 


CEREBEAL    APOPLEXY.  967 

Just  as  liable  to  apoplexy  as  he  of  the  o]oposite  condition.'  "Whether 
atrophy  of  the  brain  can  produce  sufficient  dilatation  of  the  cerebral  ves- 
sels to  cause  rupture  is  uncertain.  Cerebral  softening  may,  by  affording 
less  support  to  the  vessels,  predispose  to  hemorrhage  ;  but  is  far  more  fre- 
quently a  result  than  a  cause  of  apoplexy. 

The  exciting  cause  of  cerebral  hemorrhage  is  usually  sudden  increase  in 
the  blood  pressure,  although  apoplexy  may  occur  without  any  such  in- 
crease. Coughing,  running,  a  fall,  sudden  mental  excitement,  straining  at 
stool  or  in  passing  urine,  bending  the  head  far  over  near  the  feet,  a  cold 
bath,  the  sexual  act  (especially  in  advanced  life),  large  ingestions  of  alcohol, 
sudden  stopping  of  bleeding  piles,  use  of  opium,  and  a  too  hearty  and 
indigestible  meal  may  all  induce  a  stroke  in  one  whose  arteries  or  arterioles 
are  diseased. 

Symptoms. — Preceding  an  apoplectic  seizure  there  may  be  premonitory 
symptoms.  Vertigo,  dizziness,  muscse  volitantes,  double  vision,  temporary 
blindness  due  to  retinal  hemorrhages,  tinnitus  aurium,  flushing  or  pallor  of 
the  face,  nausea,  an  abnormally  keen  sense  of  smell,  or  a  total  loss  of  it,  are, 
some  of  them,  present  in  a  certain  proportion  of  cases.  Epistaxis  in  one 
past  middle  life  is  an  important  and  dangerous  larodromal  symptom.  These, 
however,  are  unimportant  compared  with  loss  of  memory,  tremor,  or  neu- 
ralgic pains,  irregular  or  retarded  heart  action,  difficulty  and  thickness  of 
speech,  lethargy,  stupor,  change  in  temper  and  sense  of  weight,  numbness 
or  formication,  which  very  often  are  present  before  an  apoplectic  seizure, 
and  must  always  excite  alarm  whenever  they  occur  in  one  past  middle  life. 
Partial  facial  palsy  is,  by  some,  regarded  as  a  noteworthy  precursor. '■^  In 
many  cases  none  of  these  premonitory  symptoms  are  present,  but  the  seiz- 
ure is  sudden,  the  patient  rapidly  passing  into  a  state  of  coma.  In  others 
the  comatose  state  comes  on  gradually,  and  is  preceded  by  pains  in  the  head 
and  a  feeling  of  faintness.  In  rare  instances  hemiplegia  and  aphasia  are 
the  primary  symptoms.  Convulsions  usher  in  the  attack  when  large  hemor- 
rhages occur  into  the  meninges.  With  very  small  hemorrhages  there  may 
be  only  momentary  insensibility  ;  the  patient  recollects  everything,  though 
not  clearly,  and  those  about  him  pronounce  it  a  fainting  fit,  or  bad  attack 
of  indigestion,  as  it  frequently  comes  on  after  over-indulgence  at  the 
table. 

Usually  the  coma  is  sudden  and  complete,  and  lasts  from  a  few  hours  to 
two  or  three  days.^  During  this  coma  the  respirations  are  deep,  slow, 
stertorous,  and  accompanied  by  a  puffing  sound  ;  sometimes  the  face  is  pale, 
but  more  commonly  it  is  red,  swollen,  and  turgid,  and  as  the  coma  deepens 
it  assumes  a  dusky,  livid  hue.  Pallor  may  continue  throughout  the  attack 
when  the  hemorrhages  are  gradual.  If  the  coma  lasts  from  forty-eight  to 
seventy-two  hours  the  temperature  is  lowered  on  the  second  day  in  some 

1  If,  as  H.  Jackson  supposes,  there  Is  an  hereditary  tendency  to  apoplexy,  it  must  be  transmitted  through 
arterial  disease. 

*  Trousseau  and  Hughlings  .Jackson. 

3  Apoplectic 'coma,  according  to  Niemeyer,  Hutchinson,  and  others,  is  due  to  anaemia  produced  by 
presi^ure  upon  the  capillary  vessels.  This  only  holds  good  for  large  hemorrhages  ;  and  small  hemorrhages 
sometimes  produce  coma. 


968  DISEASES   OF   THE    NERVOUS    SYSTEM. 

instances  to  96°  F.  The  third  day  it  not  infrequently  rises.  The  pulse, 
at  the  onset  of  the  attack,  is  slow  and  irregular  ;  later  it  becomes  frequent 
and  more  regular.  The  pupils  are  seldom  normal ;  they  may  be  dilated, 
or,  in  meningeal  apoplexy,  contracted.  Inequality  of  the  pupils  is  of  much 
more  serious  import  than  equal  dilatation  or  contraction.  Sometimes  when 
the  pupils  are  small,  they  quickly  enlarge  upon  rousing  or  disturbing  the 
patient.  The  patient  may  be  unable  to  swallow,  the  features  become  dis- 
torted, and,  as  the  paralysis  deepens,  the  pupils  dilate ;  the  skin  becomes 
cold  and  clammy,  and  the  urine  and  fseces  are  passed  involuntarily.  An 
apoplectic  patient  may  lie  apparently  dead,'  yet  even  in  such  cases  sudden 
death  is  rare.^  Eeflex  movements,  except  at  the  very  onset,  may  nearly 
always  be  excited,  often  more  readily  than  during  health.  Convulsive 
movements  during  the  coma  are  rare.  Hemorrhages  into  the  pons  and  me- 
dulla, implicating  the  roots  of  the  pneumogastrics,  are  generally  followed 
by  death  in  a  few  hours.  The  side  that  is  subsequently  paralyzed  may  show 
convulsive  movements  from  the  commencement,  and  tetanic  spasms  in 
sets  of  muscles  or  in  single  muscles  occasionally  occur.  In  many  cases 
the  head  and  both  eyes  are  turned  toward  the  healthy  side  for  a  short 
time. 

After  the  coma,  consciousness  returns  slowly  ;  and  in  from  forty-eight  to 
seventy-two  hours  headache,  restlessness,  wandering  or  delirium  may  come 
on.  A  slight  febrile  movement,  increase  of  the  pulse-rate  and  respiration, 
confusion  of  the  mental  faculties,  and  contraction  of  the  flexor  muscles, 
indicate  the  occurrence  of  inflammatory  changes  in  and  about  the  clot. 

Hemiplegia  upon  the  side  opposite  to  the  hemorrhage  is  one  of  the  most 
constant  attendants  of  apoplexy,  especially  in  the  aged.  It  may  be  accom- 
panied by  anaesthesia,  but  it  is  rarely  present  without  hemiplegia.  The  hem- 
iplegia is  permanent  or  temporary,  according  to  the  extent  and  location  of 
the  clot.  As  recovery  takes  place  the  thick  speech,  retracted  mouth, 
deviation  of  the  tongue,  and  other  evidences  of  facial  paralysis  gradually 
disappear.  The  leg  also  gains  more  or  less  in  strength,  but  the  arm  is 
permanently  paralyzed.  This  is  more  favorable,'  however,  than  when  the 
arm  recovers  and  the  leg  remains- paralyzed.  Sometimes  the  face  remains 
semi-paralyzed  after  the  other  signs  of  paralysis  have  disappeared.  *  Mus- 
cular contractures,  which  relax  during  sleep,  of  varying  intensity,  are 
rarely  absent. 

Diminution  of  electrical  excitability  is  the  rule  ;  and  the  temperature 
of  the  paralyzed  limb  is  below  normal.  The  muscles  are  either  hard  and 
rigid,  or  weak  and  flaccid.  They  always  show  reflex  excitability.  An- 
aesthesia soon  passes  away  ;  but  it  is  claimed  that  sensation  is  never  as 
perfect  on  the  paralyzed  as  on  the  non-paralyzed  side.  Though  anaes- 
thesia and  paralysis  are  commonly  distributed  over  the  same  region,  the 

>  Nothnagel. 

2  Wilks  :  Gm/s  Hosp.  Beiioris,  178,  1866. 

3  Trousseau. 

*  Total  loss  of  motor  power  is  called  paralysis ;  partial  loss  is  called  paresis.  Gubler  describes  some 
interesting  cases  of  crossed  or  alternate  paralysis,  where  a  left  arm  and  a  right  leg,  etc.,  were  paralyzed. 
A  few  cases  of  paralysis  of  the  facial  alone  and  of  the  musculo-spiral  alone  have  been  recorded. —  Union 
Medicate,  1854. 


CEREBKAL   APOPLEXY. 


969 


former  is  usually  confined  to  the  track  of  certain  nerves.'  Sometimes  the 
paralyzed  parts  are  hypereesthetic,  the  pain  being  diffused.'"  The  organs 
of  special  sense  are  rarely  involved.  Sight  and  hearing  may  be  altered, 
upon  increase  of  intracranial  pressure.  Hemiopia  is  not  uncommon. 
Paralysis  of  the  olfactory  is  rare ;  but  when  the  chorda  tympaui  is  aifected 
taste  may  be  abolished  on  the  fore  part  of  one  side  of  the  tongue. 

On  the  second  or  fourth  day  after  the  apoplectic  seizure  erythematous 
patches  may  appear  in  the  sacral  region  on  the  paralyzed  side.  Excoria- 
tion then  occurs,  and  the  acute  bed-sore,  the  most  important  of  the  trophic 
changes,  appears  as  a  dry  brown  crust.  The  eschar  may  slowly  extend  to 
the  sound  side.^  The  intellect  rarely  remains  as  clear  as  before  seizure, 
and  the  disposition  changes.  The  memory,  especially  for  recent  events, 
is  markedly  impaired,  and  the  will-power  is  greatly  diminished.     Some- 


Fig.  197. 
Vertical  Transverse  Section  of  the  Brain  through  the  Optic  Thalamus. 

A,  A.  Motor  tracts  of  the  cortex  ce7'eb7'i. 

B.  Optic  thalamus.  ^     ^  ^, 

C.  Radiation  of  internal  capsule  to  tlie  motor  tracts  of  the  cortex. 

D.  Lenticular  nucl£us. 

E.  Claustrum. 

F.  Caudate  nucleus.  Charcot. 

times  complete  imbecility  follows  an  apoplexy.  In  the  very  aged  there  is 
a  form  of  apoplexy  that  is  seemingly  associated  with  hemorrhage  into,  or 
rupture  of,  the  walls  of  the  ventricles ;  it  is  accompanied  by  a  general 

>  Tiirck  states  that  anaesthesia  is  permanent  when  the  inner  part  of  the  lenticular  nucleus,  tlie  super- 
ficial portions  of  the  thalamus  opticus  and  the  ad.ioiniu-  portions  of  the  corona  radiata  are  involved.  The 
anaesthesia  is  also  permanent  in  lesions  of  the  pons  and  peduncles. 

2  Charcot  has  laid  stress  on  the  arthritic  pains  that  occur  in  the  paralyzed  limhs  (spontaneous),  and 
Brown-Sequard  on  the  neuralgic  pains  that  are  so  troublesome  during  damp,  cold  weather.  The  joints 
are  swollen,  hot  and  moist,  and  there  is  pain  on  motion.  _ 

3  Some  claim  that  these  eschars  depend  upon  trophic  iniluences  due  to  local  hyperaemia.  Charcot 
states  that  they  are  due  to  irritation  of  trophic  centres  in  the  brain.  Most  authorities,  including  Charcot 
and  Nothnagel.  ascribe  little  influence  to  vaeo-motorial  changes.- CAarcoC,  Legons  sur  les  Maladies  du 
System  Nerveux.    Paris,  1872. 


970  DISEASES   OF   THE    NERVOUS    SYSTEM. 

epileptiform  attack,  lasting  from  fifteen  to  thirty  minutes,  during  which 
the  tongue  is  bitten  and  frothing  at  the  mouth  occurs.  This  is  followed, 
apparently,  by  no  serious  results,  other  than  the  gradual  development  of 
extreme  debility.  Death,  however,  usually  occurs  after  a  longer  or  shorter 
period,  which  varies  with  the  age  and  constitution  of  the  patient. 
Localization  of  cerebral  lesions. 

I.  Hemorrhage  into  the  motor  ganglia — corpus  striatum^  and  lenticular 
nucleus — occurs  in  nearly  seventy  per  cent,  of  all  apoplexies.  It  is  attended 
by  hemiplegia,  partial  paralysis  of  the  face,  some  ansesthesia,  and  slight 
ocular  disorders  and  perversions  of  the  special  senses.  Intelligence  is  modi- 
fied, memory  chiefly,  and  there  may  follow  hemi-chorea  and  athetosis.'' 
The  head  is  turned  from  the  paralyzed  side.  To  say  whether  the  lenticu- 
lar nucleus  or  the  nucleus  caudatus  is  alone  involved  is  impossible. 

II.  When  the  thalamus  opticus  is  alone  involved  there  is  angesthesia 
and  no  motor  paralysis.  No  points  (yet)  known  are'  indicative  of  exclu- 
sive implication  of  this  ganglion.' 

III.  Lesions  of  the  cortex  are  most  interesting  from  their  diverse  mani- 
festations, and  from  the  study  and  experimentation  that  have  been  ex- 
pended upon  this  subject."  The  motor  zone  of  the  cortex,  however,  em- 
braces the  anterior  and  posterior  central  convolutions  and  the  lobulus 
paracentralis.  Hemiplegia,  in  nowise  differing  from  that  due  to  lesions 
of  the  nucleus  lenticularis,  may  arise  from  hemorrhage  into  this  part. 
Aphasia,  both  ataxic  and  amnesic,  follows  destruction  of  the  island  of  Reil, 
or  of  the  third  left  frontal  convolution.  Hemorrhage  into  \hQ paracentral 
lohule  is  followed  by  paralysis  of  the  arm  and  leg  of  the  opposite  side.* 
Following  cortical  lesions  there  appear  convulsive  epileptiform  movements 
in  certain  groups  of  muscles,  or  in  single  muscles  called  "  partial  epilepsy 
of  cortical  origin." 

IV.  Extensive  cortical  hemorrhage  is  usually  associated  with  more  or 
less  meningeal  apoplexy,  and  is  to  be  distinguished  from  pachymeningitis. 
The  seat  of  meningeal  hemorrhage  may  be  at  the  base  or  convexity,  or 
spread  over  both  hemispheres.  The  symptoms  in  children  are  somno- 
lence, spasms  and  tremor.  Death  usually  occurs  rapidly  with  convulsions, 
dyspnoea  and  sudden  attacks  of  vomiting.''  In  the  adult  death  often  oc- 
curs very  suddenly,  and  most  cases  of  sudden  death  from  apoplexy  are  at- 
tended by  meningeal  hemorrhage.  Eupture  of  the  posterior  communica- 
ting artery  is  preceded  by  signs  of  compression  of  the  third,  fifth  and 
sixth  cranial  nerves.'' 

V.  Hemorrhage  into  the  pons  is  commonly  followed  by  coma  and 
speedy  death.     Convulsions  attend  the  passage  of  blood   into  the  fourth 

'  The  caudate  nuclevs. 

2  Top.  Diagnos.  d.  Gehirnkt.  Nothnagel,  1879. 

s  Hammond  and  Luys  alone  state  that  aberrations  of  the  special  senses  follow  lesions  of  this  part  of  the 
brain. 

*  Charcot  and  Pietres  state  that  destruction  of  the  infr.  parietal  lobe,  angular  gyrus,  of  the  anterior 
portion  of  the  first,  second  and  third  frontal  convolutions  produces  no  motor  paralysis. 

'•  M.  Rosenthal  states  that  psychical  disturbances  play  the  chief  part  in  cortical  (hemorrhagic)  lesions. 

*  Wiirt.  Med.  Corblatt  Elsasser. 
''  Gougoucnheim. 


CEKEBRAL   APOPLEXY.  971 

ventricle.  Incomplete  parajolegia,  facial  paralysis,  at  times  on  the  same, 
at  others  on  the  opposite  side  to  the  lesion,  contracted  pupils  that  do  not 
respond  to  light,  disorders  of  taste,  smell,  or  hearing,  indicate  ajooplexy  in 
the  median  portion  of  the  jDons.  Sometimes  hemorrhage  into  the  pons 
attended  by  slight  spasms  is  followed  by  partial  hemiplegia,'  or  by  irregu- 
lar and  difficult  breathing.  Besides  crossed  paralysis,  we  may  find  hemi- 
plegia, paraplegia  and  paralysis  of  all  the  extremities,  with  or  without 
facial  paralysis  ;  or  double  facial  ]3aralysis  with  hemiplegic  phenomena.^ 
The  mental  symptoms  are  few,  if  any.  Angesthesia  is  common  ;  and  may 
be  crossed  also.  All  authorities  note  that  articulation  is  more  difficult 
and  paralysis  of  the  abducens  is  more  likely  to  occur  with  this  than  with 
any  other  brain  lesion. 

yi.  Hemorrhages  into  the  anterior  lobe  are  commonly  attended  by  hemi- 
plegia, incomplete  paralysis  of  the  face,  and  when  on  the  left  side  by 
aphasia. 

VII.  Hemorrhage  into  the  middle  lobe  is  attended  by  amblyopia,  con- 
gestion of  the  retinal  veins,  and  injection  of  the  optic  papilla.^  Nausea, 
dizziness  and  headache  often  occur. 

VIII.  Hemorrhage  into  ihe  posterior  lobe  is  marked  by  intellectual  dis- 
turbances, and  usually  by  the  absence  of  motor  and  sensory  disturbances. 
When  hemiplegia  occurs  its  tendency  is  to  gradually  disappear.  Frequently 
no  symptoms  attend  a  hemorrhage  into  the  substance  of  the  cerebral 
lobes. 

IX.  In  hemorrhage  into  the  cerebeUur)i  vomiting  is  a  prominent  symp- 
tom.* Although  it  is  W\q,  great  co-ordinating  ganglion,  clots  in  the  cerebel- 
lum rarely  produce  disturbance  of  co-ordination.  Sensibility  is  never  dis- 
turbed, but  there  is  pain  in  the  hach  of  the  head.  Sometimes  the  eyes  are 
rolled  about  incoordinately,  and  amaurosis  and  amblyopia  occur.  In 
hemiplegia^  from  hemorrhage  into  the  cerebellum  there  is  no  lingual  or 
facial  paralysis,  though  there  is  loss  of  facial  expression.  The  patients 
can,  and  do,  lie  only  in  one  position ;  when  they  are  moved  they  immedi- 
ately return  to  it. 

X.  Hemorrhage  into  the  lateral  cerelellar  loies  is  attended  by  obstinate 
headache,  vertigo,  vomiting,  amblyopia,  amaurosis,  dilatation  of  the  pupils, 
thick  and  difficult  speech,  and  by  hemiplegia  on  the  opposite  side."  Should 
the  hemorrhage  encroach  upon  any  of  the  great  centres,  the  symptoms  will 
be  more  pronounced.  Injury  of  the  cardio-inhibitory  centre  would  be  in- 
dicated by  irregular  heart  action,  a  condition  that  frequently  occurs. 

XI.  When  the  crura  of  the  cerebellum  are  involved,  the  symptoms  resem- 
ble those  of  hemorrhage  into  the  cerebellum  ;  most  modern  pathologists, 
ascribe  all  the  symptoms  of  cerebellar  hemorrhage  to  lesions  of  the  crura. 

1  Gubler  and  Luys  state  that  crossed  paralysis  is  always  attended  by  apoplexy  in  the  pons.    Exceptions 
have  occurred,  however. —  TrovMeau,  Clin.  Med. 

*  Brown-Seqnard. 

3  White  spots  in  its  centre  were  noted,  in  addition  to  the  amaurosis,  in  Hughlings- Jackson's  cases. 
— ReyrKjldn'  System  of  Med. 

*  Berliner  Klinische  Wochenschrift.—Renvak.  1865. 

*  iMndon  Lancet,  Nov.  2, 1861. 

8  Rosenthal,  Dis.  of  Nervous  Sys.  vol.  i.,  p,  50-60. 


072  DISEASES    OP   THE   NERVOUS    SYSTEM. 

The  patients  are  sometimes  forced  to  rotate  about  the  long  axis  of  the  body, 
in  some  cases  toward,  in  others  from,  the  paralyzed  side. 

XII.  Hemorrhage  into  the  cerebral  peduncle  is  attended  by  hemiplegia 
and  alternating  facial  paralysis,  and  by  ptosis,  mydriasis,  and  diyerging 
strabismus  on  the  same  side. 

XIII.  Destruction  of  the  corpora  quadrigemina  leads  to  blindness  and 
the  pupils  become  fixed. 

XIV.  When  the  medulla  oblongata  is  'involved,  the  symptoms  are  the 
same  as  those  due  to  injury  of  the  pons.  In  addition  there  is  diabetes  and 
albuminuria  in  many  cases.  Grlosso-pharyngeal  and  hypoglossal  paralysis 
cause  dysphagia  and  loss  of  power  to  protrude  the  tongue  ;  dyspnoea,  ir- 
regular heart  action,  and  gastric  derangements  arise  from  implication  of  the 
pneumogastric. 

XV.  Finally,  when  hemorrhage  occurs  into  the  ventricles,  death  is  usu- 
ally rapid.  Eecovery  is  possible,  however.'  Spasms  and  contractions  of  the 
paralyzed  extremities  occur  in  many  of  these  cases. 

Differential  Diagnosis. — Apoplexy  may  be  mistaken  for  cerebral  congestion, 
urmmia,  alcoliolic  coma,  cerebral  embolism,  opium  poisoning,  epileptic  and 
hysterical  coma. 

Stertorous  breathing — a  common  symptom  in  apoplexy — is  absent  in  cere- 
bral congestion.  The  pupils  are  alike  in  congestion;  in  apoplexy  they  are 
unequal.  The  coma  is  of  short  duration  in  congestion  ;  in  apoplexy  it 
persists  for  some  time.  Congestion  has  a  long  prodromal  period;  in  apo- 
plexy this  is  short  or  absent.  Should  paralysis  be  present  from  congestion, 
it  is  usually  bilateral;  while  in  apoplexy  hemiplegia  is  more  or  less  complete. 

The  mental  faculties  are  rapidly  and  completely  restored  after  an  attack 
of  apoplectiform  congestion,  while  the  reverse  is  the  case  in  apoplexy. 

In  urmmia  the  previous  history  of  the  patient  is  important,  and  there  is 
more  or  less  oedema.  Hemiplegia  is  never  present  in  ursemia  ;  it  is  rarely 
absent  in  apoplexy.  Ursemic  coma  comes  on  gradually  and  is  usually  pre- 
ceded by  convulsions;  while  the  coma  of  apoplexy  is  more  sudden  in  its  ad- 
vent, and  is  followed  rather  than  preceded  by  convulsions.  Casts  and  al- 
bumen in  the  urine  are  strong  presumptive  evidences  of  ur^emic  coma. 

Profound  alcoholic  intoxication  is  often  mistaken  for  apoplexy.  A  pa- 
tient can  be  roused  from  alcoholic  coma,  but  not  from  apoplectic.  There  is 
no  stertorous  breathing  in  alcoholic  coma  ;  while  this  is  rarely  absent  in  apo- 
plexy. The  pulse,  in  alcoholic  coma  is  feeble  ;  in  apoplexy  it  is  full,  strong 
and  slow.  There  is  no  hemiplegia  in  alcoholismus,  and  the  urine  as  well 
as  the  contents  of  the  stomach  will  contain  alcohol. 

The  diagnosis  between  apoplexy  and  cerebral  embolism  is  often  difficult. 
Both  may  be  preceded  by  rheumatic  endocarditis  and  valvular  disease  of 
the  heart,  although  they  are  more  frequent  in  embolism  than  in  apo- 
plexy. In  embolism  there  is  rarely  complete  loss  of  consciousness  ;  and  if 
it  occur  it  is  of  short  duration  ;  while  loss  of  consciousness  is  the  rule  in 
apoplexy,  and  it  usually  continues  for  two  or  three  days.  The  pulse  in  em- 
bolism is  feeble  and  frequent,  and  the  face  is  pallid  ;  while  in  apoplexy  the 

1  Diseases  of  Old  Age  ;  Charcot  and  Loomis,  New  York,  1881. 


CEREBKAL   APOPLEXY.  973 

pulse  is  slow  and  full,  and  the  face  is  suffused.  Aphasia  is  the  rule  in  em- 
bolism and  the  exception  in  apoplexy.  The  pupils  are  unchanged  in  em- 
bolism ;  while  in  apoplexy  they  may  be  dilated,  contracted,  or  unequal. 
The  respiration  is  normal  in  embolism  and  stertorous  in  apoplexy.  There 
is  usually  right-side  hemiplegia  in  embolism;  if  left  side  hemiplegia  exist, 
it  is  probably  due  to  cerebral  hemorrhage.  Arterial  degeneration  is  always 
present  in  apoplexy  ;  while  in  embolism  the  arteries  may  be  normal.  The 
paralysis  is  temporary  in  embolism  and  recovery  is  comj)lete ;  while  in 
apoplexy  it  is  delayed,  and  recovery  is  partial.  Vomiting  is  a  far  more 
prominent  symptom  of  apoplexy  than  of  embolism.  Embolism  is  probable 
when  hemiplegia  occurs  suddenly  in  the  young;  apojDlexy  is  a  disease  of 
middle  and  advanced  life.  Premonitory  cerebral  symj)toms  are  never  pres- 
ent in  embolism  ;  they  may  be  in  apoplexy. 

Opium  poisoning  gives  many  of  the  symptoms  of  apoplexy.  Apoplexy 
is  usually  accompanied  by  dilated  or  irregular  pupils  ;  opium  always  pro- 
duces regular  and  generally  pin-head  pupils.  Convulsions  may  attend 
apoplexy  ;  they  are  absent  in  opium  i3oisoning.  The  coma  comes  on  more 
gradually,  and  is  not  usually  as  deep  in  opium  poisoning  as  in  aj)oplexy. 
An  exceedingly  slow  pulse  and  respiration  indicate  narcotic  poisoning. 
Stertor  and  liemiijlegia  attend  apoplexy,  and  the  pulse  may  be  irregular. 

The  coma  of  epilepsy  may  be  confounded  with  that  of  ajjoplexy ;  but 
the  blood-stained  frothing  at  the  mouth,  the  imprint  of  the  teeth  on  the 
tongue,  the  history  of  previous  convulsions,  the  rapid  recovery,  and  the 
age  of  the  patient  are  sufBcient  to  distinguish  epileptic  from  apo]3lectic 
coma. 

In  hysteria  the  coma  is  not  deep,  and  cold  will  restore  to  consciousness. 
Stertor  is  absent,  the  pupils  are  mobile  or  unchanged.  In  hysterical  hemi- 
plegia the  patient  drags  the  limb  like  an  inert  mass,  contractions  develop 
more  rapidly  than  in  apoplexy,  and  the  electro-muscular  contractility 
diminishes  after  it  has  lasted  for  a  short  time.  Hysteria  is  j)receded  by 
characteristic  hysterical  attacks  which  have  been  followed  by  abundant 
limpid  urine.  In  spinal  hemiplegia  sensation  is  preserved.  The  electro- 
muscular  contractility  is  diminished,  and  reflex  excitability  is  increased. 
Sensation  is  lost  on  the  opposite  side,  but  motion  and  contractility  are  in- 
tact. 

Prognosis. — The  prognosis  of  apoplexy  is  always  grave.  The  greater  the 
age  the  more  unfavorable  it  is.'  Death  rarely  occurs  at  the  onset  of  the 
seizure  ;  but  the  hemiplegia,  the  loss  of  mental  power,  and  the  liability  to 
recurring  attacks  render  it,  even  when  not  at  once  fatal,  a  dreaded  con- 
dition. It  is  a  favorable  sign  if  the  hemiplegia  begins  to  improve  very  soon 
after  the  attack  ;  but  if  the  period  of  unconsciousness  is  prolonged,  if  the 
coma  deepens,  if  reflex  excitability  is  wholly  lost,  the  sphincters  relaxed, 
the  breathing  irregular,  puffy,  and  noisy,  if  the  pupils  enlarge,  or  the 
temperature  after  having  fallen  rises  rapidly,  a  fatal  termination  is  in- 
dicated.    Convulsions  in  the  aged  always  indicate  great  danger. 

1  Diirand-Fardel  state  that  ventricular  and  meningeal  hemorrhages  are  frequent  after  sixty  ;  hence  an 
apoplexy  in  one  who  has  passed  that  age  must  be  regarded  as  very  serious. 


974  DISEASES   OF   THE   N"ERVOUS   SYSTEM. 

The  general  condition  of  the  patient  and  the  extent  and  degree  of  paraly- 
sis are  always  important  factors  in  the  prognosis.  Epileptic  seizures  may 
follow  a  partial  recovery  from  apoplexy.  Death  may  occur  from-  the  shock 
of  a  large  extravasation,  from  interference  with  the  medullary  centres, 
from  asphyxia,  and  sometimes  from  inanition. 

Treatment. — In  one  who  has  the  prodromal  symptoms  of  apoplexy,  or 
whose  age  and  condition  are  such  as  to  favor  its  occurrence,  prophylaxis 
may  avert  an  attack. 

The  principal  prophylactic  measures  are  the  avoidance  of  sudden  or 
violent  physical  exercise  or  strain,  and  of  strong  mental  emotions.  The 
diet  should  be  most  nutritious,  but  non-stimulating,  and  sleeping  and 
living  rooms  should  be  large  and  well  ventilated.  Great  care  should  be 
taken  that  the  functions  of  the  intestines,  liver,  and  kidneys  are  kept  at 
their  normal  standard  ;  and  moderate  exercise  should  be  taken  daily  in  the 
open  air.  Sudden  extremes  of  temperature  should  be  avoided  ;  therefore 
hot  or  cold  baths  are  to  be  forbidden.  The  body  should  always  be  warmly 
clothed  in  flannels. 

In  the  advent  of  the  premonitory  symptoms,  free  purgation  and  the 
application  of  blisters  to  the  neck  with  the  bromide  of  lithium  and  oxide 
of  zinc  are  indicated. 

When  an  apoplectic  seizure  has  occurred,  the  patient's  head  is  to  be 
elevated,  the  clothing  about  the  neck  loosened,  and  he  is  to  be  put  in  bed 
in  a  cool,  dark  and  absolutely  quiet  apartment,  with  cold  applied  to  the 
head  and  heat  to  the  feet.  If  the  fit  occur  after  a  hearty  meal,  vomiting 
must  be  induced  and  a  purge  given.  Blood-letting  is  to  be  the  exception  ; 
but  if  a  very  robust  individual  with  high  arterial  tension  is  seized,  and 
there  is  evidence  of  progressive  hemorrhage,  then  six  to  eight  ounces  of 
blood  may  be  taken.  The  condition  of  the  heart  and  the  arterial  tension 
are  the  guides  as  to  the  propriety  of  blood-letting.  In  old  age  or  in  the 
weak,  with  a  pale  face  and  feeble  pulse,  venesection  is  never  to  be  prac- 
tised. The  condition  of  the  bladder  should  be  carefully  examined,  and  the 
urine  drawn  if  necessary.  Much  of  the  turgescence  of  the  face  is  due  to 
the  falling  back  of  the  tongue,  consequently  the  patient  should  be  placed 
on  his  side.  Sinapisms  maybe  applied  to  the  nape  of  the  neck,  calves,  and 
over  the  stomach,  when  venesection  is  not  practised. 

As  the  patient  comes  out  of  the  coma  the  vital  powers  must  be  sustained, 
the  most  absolute  rest  and  quiet  enjoined,  and  the  bowels  kept  freely  open 
by  mild  salines.  Milk  and  beef  juice  are  to  be  freely  administered,  and  if 
there  is  very  great  feebleness  stimulants  may  be  given.  Stimulation  is 
demanded  very  early  in  old  and  feeble  subjects.  Narcotics  are  indicated 
when  there  is  great  restlessness  and  insomnia,  especially  in  the  aged. 

The  clot  in  the  brain  is  now  a  foreign  body  :  nothing  external  or  internal 
can  remove  it ;  hence  blisters,  ointments,  drugs,  etc.,  etc.,  are  worse  than 
useless.  The  galvanic  current  to  the  paralyzed  limbs  is  indicated  if  the 
paralysis  persists.  It  may  be  passed  directly  through  the  brain,  and  though 
the  absorption  of  the  clot  may  not  be  aided  by  it,  it  often  benefits  the 
paralyzed  limbs.     It  should  not  be  resorted  to  until  three  or  four  months 


ABSCESS   OF   THE   BRAIN.  975 

after  the  seizure ;  but  passive  motion,  gentle  friction,  and  the  application 
of  stimulating  liniments  to  the  surface  may  be  ])ractised  early  on  the  par- 
alyzed limb.  Massage  of  the  paralyzed  limb  should  always  form  part  of 
the  treatment.  When  electricity  is  used,  three  or  four  seances  a  week,  each 
lasting  from  five  to  eight  minutes,  are  suflBcient.' 

ABSCESS    OF    THE    BRAEST. 

Abscess  of  the  brain  or  suppurative  encephalitis  may  occur  in  any  part 
of  the  brain.  It  may  be  simple  or  multiple,  and  may  not  differ  in  charac- 
ter from  abscesses  in  the  connective-tissue  in  any  part  of  the  body. 

Morbid  Anatomy. — The  white  substance  of  the  middle  cerebral  lobes  is 
its  most  frequent  site.  About  16  per  cent,  of  all  cases  are  located  in  the 
cerebellum,  and  about  3  per  cent,  each  in  the  pons,  corpus  striatum  and 
thalamus  opticus.^  They  may  vary  in  size  from  a  walnut  to  the  involve- 
ment of  an  entire  hemisphere.  Usually  they  are  from  one  to  two  inches 
in  diameter.     They  are  irregularly  spherical  in  shape. 

Embolic  abscesses  are  usually  multiple.  Their  walls  are  irregular  and 
made  up  of  shreddy,  disintegrated  brain  substance,  with  projections  which 
are  found  to  surround  blood-vessels.  A  limiting  membrane  may  or  may 
not  exist.  In  recent  abscesses  it  is  either  wanting  or  incomplete.  Some 
abscesses  have  a  membrane  from  their  very  onset ;  they  are  encapsulated. 
Usually  a  zone  of  red  softening  surrounds  the  abscess,  and  around  this  is 
an  envelope  of  oedematous  brain  substance.^ 

Their  contents  are  usually  inodorous  and  composed  of  a  greenish,  creamy 
pus,  fatty  and  granular  matter,  the  debris  of  necrosed  brain-tissue.  Py- 
aemic  abscesses  may  contain  fetid  pus.  The  pus  is  decidedly  alkaline  ;  very 
rarely  is  it  acid.  When  mucin  is  present  the  pus  is  ropy,  viscid,  or  gela- 
tinous. As  an  abscess  increases  in  size  it  causes  pressure  on  the  adjacent 
brain  substance.  In  large  abscesses  the  convolutions  are  compressed,  so 
that  their  edges  are  sharpened  and  their  surfaces  flattened.  On  removing 
the  brain  a  bulging  with  a  boggy  feel  is  sometimes  noticed. 

Cerebral  abscesses  may  rupture  into  the  ventricles,  or  they  may  make 
their  way  to  the  surface  of  the  brain  and  cause  diffuse  suppurative  menin- 
gitis. In  rare  instances  they  discharge  into  the  cavity  of  the  tympanum, 
the  nasal  fossae,  or  the  orbit  of  the  eye.^  Multiple  abscesses  are  small  ; 
they  are  found  scattered  throughout  the  brain.  The  processes  by  which 
the  formation  of  a  cyst  wall  is  effected  in  these  abscesses  have  been  de- 
scribed by  Rindfleisch  as  follows  :   a  fibrinous  wall,  sometimes  a  quarter  of 

1  The  subcutaneous  injection  of  strychnia  into  the  paralyzed  limb  has  been  recommended,  and  hypo- 
dermics of  ergotin  have  been  advocated  during  the  attack  and  at  the  commencement  of  the  subsequent 
coma.  Dr.  Cel borne  reports  a  case  where,  after  an  hour  and  a  quarter's  persistent  practice  of  artificial 
respiration  by  the  Sylvester  Method,  asphyxia  was  averted.  —Jour.  Med.  Chirur.  Pesth.,  Dr.  Foster,  N.  Y. 
Med.  Rec,  1876. 

2  Hammond  states  that  the  gray  matter  is  involved  first,  the  white  secondarily.  Gull  and  Sutton  state 
just  the  contrary. 

3  Rokitansky  states  that  yellow  (chronic)  softening  surrounds  cerebral  abscess  in  a  large  majority  of 
cases. 

••  Niemeyer  states  that  the  pus,  after  reaching  the  surface  of  the  brain,  may  perforate  outwardly  through 
the  bones,  provided  extensive  meningitis  has  not  been  excited. —  Text-Book  of  Pract.  Med.,  vol.  ii.,  p.  227. 


976  DISEASES    OF   THE   IS'EKVOUS   SYSTEM. 

an  inch  thick,  may  envelop  tiie  abscess.  The  innermost,  lining  membrane 
of  this  cyst-wall  consists  of  a  yellow,  smooth  layer  of  cells.  Tortuous 
venous  vessels  traverse  it ;  it  is  sometimes  called  the  pyogenic  membrane. 
Next  to  it  is  a  layer  of  germ-tissue,  irregular  in  thickness.  Externally  is  a 
stratiform,  spindle-celled  tissue,  that  forms  a  direct  transition  into  the  sur- 
rounding brain  matter ;  in  spite  of  which,  however,  the  abscess  can  be 
enucleated.  A  zone  of  fatty  degeneration  surrounds  the  outermost  (fibrous) 
layer  of  the  cyst-wall.  The  pus,  Eindfleisch  further  states,  is  greasy, 
greenish-yellow,  acid,  and  usually  odorless.  It  is  to  be  noted  that  Grull 
and  Sutton  state  the  pus  to  be  decidedly  alkaline  and  very  fetid  in  old 
abscesses. 

Hseraatoidin  crystals,  margarin,  and  cholesterin  are  not  infrequently 
found  mingled  with  the  pus,  and  the  entire  capsule  is  to  be  regarded  as  a 
neuroglia  production.  Absorption,  cheesy  degeneration,  and  the  forma- 
tion of  chalky  masses  are  said  to  occur  in  cerebral  abscesses.  The  cyst- 
wall  retracts  and  finally  disappears.* 

Etiology. — Cerebral  abscess  occurs  at  all  ages.  Males  are  more  subject 
to  it  than  females.  Among  its  chief  causes  are  suppurative  otitis  and 
traumatism,  especially  blows  on  the  head.  It  may  result  from  suppurative 
inflammation  of  the  face  and  scalp,  and  from  suppuration  about  the  orbit 
or  nose.  Syphilitic  and  other  diseases  of  the  bones  of  the  skull,  the  tem- 
poral especially,  are  not  infrequently  followed  by  abscess.  Pyaemia  and 
glanders  are  among  its  frequent  causes.  Eed  inflammatory  softening  is  the 
first  stage  of  abscess.  Ulcerative  endocarditis  and  osteo-myelitis  are  espe- 
cially liable  to  give  rise  to  it ;  the  embolus  in  these  cases  has  a  special 
character.  There  are  cases  in  which  no  cause  can  be  found  for  their  de- 
velopment. 

Symptoms. — Headache  is  the  most  constant  and  prominent  symptom  of 
abscess  of  the  brain.  In  some  cases  it  is  not  severe  but  is  constant,  in 
others  it  is  so  severe  that  patients  are  not  able  to  bear  it  without  an  anodyne. 
It  may  be  so  circumscribed  as  to  localize  the  very  site  of  the  abscess.  With 
the  headache  there  is  vomiting  and  dizziness.  Delirium  and  disturbance 
of  intellect  may  be  marked  but  transitory  ;  it  may  alternate  with  stupor. 
Epileptiform  convulsions,  and  signs  of  cerebral  pressure  may  end  in  coma. 
Incontinence  of  urine  and  faeces  is  a  prominent  symptom  in  most  cases. 

It  is  to  be  remembered  that  large  abscesses  have  been  found  in  the  brain 
of  those  who  during  life,  gave  no  cerebral  symptoms.  Otitic  abscesses 
of  the  brain  are  preceded  by  all  the  signs  of  the  (causative)  local  disease. 
Headache,  vomiting,  delirium,  fever  and  irregular  chills,  spasmodic  move- 
ments in  the  muscles  of  the  face  or  limbs,  then  hemiplegia,  coma  and  death 
— this  is  the  usual  course  of  such  an  abscess.  But  cases  are  reported  where 
an  artificial  or  spontaneous  exit  to  the  pus  has  been  followed  by  recovery.^ 
In  some  cases  optic  neuritis  has  been  found.  ^  Rapid  and  progressive 
emaciation  usually  accompanies  cerebral  abscess.  At  times  there  will  be 
hyperaesthesia  and  abnormal  acuteness  of  the  special  senses  at  the  onset ; 

1  Rosenthal,  Diseases  of  Nervous  System,  vol.  i. 

a  Schloz.  3  HughlingB-JackBon. 


TUMOES    OF   THE   BHAIIT    AND    MENINGES.  977 

and  this  will  be  followed  by  sopor,  ansesthesia,  formication^  numbness,  etc., 
etc.  If  the  abscess  involves  the  motor  tract,  hemiplegia  or  local  paralyses 
will  occur. 

When  pysemic  abscesses  occur  in  the  brain,  they  are  chiefly  diagnosticated 
by  the  constitutional  symptoms.  It  will  begin  with  rigors  and  run  an. 
acute  course  ;  the  temperature  may  reach  1.05°  F.  Ague-like  rigors  and 
the  initial  signs  of  abscess  coming  on  when  the  conditions  of  pyaemia  exist 
must  lead  to  the  suspicion  of  multiple  cerebral  abscess. 

Sometimes  in  chronic  abscess  of  the  brain  there  is  a  long  latent  period.' 
During  this  time  epileptiform  convulsions,  facial  paralysis,  and  hemiplegia 
and  aphasia  accompanied  by  intermittent  chills  and  headache  may  occur  ; 
After  which,  acute  symptoms  may  be  present  for  a  few  days  and  end  in 
death.  The  acute  symptoms  differ  widely  in  diiferent  cases  ;  there  may 
be  localized  headache  over  the  abscess,  delirium,  nausea,  vomiting,  well- 
marked  signs  of  cerebral  irritation,  ending  by  a  fall  in  temperature  and 
pulse,  deep  coma  and  death. 

Differential  Diagnosis. — It  is  always  difficult  to  distinguish  cerebral  ab- 
scesses from  cerebral  tumor.  Abscess  is  accompanied  by  greater  emacia- 
tion and  is  of  shorter  duration  than  tumor.  Local  paralyses  of  long 
standing  are  common  in  tumors,  rare  in  abscess.  Rigors  and  more  or  less 
fever  usually  attend  abscess.  An  ozoenal  or  otorrhoeal  discharge,  the  his- 
tory of  traumatism,  or  the  fact  of  a  latent  period  having  existed,  is  in  favor 
of  abscess.  Softening  may  be  mistaken  for  abscess.  The  age  of  the 
patient,  the  condition  of  the  blood-vessels,  the  slow  development  of  the 
hemiplegia,  the  absence  of  constant  or  intense  localized  pains  in  the  head 
and  the  gradual  loss  of  mental  power,  distinguish  softening  from  abscess. 

Prognosis. — Acute  abscess  of  the  brain  is  always  fatal  in  from  four  to 
twenty  days.  Chronic  abscess  terminates  fatally  from  its  complications, 
the  commonest  of  which  are  meningitis,  cerebral  hemorrhage,  oedema, 
softening,  thrombosis  of  the  cerebral  sinuses,  serous  effusions  into  the 
meshes  of  the  pia  mater  and  the  ventricles,  and  pulmonary  hypostasis. 
When  abscesses  are  situated  away  from  the  motor  tract  and  surface  of  the 
brain,  they  may  exist  for  years  and  give  rise  to  no  symptoms. 

Treatment. — The  treatment  of  cerebral  abscess  is  altogether  surgical. 
The  operation  of  trephining  for  traumatic  abscess,  and  the  treatment  of 
chronic  aural  disease,  are  found  in  modern  surgery  and  in  special  works 
upon  diseases  of  the  ear.  Recently  the  withdrawal  of  pus  from  the  brain 
has  received  much  attention,  and  marked  success  has  attended  surgical 
operations  for  the  accomplishment  of  this  end.  Anodynes  are  always  indi- 
cated for  the  relief  of  the  intense  headache. 

TUMORS    OF   THE    BEAIN    AND    MEISTHSTGES. 

The  most  frequent  intracranial  growths  are  tubercle,  cancer,  gummata 
and  gliomata.  Apoplexy  and  abscess,  which  have  much  in  common  with 
tumors  of  the  brain,  are  elsewhere  described.     Some  intracranial  growths 

'  Lebert  says  from  one  to  two  mouths. 
62 


978 


DISEASES   OE   THE   NEEVOUS    SYSTEM. 


are  peculiar  to  the  brain,  e.  g.,  psammomata ;  but  the  majority  (cancer, 
tubercle,  gummata,  etc.)-  do  not  differ,  in  their  anatomical  characteristics 
from  similar  growths  elsewhere  in  the  body. 
Intracranial  tumors  may  have  their  origin  in  the  meninges,  as  sarcomata. 


Fig.  198. 
Cerebral  Tumors. 
Sketch  showing  at  A  a  Fibroma  of  the  Cerehdlum^frmn  Lebert. 


myxomata,  lipomata,  cholesteatomata  and  psammomata  ;  in  the  Hood-ves- 
sels as  angiomata,  aneurisms,  and  a  peculiar  tumor  in  rare  instances  found 
in  the  third  yentricle — the  epithelioma  myxomatodes  psammomum  ;*  and 
in  the  neuroglia,  as  gliomata,  gummata  and  fibromata. 

Morbid  Anatomy. — The  commonest  form  of  cerebral  tumor  is  the  tuter- 
culous.  These  growths  yary  in  size  from  a  pea  to  an  orange.  They  are  hard 
and  compact,  their  exterior  being  gray,  semi-transparent,  and  intimately 
blended  with  the  surrounding  brain-tissue.  Their  centres  are  soft  and  yel- 
low. They  develop  slowly  and  may  calcify.  The  vessels  going  to  them  are 
dilated,  and  at  the  centre  of  the  growth  they  are  indistinguishable.  Tu- 
bercular tumors  occur  in  the  hemispheres,  cerebellum,  optic  thalami,  cor- 
pora striata,  peduncles,  pons  Varolii  and  ependyma  of  the  ventricles  f  but 
the  cerebellum^  is  their  favorite  seat.  At  times  tubercular  growths  are 
encysted. 

Cancer  of  the  brain  may  originate  in  the  cranial  bones,  the  dura  mater, 
the  pia  mater,  the  cerebellum,  the  cerebrum,  the  pons,  or  the  medulla  oblon- 
gata. Encephaloid  cancer  is  the  commonest  variety.  The  color  depends  on, 
(1)  their  vascularity,  (2)  the  kind  of    softening  about  them,  and  (3)  on 


'»  E.  Long  Fox,  in  Quain's  Dictionary,  p.  157. 
^  Forster. 


3  Jenner. 


TUMOES    OF   THE    BRAIK    AND   MENINGES.  979 

the  amount  of  retrogressive  degenerative  changes  that  have  occurred  at 
their  centres.  When  more  than  one  tumor  is  present,  they  develop  sym- 
metrically, and  are  liable  to  involve  homonymous  parts  of  the  brain  (Eoki- 
tansky). 

Guminata,  or  syphilomata,  may  appear  as  soft,  red-gray,  jelly-like 
masses,  irregular  in  form,  and  intimately  blended  with  the  adjacent  brain 
substance.  They  are  chiefly  composed  of  round  cells,  but  spindle  and 
stellated  cells  are  sometimes  found.  They  may  have  an  alveolar  frame- 
work. Capillaries  are  not  numerous  in  their  substance.  There  may,  how- 
ever, be  small  points  of  extravasation.  There  are  rare  forms  of  gummata 
which  consist  of  a  well-defined  homogeneous  mass,  which  is  dry,  friable 
and  cheesy.  Atrophied  neuroglia  and  round  and  spindle  cells  in  a  state 
of  fatty  degeneration  are  often  found  throughout  the  gummy  masses. 
Syphilomata  are  generally  found  at  the  circumference,  and  especially  at 
the  base  of  the  brain.  They  may  have  their  origin  in  the  membranes,  the 
vessels,  or  the  neuroglia.  The  surrounding  inflammation  joins  them  to 
the  meninges.  If  the  latter  be  joined  to  the  dura  mater,  granules  are  de- 
yeloped  in  the  pia,  which  vary  in  size  from  a  pea  to  that  of  a  small  egg. 
Syphilitic  tumors  in  the  interior  of  the  brain  are  very  rare. ' 

So-called  syphilis  of  the  brain  may  appear,  (1)  as  well-defined  hard 
tumors,  (2)  as  thickenings,  adhesions,  and  contractions  or  puckerings  of 
the  meninges,  (3)  as  disease  of  the  walls  of  the  vessels,  and  (4)  as  sjDots 
of  softening  or  diffuse  gelatinous  accumulations.^ 

Gliomata  ^  may  develop  either  in  the  brain  substance,  or  in  the  meninges 
along  the  course  of  the  cephalic  nerves,  or  in  the  retina.  On  account  of 
its  vascularity,  hemorrhages  are  liable  to  take  place  into  its  substance.  At 
times  a  light  brown  coagulum  causes  the  tumor  to  resemble  tuberculous  or 
gummatous  growths.  It  is  often  difficult  to  distinguish  a  glioma  from  nor-, 
mal  brain  substance.  These  tumors  may  be  either  hard  or  soft ;  soft  gli- 
omata contain  only  a  small  quantity  of  intercellular  substance.  Hard 
gliomata  have  bundles  of  parallel  or  interlacing  fibrillse  as  their  fundamen- 
tal substance.  They  vary  in  size  from  minute  masses  to  masses  as  large 
as  an  orange.  They  grow  slowly  and  are  usually  solitary.  There  are  fat 
granules,  cholesterin  crystals,  neuroglia  nuclei,  a  debris  of  nerve-tissue, 
and  more  or  less  redness  and  softening  in  the  immediate  neighborhood  of 
gliomata."  Diffuse  gliomatous  masses  were  once  thought  to  be  infiltrated 
cancer  of  the  brain. 

Psammomata,  or  Yirchow's  sandy  tumor,  are  soft,  juiceless  sarcomata 
whose  cells  are  thin,  flat,  irregular  in  outline  but  very  large.  The  vessels 
are  in    direct  connection  with  the  cells.     Psammomata  usually  develop 

1  Rindfleisch  states  that  sj'philomata  develop  in  the  brain  substance  along  the  lymphatic  sheaths  and 
the  vessels,  and  that  they  produce  spots  of  softening  by  compression  of  the  vessels  and  arrest  of  the  cir- 
culation. 

2  Niemeyer  states  that  gummata  are  more  frequent  as  diffuse  infiltrations.  Virchow,  Charcot  and  West- 
phal  have  found  gummata  in  the  white  substance  of  the  hemispheres,  in  the  thai,  opticus,  the  pituitary 
gland,  the  optic  tracts,  the  cerebral  pc^duncles,  the  pons,  and  in  the  cerebellum. 

3  The  neuroglia-sarcomata  of  Cornil  and  Ranvier. 

<  Ernest  Wagner  and  Obermeier  regard  hyperplasia  of  the  pineal  gland  as  essentially  the  same  as  a  glio- 
matous neoplasm. 


980  DISEASES   OF  THE   JSTEEVOUS   SYSTEM. 

from  the  dura.  They  may  reach  the  size  of  a  pea,  and  are  hard,  smooth, 
and  spherical.  These  calcareous  tumors  often  have  a  concentric  or  lami- 
nated structure. 

Cholesteatoma  (called  pearl  tumors  from  their  lustre)  do  not  always 
contain  cholesterin,  but  consist  of  concentric  layers  of  epithelial  cells 
that  haye  partially  undergone  fatty  degeneration.  They  may  have  an  in- 
distinct fibrous  envelope.  They  rarely  exceed  one  and  one-half  inch 
in  diameter.  They  are  aggregations  of  crystalline,  pearly  masses,  the 
size  of  a  mustard-seed  ;  they  grow  slowly  from  the  pia  at  the  base  of  the 
brain,  or  in  some  depression  of    it.     They  are  pathologically  insignificant. 

Cysts  (independent  of  cystic  developments  from  echinococci,  etc.,  etc.) 
are  rare.  They  seldom  exceed  the  size  of  a  pin  head,  and  are  found  on  the 
walls  of  the  lateral  ventricle.  They  may  occur  singly  or  in  groups.  Trans- 
parent serous  cysts  developing  from  the  vessels  of  the  choroid  plexus  are 
not  rare. 

Medullary  or  ganglionic  neuromata — tumors  of  nerve-cells  and  ganglia 
— occur  in,  and  on  the  brain  ;  they  are  seldom  larger  than  a  pea,  and  are 
found  on  the  ventricular  surface,  in  the  white  substance,  or  in  the  cor- 
pora striata.^  A  tumor  to  be  a  neuroma  must  contain  a  large  number  of 
nerve-cells. 

Sarcomata  appear  as  well-defined,  round  or  lobulated  tumors,  varying  in 
consistency,  and  in  size  from  that  of  a  walnut  to  an  apple.  They  may 
originate  in  the  cerebral  hemispheres,  but  more  frequently  they  arise  from 
the  dura,  especially  at  the  base  of  the  skull.  There  are  two  forms,  the 
hard  sarcoma  with  compact  hard  fundamental  tissue  and  small  cells,  and 
the  soft  sarcoma  with  loose,  scanty  intercellular  substance  and  numerous 
cells  of  large  size.  They  are  separated  from  the  surrounding  brain  sub- 
stance by  a  very  vascular  zone. 

Myxomata  appear  either  as  well-defined  tumors  or  as  infiltrated  masses 
whose  seat  and  size  resemble  those  of  sarcomata.  Indeed,  to  determine 
whether  a  tumor  is  a  sarcoma  that  has  undergone  mucous  transforma- 
tion, or  a  myxoma  with  patches  of  embryonic  tissue,  is  always  very  diffi- 
cult. 

A  true  myxoma  or  sarcoma  may  result  from  a  glioma  i^q.  v.),  the  tran- 
sition being  gradual ;  these  various  sarcomatous  tumors  are  found  in  the 
hemispheres,  the  anterior  lobes,  thalamus  opticus,  cerebral  peduncles,  or 
they  may  involve  the  pons  and  tubercular  quadi-igemina.^ 

Lii^omata  are  rare,  and  are  only  found  at  the  raph6  of  the  corpus  cal- 
losum  and  fornix.^ 

Osteomata,  new  formations  of  bone,  independent  of  ossification  or  other 
neoplasia,  are  not  frequent.  Osteoma  of  the  cerebellum  has  been  found  to 
follow  encephalitis.  Osseous  new  growths  must  not  be  confounded  with 
syphilitic  or  other  exostoses. 

1  Cornil  and  Ranvier,  Pathol.  Histologiqve. 
*   Transac.  Pathol.  Society,  Dr.  Caylej',  vol.  xvi.,  p.  33. 

3  Virchow.    Benjamin  reports  a  case  where  ossification  had  occurred  ;  Niemeyer  describes  lipomata  as 
■"  small  lobulated  tumors  starting  from  the  dura." 


TUMOKS    OF   THE   BRAIN    AND    MENINGES.  981 

Fapillomata  are  the  rarest  form  of  cerebral  tumors.  They  are  cauli- 
flower-like, budding  growths,  with  abundant  milky  Juice,  very  vascular, 
and  surrounded  by  a  zone  of  cerebral  softening.  A  large  one — situated  on 
the  ependyma  of  the  third  ventricle — is  described  by  Cornil  and  Ranvier.' 

Fibromata  appear  as  hard,  fibrillar  tumors,  small,  and  rarely  peduncula- 
ted. In  one  case  seventeen  fibrous  tumors  were  found  on  the  ependyma  of 
the  lateral  ventricle.  The  pons  and  the  cerebral  peduncle  are  sometimes 
implicated  by  this  tumor. 

Angiomata,  or  erectile  tumors,  are  masses  composed  of  vessels  of  new 
formation.  They  are  found  in  the  cerebral  substance,  corpus  striatum, 
cerebellum,  and  floor  of  the  fourth  ventricle.      They  may  be  multiple.'^ 

Aneurisms  are  not  uncommon ;  they  do  not  attain  a  large  size.  They 
involve  the  basilar  artery,  the  vessels  in  the  Sylvian  fossa  and  corpus  cal- 
losum,  the  anterior  communicating — rarely  other  than  basic  vessels  ;  from 
their  position  they  are  liable  to  compress  some  of  the  nerves  at  the  base  of 
the  brain.  Miliary  aneurisms  have  been  considered  in  the  history  of  apo- 
plexy. 

Hydatids  or  ecMnococcus  cysts  usually  exist  as  solitary  tumors  Avhich  may 
attain  any  size.  They  are  generally  located  at  the  centre  of  the  white  matter 
of  a  hemisphere.  The  cyst-wall  is  always  absent  when  the  hydatid  is  in  the 
ventricle.  Some  claim  that  it  is  absent  even  when  located  elsewhere  in  the 
brain.  They  grow  slowly,  producing  atrophy  of  the  brain.  Five  large  hy- 
datid cysts  have  been  found  in  various  parts  of  the  same  brain. 

Cysticerci  in  the  brain  form  small  serous  cysts  that  may  occur  in  any  part 
of  the  organ,  and  are  rarely  solitary.  Cruveilhier  describes  a  case  where 
one  hundred  were  found.  When  the  cysticercus  is  lodged  in  cavities,  it  is 
Don-encysted  and  tends  to  grow  easily  into  the  form  of  a  tape-worm.  These 
parasites  may  be  found  dead  and  changed  to  a  chalky  mass  in  which  some 
of  the  booklets  are  embedded. 

Etiology. — Tumors  of  the  brain  are  twice  as  frequent  in  males  as  in  fe- 
males. Tuberculous  tumors  are  most  frequent  in  children  ;  they  usually 
do  not  develop  until  after  the  second  year.  Cancer  is  rare  before  forty  ;  it 
is  primary  in  fifty  per  cent,  of  the  cases.  Syphilitic  growths  are  a  mani- 
festation of  tertiary  syphilis.  Hydatids  occur  between  the  ages  of  ten  and 
thirty-five  ;  while  cysticerci  are  rarely  found  before  forty.  Aneurisms  oc- 
cur in  middle  life,  and  are  associated  with  evidences  of  arterial  degenera- 
tion. 

Symptoms. — Cerebral  tumors  of  large  size  may  give  rise  to  no  symptoms, 
but  in  most  cases  their  development  is  attended  by  more  or  less  marked  gen- 
eral or  local  symptoms.  These,  however,  cannot  be  stated  in  any  order 
that  is  applicable  to  all  cases.  I  shall  only  consider  the  more  important 
and  constant  of  the  general  symptoms.  The  most  characteristic  are  head- 
ache and  disturbance  of  the  intellectual  faculties.  The  most  constant  local 
symptom  is  local  paralysis.     Headache  is  generally  a  prominent  and  per. 


>  Path.  Hist.,  p.  378. 

2  Obermeier  gives  the  name  pachymeningitis  hemorrhagica  bregmatica  to  angiomatous  growths  upon  the 
Inner  surface  of  the  dura. 


982  DISEASES   OF  THE  NERVOUS   SYSTEM. 

sistent  symptom.  It  is  more  severe  than  in  any  other  cerebral  disease,  ex- 
cept meningitis  ;  it  is  constant,  and  is  increased  by  light,  sound,  or  move- 
ments of  the  head.  With  the  headache  there  are  tinnitus  aurium,  morbid 
acuteness  of  hearing,  disturbance  of  vision,  strabismus,  with  more  or  less 
perversion  of  the  special'  senses,  local  hypersesthesia,  anaesthesia,  and  im- 
pairment of  the  mental  faculties.  Vertigo,  when  the  patient  assumes  the 
upright  position,  is  almost  always  associated  with  the  headache,  and  vom- 
iting occurs  at  irregular  intervals  without  any  apparent  cause.  There  are 
rarely  any  febrile  symptoms,  except  when  injlammation  occurs  about  the 
tumors.  A  slow  irregular  pulse  is  of  frequent  occurrence  during  the  early 
stage  of  their  development,  and  the  respirations  are  often  irregular  and 
slowed.  Spasm  of  single  muscles  or  groups  of  muscles  and  general  epilep- 
tiform or  choreic  seizures  often  follow  severe  attacks  of  vertigo. 

Hemiplegia  is  entirely  absent  in  a  large  number  of  cases.  If  present  it 
may  come  on  slowly,  or  suddenly  after  an  epileptiform  seizure ;  facial  paral- 
ysis on  the  same  side  as  the  hemiplegia,  is  present  in  some  cases,  and  rigid- 
ity of  the  affected  muscles  is  common.  Double  hemiplegia  is  not  infrequent ; 
one  side  being  implicated  some  time  after  the  other.  If  paraplegia  exists 
it  indicates  a  median  tumor,  usually  at  the  base  or  in  the  cerebellum. 

If  the  tumor  involves  the  island  of  Eeil  or  the  posterior  portion  of  the 
third  convolution  there  will  be  aphasia.  The  intellectual  disturbances  are 
varied.  Melancholia  and  paroxysms  of  grief  or  Joy  are  frequent.  Incoher- 
ence of  speech,  failure  of  memory,  temporary  loss  of  consciousness,  and  a 
gradual  passage  into  a  condition  of  imbecility  and  helplessness  are  a  part  of 
its  history.  This  is  especially  liable  to  occur  in  cases  where  the  tumors  are 
rapidly  developed. 

The  choked  disc  or  congested  papilla,  and  the  neuro-retinitis  as  revealed 
by  the  ophthalmoscope,  are  regarded  by  some  as  important  in  the  diagnosis 
of  cerebral  tumors.  Such  conditions  may  cause  amaurosis  and  amblyopia/ 
If  there  is  loss  of  sight  from  involvement  of  the  optic  nerves,  the  pupils 
will  be  dilated  and  they  will  not  contract  under  the  influence  of  light.  If 
the  tumor  is  situated  above  the  corpora  geniculata,  although  there  is  loss  of 
sight,  the  pupils  will  respond  to  light.  As  the  tumor  increases  in  size,  the 
paralysis  advances  from  one  set  or  group  of  muscles  to  another,  and  this  ad- 
vancing paralysis  is  a  most  important  diagnostic  sign.  Its  course  is  usual- 
ly from  above  downward. 

On  account  of  the  local  disturbances  which  result  from  the  complicating 
encephalitis,  abscess,  softening,  or  oedema  may  occur  and  give  rise  to  their 
own  peculiar  symptoms.  The  bowels  are  usually  obstinately  constipated. 
Clinically  there  may  be  recognized  three  classes  of  cases :  (1)  those  which  are 
attended  by  no  symptoms,  (2)  those  in  which  the  symptoms  are  slowly  de- 
veloped and  intermittent  and  extend  over  a  number  of  years,  (3)  those  in 
which  the  symptoms  come  on  suddenly  and  are  rapidly  fatal. 

Differential  Diagnosis. — Tumors  of  the  brain  may  be  mistaken  tor  abscess , 

>  Annnske  (in  v.  Graefe's  Archiv)  states  that  optic  neuritis  occupies  the  first  rank  among  the  symptoms  of 
intracranial  neoplasia. 


TUMOES   OF   THE   BKAIN   AND    MENINGES.  983 

cerebral  softening,  epilepsy  and  chronic  meningitis.  The  points  of  diagnosis 
between  the  first  two  have  already  been  considered. 

An  apoplectic  or  hysterical  seizure  will  hardly  ever  be  mistaken  for  a  cere- 
bral tumor. 

Epilepsy  is  a  paroxysmal  disease ;  it  usually  occurs  early  in  life  and  is 
rarely  accompanied  by  any  of  the  local  phenomena  of  tumor. 

In  chronic  meningitis  the  pain  is  not  so  severe  or  as  constant  as  in  cere- 
bral tumor,  the  mind  is  perverted  and  weakened,  epileptiform  convulsions 
are  rare,  and  the  special  senses  and  facial  nerves  are  not  implicated. 

The  differential  diagnosis  of  the  different  varieties  of  cerebral  tumor 
may  be  briefly  summarized  as  follows  : — tubercular  growths  are  met  with 
in  early  life  ;  they  are  accompanied  by  fever,  have  a  tubercular  history,  or 
have  the  evidences  of  tuberculosis  in  other  parts  of  the  body.  They  are 
usually  located  either  in  the  cerebellum  or  pons.*  Cancer  of  the  brain 
may  be  suspected  when  the  patient  is  over  forty,  when  there  is  a  marked 
cachexia  with  progressive  emaciation,  when  there  is  an  hereditary  cancerous 
history,  or  when  cancer  exists  in  other  organs,  and  when  the  development 
of  the  cerebral  symptoms  has  been  rapid.  Implication  of  the  cranial  bones 
by  the  tumor  always  indicates  cancer. 

Syphilomata  are  attended  by  nocturnal  headache,  by  the  constitutional 
signs  of  syphilis  or  evidences  of  previous  syphilitic  disease.  Their  symp- 
toms remit  and  sometimes  disappear  under  anti-syphilitic  measures.  Ptosis 
and  dilatation  of  the  pupil  are  more  often  met  with  in  syphilitic  tumors 
than  with  any  other. 

Gliomata  follow  traumatic  injuries  to  the  skull,  and  progress  slowly  with- 
out any  interference  with  the  general  health. 

Aneurism  may  be  suspected  in  the  aged,  with  the  signs  of  general  arterial 
degeneration. 

Cysticerci  occur  after  forty,  and  produce,  at  first,  subacute  epileptiform 
attacks,  which  become  very  frequent.  One  hundred  epileptic  seizures  have 
occurred  in  a  day  with  cysticerci  in  the  brain.  Paralysis  of  the  limbs  and 
hemiplegia  are  very  rare,  while  the  psychical  disturbances  are  marked,  and 
occur  very  early. 

The  diagnosis  of  hydatids  is  exceedingly  diflBcult.  The  tumor-symptoms 
are  inconstant ;  the  intellect  is  unaffected,  and  there  may  be  oedema  of 
eyelids. 

The  rules  which  will  aid  in  the  localization  of  cerebral  tumors  are  as  fol- 
lows : — tumors  of  the  convexity,  even  when  large,  may  give  rise  to  no 
symptoms.  Usually,  however,  they  cause  headache,  motor  disturbances, 
delirium,  convulsions  ;  but  rarely  disturbances  of  sensation  or  paralysis. 

Tumors  of  the  anterior  lobes  cause  diffuse  or  circumscribed  headache, 
convulsions,  and  epileptiform  attacks,  hemiplegia,  arid  aphasia.  The 
special  senses  are  undisturbed,  except  the  sense  of  smell. 

In  tumors  of  the  middle  lobes  the  special  senses  (especially  sight)  are 
affected,  and  there  is  usually  anaesthesia  of  the  surface  on  the  side  opposite 
the  tumor. 

1  Hirschberg. 


984  DISEASES   OF   THE   ITEEVOUS    SYSTEM. 

Tumors  in  the  posterior  lobes  cause  greater  psychical  disturbances  than 
those  in  any  other  position.  Motion,  sensation,  and  the  special  senses 
(sight  excepted)  are  more  or  less  disturbed.  Vertigo  and  convulsions  are 
common. 

Tumors  in  the  corpus  striatum  and  lenticular  nucleus  are  accompanied 
by  hemiplegia,  convulsions,  facial  paralysis,  difficulty  in  articulation,  dis- 
turbance of  intelligence ;  but  the  special  senses  are  not  impaired.  The 
symptoms  correspond  to  those  of  apoplexy,  but  they  are  of  slower  develop- 
ment. 

Tumors  in  the  tubercula  quadrigemina  are  attended  by  convulsive  spasms, 
paralysis  of  the  motor  oculi,  disorders  of  vision  on  loth  sides,  slight  paral- 
ysis of  the  face,  and  unilateral  paralysis  of  the  limbs. 

Tumors  in  the  cerebral  peduncles  induce  headache,  vertigo,  hemiplegia 
alternating  with  sensory  disturbances,  paralysis  of  the  motor  oculi  on  the 
same  side,  neuro  retinitis,  difficulty  of  micturition,  but  no  intellectual  dis- 
turbances. 

Tumors  in  the  pojis  Varolii  induce  crossed  paralysis  of  motion  (and 
sometimes  of  sensation  also),  amblyopia,  amaurosis,  choked  disc,  dysphagia, 
strabismus,  difficulty  in  articulation,  but  no  convulsions.  There  is  usually 
paralysis  of  the  bladder. 

When  the  cerelellar  peduncles  are  involved  the  gait  is  tottering  and  un- 
steady ;  the  patient  tends  to  fall  to  one  side,  or  rotate  around  the  median 
line. 

In  cerebellar  tumors,  there  will  be  occipital  headache,  oscillatory  move- 
ments, unsteady  gait,  intense  vertigo,  strabismus,  amblyopia,  and  amaurosis; 
but  there  are  no  disturbances  of  the  intellect  or  sensation. 

In  tumors  of  the  medulla,  the  symptoms  not  infrequently  resemble 
glosso-labio-laryngeal  paralysis.  There  is  dysphagia,  disturbances  of  sensa- 
tion, convulsions,  occasionally  saccharine  urine,  and  difficulty  in  articula- 
tion. 

Prognosis. — The  character  of  cerebral  tumors  varies  with  their  structure. 
The  prognosis  is  always  unfavorable  ;  carcinomatous  and  tuberculous 
tumors  are  progressive  and  early  fatal.  In  hydatids  and  aneurism,  though 
life  may  be  prolonged,  death  is  a  certain  result.  In  syphiloma,  life  may 
be  prolonged  for  years  by  judicious  and  timely  treatment.  The  average 
duration  of  cancer  is  about  one  year.'  Echinococci  tumors  have  been 
cured.^  In  any  case  of  cerebral  tumor  which  is  attended  by  intense  pain 
and  progressive  emaciation,  the  course  is  rapid,  and  the  prognosis  un- 
favorable. Death  may  occur  from  continued  convulsions,  paralysis, 
cerebral  softening,  oedema  or  hemorrhage.  Secondary  inflammation  with 
abscess,  and  meningitis,  and  pulmonary  complication,  may  be  the  cause 
of  death.  Anaemia  and  exhaustion  are  common  modes  of  death  in  specific 
tumors. 

Treatment. — In  a  case  of  cerebral  tumor  where  syphilis  can  even  be  sus- 

1  Lebert  states  that  three  months  and  five  years  are  the  extremes. 

5  Mouline  trephined,  and  Fletcher  incised,  a  frontal  tumor,  withdrawing  the  hydatids.  These  are 
phenomenal  cases. 


SCLEROSIS   OF   THE   BRAIK. 


985 


pected,  mercury  and  iodide  of  potassium  in  large  doses  should  be  admin- 
istered. The  diet  and  hygienic  surroundings  should  be  carefully  regulated, 
the  patient  restricted  in  exercise,  the  pain  and  sleeplessness  should  be  re- 
lieved by  anodynes. 


SCLEROSIS    OF    THE    BRAEST. 


Independent  of  cerebro-spinal  ^^erosis,  this  is  a  comparatively  rare  con- 
dition.  Cerebral  sclerosis  is  a  chronic  interstitial  inflammation,  following 
hypersemia  of  the  neuroglia.'     It  may  be  diffused  or  multiple. 


Pig.  199. 

Diagram  showing  the  Connective-tissues  of  Medallated  Nerve  Structure. 

AA.  Two  bundles  ofmedullated  nerves. 
BB.  Epinevnum. 
CC.  Penneurivm. 
DD.  Endonevnum. 

E,  Axis-cylinders. 

F.  Neuroglia  cells. 

Morbid  Anatomy. — The  medullary  substance  is  the  favorite  seat  of  mul- 
tiple cerebral  sclerosis. 

On  section,  masses  of  gray,  hard,  well-defined,  transparent  sclerotic  tissue 
are  found — sclerotic  islands  varying  in  size  from  one-fourth  to  one  inch. 
They  may  be  so  numerous  and  small  as  to  be  scarcely  discoverable.^ 

The  cut  surface  of  a  sclerosed  patch  is  moist  with  serum ;  and  usually 
shows  small  blue  or  gray-red  spots. 


1  The  tissue  forming  the  siteleton  framework  of  the  brain  is  called  the  neuroglia  by  Virchow.  It  is 
analogous  to  the  connective-tissue  framework  between  the  liver-lobules  and  kidney  tubules. 

"  Comil  and  Ranvier  describe  cerebral  sclerosis  as  almost  exclusively  involving  the  convolutions,  and 
consisting  of  a  first  stajje  where  hyperplasia  of  the  neuroglia  produces  a  vascular,  pulpy,  gelatinous  mass  ; 
and  of  a  second  stage  where  atrophy  of  the  new  elements  is  accom))anied  by  development  of  a  vascular 
structure,  hard  and  resistant. 


086 


DISEASES    OF   THE    NERVOUS    SYSTEM. 


A  microscopical  examination  of  the  patch  in  its  soft  stage  shows  active 

hyperplasia  of  the  neuro- 
glia-cells.  Later,  com- 
pression of  nerve  -  sub- 
stance occurs  from  the 
pressure  of  the  hyper- 
plastic neuroglia  tissue, 
which,  at  this  period,  ex- 
ists as  fibrillated  connec- 
tive-tissue, whose  fibrils — 
extremely  fine  and  inter- 
lacing in  all  directions — 
form  a  network  contain- 
ing atrophied  nerve  ele- 
ments and  small  round  or 
oval  nucleated  cells.  The 
axis  -  cylinders  are  pre- 
served, and  are  sometimes 
markedly  hypertrophied 
at  their  periphery.  At 
the  centre  of  the  mass 
are  found  numerous  amy- 
loid corpuscles,  a  few 
atrophied  axis-cylinders, 
fat  granules,  and  new 
formed  fibres  that  entirely 
replace  the  normal  elements.  The  walls  of  the  vessels  are  thickened.  In 
the  brain  any  portion  of  the  white  substance  may  exhibit  this  lesion. 

Etiology. — The  causation  of  cerebral  sclerosis  is  obscure.  It  unques- 
tionably is  intimately  connected  with  changes  in  the  vascular  system,  for 
the  localities  in  which  it  is  developed  are  the  terminal  arteries,  i.  e.,  ar- 
teries that  do  not  anastomose,  or  anastomose  slightly.  Sclerosis  is  often 
found  in  epileptics  and  in  the  insane.  It  is  occasionally  met  with  in  ad- 
vanced life. 

Symptoms. — The  symptoms  of  cerebral  sclerosis  are  a  gradual  enfeeble- 
ment  of  the  mental  powers,  especially  memory,  muscular  tremors,  headache, 
dizziness  and  vertigo.  Accompanying  these,  one  group  of  muscles  after 
another  becomes  paralyzed.  There  is  no  regular  order  in  the  development 
of  the  paralysis,  first  a  lower,  then  an  upper  extremity,  then  some  of  the 
facial, muscles  are  involved.  Melancholia,  pains  in  the  extremities,  and  a 
sense  of  formication  are  common.  The  nutrition  is  rarely  interfered  with  ; 
many  patients  gain  flesh.  Convulsions  and  disturbances  of  special  sense 
are  rare.     Strabismus  may  be  present. 

A  peculiar  symptom  is  /est ination,— the  patient  bends  forward  and  trots 
along  like  one  trying  to  run  after  he  is  tired  out.  Late  symptoms  are 
paralyses  of  the  muscles  of  deglutition,  speech  and  respiration.  In  rare 
instances  the  first  and  only  symptoms  are  convulsions  of  an  epileptiform 


Pig.  200. 

Sclerosis  of  the  Brain. 

Section  of  Cerebrum  throvgh  a  patch  of  sclerosed  tissue. 

The  normal  brain  structure  has  entirely  disappeared^  and  is  re- 
placed by  interlacing  fibrils  of  connective-tiss^je,  in  the  meshes  of 
which  are  shown  small  nucleated  cells,  atrophied  nerve  fibres  and 
fat  granules,     x  300. 


HYPERTROPHY    OF   THE    BRAIN.  987 

character,  followed  by  hemiplegia.'  Labio-glosso-pharyngeal  paralysis  may 
exist  in  sclerosis.  Electrical  reactions  are  not  changed,  when  the  cord  is 
uninvolved.  Inanition,  emaciation,  muscular  contractures,  and,  rarely,  an 
unexplainable  rise  in  temperature,  precede  death,  which  occurs  in  collapse 
with  loss  of  consciousness. 

Differential  Diagnosis. — Sclerosis  of  the  brain  may  be  mistaken  for  cere- 
hral  softening,  paralysis  agitans,  or  tumors. 

Softening  occurs  in  old  age  ;  the  j)aralysis  is  in  one  set  or  group  of  mus- 
cles, and  if  it  extends,  does  so  in  an  orderly  manner.  There  is  ancesthesia, 
and  the  symptoms  develop  more  suddenly  than  in  sclerosis. 

Paralysis  agitans  is  marked  by  rhythmic  tremor  passing  from  one  upper 
to  the  corres23onding  lower  limb  ;  there  is  a  peculiar  deformity  of  the  fingers 
and  toes ;  the  facial  muscles  are  not  affected,  and  the  patient  inclines  to 
the  paralyzed  side  in  walking.  Paralysis  agitans  occurs  only  after  the  fo"- 
tieth  year,  and  is  accompanied  by  qio  cerebral  symptoms. 

Cerebral  tumors  are  attended  by  headache,  convulsions,  and  signs  of 
brain  irritation  without  loss  of  mental  power. 

Prognosis. — Sclerosis  of  the  brain  may  continue  from  five  to  eight  years, 
but  it  is  progressive  and  always  fatal.  Death  may  occur  from  inanition,  or 
complications  such  as  pneumonia,  bed-sores,  pleurisy,  tuberculosis,  ma- 
rasmus, or  cerebral  paralysis. 

Treatment. — Little  can  be  done  for  this  disease  except  to  improve  the 
general  health.  Yet  it  should  be  mentioned  that  Vulpian  recommends 
chloride  of  iron,  Mitchell  the  bi-chloride  of  mercury,  Hammond  the  chlo- 
ride of  barium,  and  many  the  phosphite  of  zinc.  Nitrate  of  silver  and 
strychnia  are  said  to  relieve  tremor. 

HTPEETROPHT    OF   THE    BEAIlSr. 

Cerebral  central  hypertrophy  is  an  increase  in  the  neuroglia  (the  nerve 
filaments  and  ganglia  are  uninvolved),  and  may  be  partial  or  general.  The 
term  cerebral  hypertrophy  is  really  a  misnomer.^ 

Morbid  Anatomy. — On  removal  of  the  skull-cap  the  brain  protrudes  be- 
yond the  cranial  bones.  The  skull-bones  are  thinned.  If  the  disease  be- 
gins very  early  in  life,  the  head  may  become  as  large  as  in  congenital  hy- 
drocephalus, and  the  sutures  will  be  separated.  The  convolutions  and  sulci 
are  lessened  by  pressure,  and  the  membranes  are  thin  and  dry.  The  dura 
mater  maybe  adherent.  The  ventricular  fluid  is  absent.  Intense  anaemia 
always  exists ;  the  brain  matter,  both  white  and  gray,  is  wliite,  and  tough 
and  elastic.  The  brain  is  heavier  than  normal.  The  cerebrum  is  usually 
involved.  But  hypertrophy  of  the  cerebellum,  thalamus  opticus,  corpus 
striatum,  pons  Varolii,  and  medulla  oblongata  may  also  occur. 

Etiology. — Hypertrophy  of  the  brain  may  be  congenital.     It  appears, 

'  Charcot  states  that  cerebral  sclerosis  not  infrequently  commences  with  nausea,  headache,  vertigo,  syn- 
copal and  apoplectiform  attacks,  followed  by  diplopia,  amblyopia,  nystagmus,  disturbances  of  mind  and 
of  speech. 

2  Virchow  in  1862  and  1867  published  his  article  on  hypertrophy  of  the  brain  ;  his  views  were  based  on 
the  results  of  autopsies,  and  to  these  wc  are  indebted  for  our  knowledge  of  this  subject. 


988  DISEASES    OF   THE   NERVOUS    SYSTEM. 

when  not  congenital,  in  childhood  before  the  third  year.  It  may  be  hered- 
itary, i.  e.,  it  may  occur  in  several  members  of  the  same  family.  It  may 
be  the  result  of  traumatism,  lead  poisoning,  chronic  alcoholismus,  or  epi- 
lepsy. It  not  infrequently  accompanies  idiocy  and  insanity.  In  children, 
swelling  of  the  lymphatics  and  thymus  gland,  and  the  evidences  of  rickets 
precede  or  coexist  with  its  development.  Dwarfs  are  often  the  subjects  of 
cerebral  hypertrophy. 

Symptoms. — Virchow  makes  two  forms,  acute  and  chronic.  In  the  former, 
headache,  epileptiform  convulsions,  retardation  or  great  acceleration  of  the 
pulse,  vertigo,  delirium,  sympathetic  vomiting,  dyspnoea,  and  dysphagia 
occur.  In  children  there  is  weakness,  tremor,  and  a  tottering  gait,  and 
the  head  inclines  to  one  side.  Convulsive  movements  of  the  eye  or  arm 
occur.  There  may  be  permanent  strabismus.  The  child  may  be  very  pre- 
cocious at  first ;  later  he  becomes  feeble-minded  or  idiotic.  Periodical  lar- 
yngeal spasm  (thymic  asthma)  may  occur.  Bulimia  is  marked  ;  and  the 
child  is  constantly  somnolent.  The  tongue,  often  larger  than  normal,  pro- 
trudes from  the  mouth,  and  children  often  persistently  suck  it.  Headache 
is  rarely  absent.  It  is  steadily  progressive,  and  e7ids  in  coma,  preceded  by 
dilated  pupils,  slowed  pulse,  vomiting,  and  repeated  convulsive  attacks. 

DifFerential  Diagnosis. — It  is  very  often  impossible  to  differentiate  between 
chronic  hydrocephalus  and  hypertrophy  of  the  brain.  In  hypertrophy  the 
child  has  been,  or  is,  bright  and  precocious  ;  in  hydrocephalus  he  is  always 
stupid.  The  fontanelles  pulsate  in  hydrocephalus  ;  they  do  not  in  hyper- 
trophy. The  cerebral  souffle  may  be  heard  in  hypertrophy  but  not  in  hy- 
drocephalus. 

Prognosis. — It  always  terminates  in  death.  It  may  end  either  by  pro- 
gressive stupor  or  from  complications. 

ATEOPHT    OF   THE   BEAEST. 

Atrophy  of  the  brain  may  be  either  infantile  or  senile;  it  is  never  met 
with  in  adult  life. 

Morbid  Anatomy. — In  children  the  disease  begins  in  utero.  The  skull  is 
oblique  ;  one-half  is  thick,  smaller  than  normal,  and  misshapen.  The  cor- 
responding parts  of  the  brain  are  atrophied,  hard,  altered  in  color,  and  are 
studded  with  collections  of  serum.  (Rosenthal.)  Atrophy,  or  absence,  of 
the  corpus  callosum  is  the  result  of  defective  foetal  development.  It  is 
generally  accompanied  by  intra-uterine  hydrocephalus.  Physiologically, 
the  brain  begins  to  diminish  in  R^eight  after  the  sixtieth  year;  at  thai 
time  it  is  one-fifteenth  lighter  than  during  early  adult  life.  Hence. 
slight  atrophy  is  physiological  in  old  age.  But  in  senile  atrophy  ther^ 
is  more  or  less  marked  diminution  in  the  anatomical  elements  of  the 
brain,  and  a  loss  in  the  interstitial  connective-tissue.  The  cells  of  the 
cortex  are  swollen  and  pigmented  ;  and  pigmentation  also  occurs  in  the 
walls  of  the  vessels,  which  often  undergo  more  or  less  fatty  degeneration. 
The  cortex  is  thinned,  and  in  it  are  found  corpora  amylacea.  The  fat  in 
the  cerebral  substance  is  lessened,  the  water  increased.     Senile  atrophy  is 


ATEOPHY    OF   THE    BRAIN".  989 

usually  general ;  but  when  partial  it  affects  the  left  hemisphere.  There  is 
unequal  thinning  of  the  convolutions,  and  the  sulci  are  large  and  deep. 
The  meninges  are  somewhat  clouded.  The  brain  is  usually  tougher  than 
normal,  and  the  ventricles  contain  from  two  to  twelve  drachms  of  fluid. 
This  is  a  purely  conservative  process.  The  ependyma  is  granular  and 
nodular.  More  or  less  serum  distends  the  meshes  of  the  pia  mater.  The 
medullary  substance  and  the  corpora  striata  are  riddled  with  holes,  etat 
crihU.^ 

On  section  the  brain  has  a  leathery  toughness  ;  it  may  be  corrugated.  The 
cortex  is  of  a  dirty  gray  color;  and  the  medullary  substance  is  a  dull  white 
or  drab  color.  Partial  atroj)hy  may  extend  to  the  cortex,  or  it  may  follow 
the  fibres  through  the  peduncles,  pons  Varolii,  and  pyramids.  A  crossed 
lesion  may  sometimes  be  met  with,  due  to  atrophy  of  one  cerebral  and  of 
the  opposite  cerebellar  hemisphere.  There  are  remarkable  instances  of 
diminution  of  the  cerebellum  to  one-half  its  normal  size  and  weight. 

The  loss  in  weight  of  the  brain  in  the  general  j}aralysis  of  the  insane  is 
greater  than  in  any  other  disease.  The  cerebellum  and  basal  portions  of 
the  cerebrum  are  unaffected  ;  the  most  striking  degree  of  atrophy  being  in 
the  frontal  lobes,  the  convolutions  exhibiting  it  most  of  all.  Of  all  the 
changes  accompanying  this  form  of  atrophy  those  in  the  dura  are  most 
marked  ;  it  is  adherent  to  the  bone,  and  hemorrhages  into  its  substance  are 
frequently  met  with.  Pachymeningitis,  hsematoma,  ruptures  and  foldings 
of  the  dura  over  the  brain  are  often  met  with.  Some  regard  these  as  the 
specific  lesions  of  general  paralysis.  The  p)ia  mater  is  oedematous  and 
thickened,  either  continuously  or  in  patches. 

Etiology. — Cerebral  atrophy  may  be  congenital  or  occur  as  a  part  of 
senile  change.  It  may  follow  cerebral  hemorrhage  or  softening,  and  is 
occasionally  caused  by  tumors,  meningeal  inflammation,  and  internal  or 
external  hydrocephalus.  Injury  or  destruction  of  the  peripheral  nerves 
may  induce  secondary  cerebral  atrophy.  Excess  in  venery,  the  opium 
habit,  and  alcoholismus  are  adduced  as  its  causes."  It  is  met  with  oftenerin 
males  than  in  females.     Senile  marasmus  is  its  chief  cause. 

Symptoms. — Senile  cerebral  atrophy  is  attended  by  gradual  failure  of  the 
mental  faculties.  Memory  is  impaired,  the  special  senses  3.re  markedly 
dulled  ;  and  the  movements,  at  first  unsteady,  are  soon  accom|)anied  by 
tremor.  The  patient  is  somnolent ;  indeed,  he  sleeps  the  greater  part  of  the 
time.  Soon  the  condition  popularly  known  as  "second  childhood"  is 
reached.  There  is  often  more  or  less  complete  loss  of  power  over  the 
sphincters.  Atrophic  degenerations  of  that  half  of  the  body  on  the  same 
side  as  the  atrophied  cerebellum,  or  on  the  opposite  side  to  the  atrophied 
cerebrum  are  apt  to  occur.  Incomplete  paralysis  accompanies  these  atrophic 
changes.  Epileptiform  attacks  are  quite  frequent ;  choreic  attacks  occa- 
sionally occur. 

Only  a  brief  mention  can  here  be  made  of  the  symptoms  of  the  extensive 
atrophy  which  occurs  in  general  paralysis  of  the  insane.  Headache,  dizzi- 
ness, irritability  of  temper,  weakness  of  memory  pre-eminently,  thickness 

>  Durand-Fardel  and  Parchappe. 


990  DISEASES    OF    THE    NEEVOUS    SYSTEM. 

of  sjDeech,  change  in  the  character  of  the  voice,  a  feeling  of  self-importance, 
grandeur  and  great  riches, — these  are  very  common.  Sudden  and  uncalled- 
for  outbursts  of  rage  are  common.     It  is  very  much  like  senile  dementia. 

Atrophy  of  the  brain  ultimately  involves  the  medulla,  implicates  the 
great  life-centres  situate  therein,  and  deglutition  or  respiration  is  so  much 
interfered  with  that  death  results.  In  general  paralysis  of  both  sides  of  the 
body  there  is  usually  complete  imhecility. 

Differential  Diagnosis. — Senile  cerebral  atrophy  may  be  mistaken  for 
cerehral  hemorrhage  and  softening.  The  history  of  the  case  is  essential  in 
its  differential  diagnosis.  Atrophy  of  the  cerehellum  may  be  mistaken  for 
tabes  dorsalis  and  multijjle  sclerosis.  From  the  former  it  is  diagnosticated 
by  the  absence  of  vesical  symptoms  and  by  more  intense  pains ;  the  anaes- 
thesia about  the  dorsal  vertebrae  is  a  valuable  point,  as  it  is  always  present 
in  tabes  and  not  in  atrophy.  The  intra-uterine  variety  of  cerebral  atrophy 
is  easily  recognized  by  the  paralyses  and  spasmodic  seizures  that  occur 
directly  after  the  birth  of  the  child. 

Prognosis. — Congenital  atrophies,  or  those  occurring  in  the  early  life, 
usually  terminate  during  the  fourth  year.  Senile  atrophy  is  steadily  pro- 
gressive to  a  fatal  termination.  No  estimate  of  its  duration  can  be  made. 
It  may  be  complicated  by  hypostasis  in  the  lungs,  bronchitis,  pulmonary 
cedema,  pneumonia,  acute  bed-sores,  or  by  disease  of  the  bladder  or  kidneys. 
In  the  general  paralysis  of  the  insane  its  duration  is  rarely  more  than  a  year. 
Death  is  reached  by  intercurrent  apoplexies,  exhaustion  from  large  bed- 
sores, ansemia  or  pulmonary  complications. 

Treatment. — Improvement  of  the  general  health  is  regarded  as  the  most 
important  indication.  Some  advocate  exercise  and  massage  of  the  para- 
lyzed limbs.  Niemeyer  recommends  cold  douches.  In  atrophy  in  general 
paralysis,  galvanism,  iodide  of  potash,  calabar  bean,  morphia,  and  chloral, 
alone  or  together,  prolonged  tepid  baths,  and  attention  to  the  bowels  and 
bladder  have  been  recommended. 


DISEASES  OF  THE  SPINAL  COED. 

Diseases  of  the  spinal  cord  and  its  membranes  will  be  considered  under 
the  following  heads  : 

I.  Spinal  Ilyijercemia.  IX.  Acute  Spinal  Paralysis  of  Adults, 

II.  Spinal  Meningitis.  X.  Chronic  Anterior  Myelitis. 

■  HI.  Acute  Myelitis.  XI.  Progressive  Muscular  Atrophy. 

IV.   Chronic  Myelitis.  XII.  Cerebro- Spinal  Sclerosis. 

V.  JSfon-Inflammatory  Soften-   XIII.  Locomotor  Ataxia. 

ing.  XIV.  Spasmodic  Tabes  Dorsalis. 

VI.  Acute  Bulbar  Paralysis.        XV.  Amyotrophic  Lateral  Sclerosis. 

VII.  Progressive  Bulbo-Nuclear  XVI.  Pseudo-Hypertrophic  Paralysis. 

Paralysis.  XVII.  Spinal  Apoplexy. 

VIII.  Lnfantile  Spinal  Paralysis. 


HYPEE^MIA   OP   THE   SPINA L   COED    AND    MENINGES.  991 


HYPEREMIA    OF    THE    SPINAL   CORD    AND    MENINGES. 

Hyperaernia  of  the  spinal  cord  may  be  active  or  passive. 

Morbid  Anatomy. — The  most  intense  active  or  passive  hyperaemia  of  the 
spinal  meninges  may  disappear  between  death  and  the  time  of  a  post-mortem, 
and  a  gravitation  from  position  may  induce  a  congestion  which  is  decidedly 
misleading.  In  active  hyperasmia  the  arterioles  are  injected  and  the  parts 
assume  a  rosy  color  marked  possibly  by  numerous  points  of  extravasation. 
In  passive  hyperaemia  the  veins  of  the  cord  and  membranes  are  distended 
with  dark  blood.  .  Chronic  congestion  results  in  thickenings,  pigmentation 
and  opacities  of  the  membranes,  attended  by  development  of  new  con- 
nective-tissue which  may  be  the  starting-point  of  a  general  sclerosis. 

Etiology. — Active  hypermmia  may  result  from  muscular  exertion,  or  ex- 
cesses in  venery,  from  vaso-motpr  paralysis  due  to  exposure  to  cold  and  wet, 
concussion,  and  suppression  of  menstrual  or  hemorrhoidal  fluxes.  Hy- 
peraemia is  always  an  attendant  of  general  or  local  myelitis.  It  occurs  with 
acute  infectious  diseases,  typhoid,  small-pox,  scarlet  fever,  and  measles, 
with  chronic  malarial  infection,  and  in  some  cases  of  rheumatism  and 
puerperal  fever.  It  may  also  result  from  poisoning  by  carbonic  oxide, 
strychnia,  nitrite  of  amyl,  alcohol,  etc'  Intense  active  hypereemia  has 
been  found  in  those  who  have  died  of  spasmodic  affections,  or  who  have 
worked  in  compressed  air,  as  in  caissons.'' 

Passive  liypercemia  is  caused  by  any  obtrusive  disease  of  heart,  liver  or 
lungs,  and  by  mechanical  pressure  uj)on  venous  trunks,  by  tumors,  fluid 
effusion,  etc. 

Symptoms. — The  onset  of  active  hypereemia  may  be  sudden,  while  pas- 
sive hyperaemia  generally  comes  on  slowly  and  often  insidiously.  In  most 
instances  there  is  pain  along  the  spine,  especially  in  the  lumbar  region, 
which  radiates  down  the  thighs  and  is  increased  by  movement  and  pressure. 
There  is  hypersesthesia  of  the  lower  limbs  associated  with  itching,  burn- 
ing, or  formication,  and  reflex  irritability  is  augmented. 

Hyperaesthesia,  sharp  pains,  spasms,  and  symptoms  of  irritation  would 
rather  point  to  ac^^/'ve  hyperaemia,  while  numbness,  anfesthesia,  heaviness  of 
the  limbs  and  vesical  paresis  are  more  commonly  associated  with  congestion.^ 
In  rare  cases  the  disease  is  so  sudden  in  its  onset  that  the  patient  may 
awake  to  find  himself  in  a  state  of  incomplete  paraplegia.  During  the 
whole  course  there  is  no  fever  and  little,  if  any,  change  in  the  pulse. 
Dyspnoea  occurs  when  the  nerve  roots  are  involved  high  up  in  the  cord.* 
Quite  often  during  attacks  of  spinal  congestion,  persistent  priapism  occurs 
and  the   iron-band   sensation  about  the  waist  is  a  frequent  symptom.* 

1  Magnan  has  experimented  with  absinthe  on  animals,  and  found  it  to  produce  intense  hj'perisemia  when 
given  in  large  doses. 

*  /S'/.  Lovw  Med.  and  Svrg.  Jour. — Dr.  Clark. 

s  Ro.senthal  states  that  violent  emotions  and  sometimes  the  dorsal  decubitus  increase  the  rachialagia. 

*  Steiner  reports  a  case  where  facial  paralysis  occwvr Qd.—ArcMv  der  Heilk.  11,  1870,  p.  23.3. 

^  Fabra  has  observed  pain,  ana3sthesia,  hyperajsthesia,  slight  paresis,  and,  rarely,  convulsive  phenom- 
ena occurring  in  tho  last  stages  of  heart  disease,  which  seemed  to  be  due  to  ^awiw  hyperasmia  of  the 
cord.— Gaz.disUoi).,  1870,  No.  147. 


992  DISEASES    OF   TEE   NEEVOUS    SYSTEM. 

When  convulsions  occur  in  sucli  diseases  as  tetanus  there  is  intense  hj  - 
pergemia  of  the  gray  matter  of  the  cord. ' 

Differential  Diagnosis. — Hyperaemia  of  the  cord  may  be  mistaken  for 
spinal  ancBmia,  meningitis,  myelitis  or  apoplexy. 

In  anmmia  the  symptoms  are  relieved  by  the  recumbent  posture,  while 
they  are  increased  in  hypergemia.  Anaemia  occurs  suddenly,  as  from  em- 
bolism and  thrombosis.  Women  suffer  most  frequently  from  anaemia, 
men  from  hyperaemia.  Vesical  complications  follow  congestion,  but  not 
anaemia. 

In  inflammation  of  tlie  cord  there  will  be  fever,  paraplegia,  paralysis  of 
the  sphincters,  loss  of  electro-contractility,  with  bed-sores  and  subsequently 
wasting  of  the  muscles. 

The  onset  of  spinal  apoplexy  is  sudden,  j)araplegia  is  complete  within  a 
few  hours,  and  accompanied  by  anaesthesia,  paralysis  of  the  bladder  and 
rectum,  the  early  development  of  gangrenous  bed-sores,  and  in  most  cases 
by  the  symptoms  of  cystitis  and  myelitis. 

Prognosis. — The  prognosis  is  favorable,  although  the  condition  is  one 
which  has  a  marked  tendency  to  become  chronic.  Complete  recovery  is 
slowly  reached,  except  in  those  cases  where  the  cause  is  permanent. 

Treatment. — If  its  cause  can  be  reached,  it  should  at  once  be  removed. 
Severe  and  sudden  congestion  demands  local  abstraction  of  blood  by  wet 
cups  along  the  spine  or  leeching  about  the  anus.  The  patient  should  be 
kept  quiet  on  his  side.  In  recent  cases  ice-bags  to  the  spine,  hot  foot  baths, 
and  a  brisk  purge  will  relieve  the  pain.  Ergot  and  belladonna  and  hot 
douches  along  the  spine  are  highly  advocated  in  chronic  passive  hyperaemia. 
In  reflex  hyperaemia,  or  hyperaemia  due  to  vaso-motor  disturbances,  elec- 
tricity may  afford  relief. 

SPINAL    MENINGITIS. 

Spinal  meningitis  may  be  acute  or  chronic. 

Morbid  Anatomy. — Acute  inflammation  of  the  spinal  meninges  is  gener- 
ally diffuse,  and  runs  a  course  similar  to  acute  cerebral  meningitis.  The 
pia  mater  is  hyperaemic,  swollen  and  studded  with  ecchymoses.  The  ex- 
udation takes  place  into  the  meshes  of  the  membrane,  and  the  effusion  maj 
be  sero-fibrinous,  or  purulent.  The  pia  mater  is  thickened,  opaque,  and 
cedematous,  and  a  turbid  fluid  fills  more  or  less  completely  the  spinal 
canal.  Although  the  exudation  is  more  abundant  upon  the  posterior  sur- 
face, it  usually  envelops  more  or  less  completely  the  whole  cord,  whose 
substance  may  either  be  pale  and  anaemic,  or  exhibit  changes  of  com- 
mencing myelitis  and  softening.  The  roots  of  the  nerves  are  embedded  in 
the  exudation,  and  present  changes  similar  to  those  in  the  cord.  The 
exudation  may  be  wholly  absorbed,  and  the  membranes  and  the  cord  return 
to  their  normal  condition  ;  but  more  frequently  the  inflammation  becomes 
chronic. 

In  chronic  spinal  meningitis  there  are  found  the  opacity,  thickening, 
adhesions,  and  puckerings  so  characteristic  of  chronic  interstitial  inflam- 

1  j?einberg. 


SPINAL  MENINGITIS.  993 

mation  in  similar  membranes.  The  membrane  is  tough,  dark,  bluish -gray 
in  color,  pigmented,  and  contains  calcareous  plates.  It  is  adherent  at 
various  points  to  the  thickened  dura  mater  (pachymeningitis  spinalis). 
The  fluid  in  the  spinal  canal  is  always  increased  in  amount ;  it  may  be  clear 
serum,  or  contain  lymph  flocculi,-  blood,  or  pus.  The  irregular  and  local- 
ized adhesions  and  retractions  produce  sclerosis  of  the  cord,  and  also  induce 
anaemia,  atrophy,  and  degeneration  of  the  nerve  roots. 

Etiology. — Spinal  meningitis  is  a  disease  of  youth  and  early  adult  life, 
and  may  follow  a  traumatism,  as  in  a  fall,  blow,  dislocation,  fracture,  or 
other  injury  to  the  vertebrae,  or  concussion,  which  is  thought  to  be  a  fre- 
quent cause.  It  may  arise  from  extension  of  inflammation  from  the 
cerebral  meninges,  from  any  disease  of  the  spine,  such  as  caries,  cancer, 
etc.  Prolonged  exposure  to  cold — especially  damp  cold — or  brief  exposure 
to  intense  cold  when  the  body  is  heated,  as  well  as  exposure  to  intense  heat, 
will  induce  spinal  meningitis.  Operations  for  sjDina  bifida  have  been  fol- 
lowed by  rapid  and  fatal  spinal  meningitis. 

Eheumatism  is  said  to  be  an  occasional  cause,  and  some  authors  regard 
all  febrile  and  infectious  diseases  as  liable  to  be  complicated  by  it.'  Syph- 
ilis, venereal  excesses,  alcoholismus,  chorea,  tetanus,  and  hydrophobia  may 
each,  in  rare  instances,  induce  spinal  meningitis  f  and  scrofulosis,  tuber- 
culosis and  wasting  diseases  are  very  apt  to  be  complicated  by  it. 

The  chronic  form  is  often  a  sequel  of  the  acute,  and  is  very  apt  to  accom- 
pany alcoholismus,  syphilis,  impeded  venous  return,  and  diseases  of  the 
cord.  The  latter  are  the  most  frequent  of  all  causes.  Chronic  or  acute 
inflammation  of  the  cord,  or  any  neoplasm  that  encroaches  upon  the  spinal 
canal,  will  lead  to  localized  chronic  meningitis.  Excessive  use  of  tobacco 
or  narcotics,  and  anti-hygienic  surroundings  are  jaredisposing  causes. 

Symptoms. — When  spinal  meningitis  is  associated  with  cerebral  inflamma- 
tion its  symptoms  are  less  distinct  than  when  it  is  uncomplicated.  Severe 
pain  in  the  back  is  the  earliest  and  most  prominent  symptom.  The  pain 
at  first  is  localized  about  the  seat  of  the  inflammation,  but  later  becomes 
diffused  and  shoots  down  the  legs  and  arms.  It  is  constant,  and  is  made 
sharp  and  lancinating  by  motion,  so  that  the  patient  holds  himself  in  a 
fixed  position  with  rigidly  contracted  muscles ;  pressure  along  the  spine 
may  increase  the  pain.  A  chill  or  distinct  rigor  accompanies  the  pain,  and 
is  followed  by  rise  in  temperature,  nausea,  vomiting,  and  a  sense  of  general 
malaise.  The  fever  is  never  high  and  the  pulse-rate  is  frequently  below  the 
normal.  The  muscles  along  the  spine  become  rigid,  and  if  the  cervical  re- 
gion is  involved  there  is  ojDisthotonos.  Convulsive  twitching  of  groups  of 
muscles  is  attended  by  the  most  excruciating  pain.  The  surface  of  the  body 
becomes  hyperaesthetic  in  the  area  of  motor  derangement,  and  reflex  activ- 
ity is  increased.  In  a  few  instances  all  the  extremities  are  involved,  but 
usually  there  is  only  incomplete  paraplegia.  There  is  constipation,  and 
the  abdomen  has  the  well-known  boat-shaped  appearance. 

'  ('.  B.  Rndcliffe,  in  Reynold's  SijHtfm,. 

'■'  Koehler  states  that  any  pulmonary  or  cardiac  disease  that  impedes  proper  venous  return  affords  a 
marked  predisposition  to  spinal  meningitis. 

63 


99-4  DISEASES   OF   THE   NERVOUS   SYSTEM. 

At  the  commencement  of  the  attack  there  is  a  constant  desire  to  mictu- 
rate. Later,  paralysis  of  the  bladder  and  retention  of  urine  accompany  the 
para-paresis,  so  that  catheterization  must  be  resorted  to.  If  the  paralysis 
involves  the  respiratory  muscles  there  will  be  dyspnoea,  and  the  temperature 
will  rise  to  106°  or  107°  P.,  and  be  followed  by  coma  and  death.  If  the 
meningitis  is  limited  to  the  lower  portion  of  the  cord,  the  case  will  be  pro- 
tracted, but  marked  by  periods  of  slight  improvement.  In  such  cases  bed- 
sores may  develop,  with  incontinence  of  urine,  and  death  finally  occur  from 
exhaustion.  Sudden  and  profuse  sweats  may  result  from  vaso-motor  impli- 
cation. 

Glironic  spinal  meningitis  is  generally  a  sequel  of  acute,  although  it  may 
develop  without  any  acute  symptoms.  When  the  acute  passes  into  the 
chronic  form,  i)ain  and  rigidity  of  the  spine  remain  after  the  other  symp- 
toms have  subsided.  The  limbs  are  hypersesthetic,  and  the  seat  of  burning, 
formication,  or  itching.  There  maybe  a  sensation  as  of  a  tight  band  about 
the  waist,  accompanied  by  weight  and  uneasiness  in  the  limbs,  which  may 
develop  into  incomplete  paraplegia.  The  bowels,  at  first,  are  constipated, 
but  later  the  passages  may  be  involuntary.  The  bladder  is  frequently  par- 
alyzed, incontinence  of  urine  occurs,  bed-sores  form,  and  a  well-marked 
marasmus  is  developed.  Finally  the  paralysis  will  vary  in  degree  with  the 
posture  of  the  patient — and  also  from  day  to  day. 

Differential  Diagnosis. — Acute  spinal  meningitis  may  be  confounded  with 
myelitis,  tetanus,  and  muscular  rheumatism.  In  tetanus  the  locked  jaw, 
the  |)eculiar  implication  of  the  facial  muscles  causing  the  risus  sardonicus, 
and  the  intense  cutaneous  hypersesthesia,  with  recurring  paroxysms  with- 
out paralysis,  are  in  marked  contrast  to  the  symptoms  of  spinal  meningitis. 
In  the  latter  disease  there  is  great  pain  on  motion,  little  or  none  on  pres- 
sure, and  muscular  spasm  is  produced  by  attempts  at  movement  rather  than 
by  irritation.     There  is,  usually,  a  traumatic  history  in  tetanus. 

Rheumatism  in  the  muscles  of  the  hack  is  accompanied  by  local  pain  only 
when  movements  are  made  :  but  there  is  never  that  rigidity  of  the  spine 
which  is  present  in  meningitis,  nor  the  cutaneous  hyperaesthesia,  paralysis, 
spasms,  or  febrile  phenomena. 

Spinal  irritation  may  be  mistaken  for  meningitis,  but  the  pain  on  press- 
ure confined  to  one  spot,  the  absence  of  pain  upon  ordinary  or  slight  mo- 
tion, and  the  disposition  to  a  sudden  transference  of  the  diseased  action 
from  one  organ  or  part  to  another,  with  possibly  the  occurrence  of  hyster- 
ical symptoms,  will  be  sufficient  to  distinguish  between  them. 

Chronic  meningitis  may  be  mistaken  for  chronic  myelitis.  In  meningitis 
pain  is  a  far  more  prominent  symptom  than  in  myelitis  ;  and  it  is  increased 
by  motion  but  not  by  pressure,  the  reverse  of  which  occurs  in  myelitis. 
Paralysis  is  never  complete  in  meningitis,  and  anaesthesia  and  muscular 
atrophy  are  rare  as  compared  with  myelitis. 

Prognosis. — Acute  spinal  meningitis  runs  a  variable  course  ;  should 
death  occur  within  twenty-four  or  thirty-six  hours  the  case  is  to  be  re- 
garded as  epidemic.  The  usual  duration  of  the  acute  form  is  from  seven 
to  ten  days.     The  majority  of  cases  are  fatal,  more  especially  those  in  which 


ACUTE    MYELITIS.  995 

the  membranes  of  the  cervical  cord  are  involved.  In  these  cases,  death  re- 
sults from  paralysis  of  the  muscles  of  respiration,  and  will  be  preceded  by- 
intense  dyspncea  and  cyanosis.  Even  when  recovery  occurs,  convalescence 
is  tedious ;  and  though  the  general  health  is  restored,  pain,  paralysis, 
and  stiffness  or  atrophy  of  muscles  are  apt  to  continue  for  many  months. 
Karely  is  convalescence  rapid.  In  many  acute  cases  death  occurs  from 
simple  asthenia. 

.  Chronic  spinal  meningitis  runs  a  very  protracted  course,  and  may  ter- 
minate in  death  from  exhaustion,  anaemia  or  marasmus.  It  jorogresses  by 
stages ;  and  although  the  prognosis  is  not  so  unfavorable  as  in  the  acute 
form,  complete  recovery  is  rare.  Both  acute  and  chronic  are  most  severe 
in  the  very  young  or  the  very  old  and  enfeebled. 

Treatment. — The  same  principles  guide  the  treatment  of  acute  spinal 
meningitis  as  were  advised  in  acute  cerebral  meningitis.  The  patient 
should  be  placed  in  bed  in  a  cool  room  and  a  brisk  purge  administered. 
Ice  or  counter-irritation  may  be  applied  along  the  spine,  and  from  the  on- 
set the  patient  should  be  kept  in  a  condition  of  semi-narcotism.  Ergotin 
and  belladonna  hypodermically  are  said  to  produce  contraction  of  the 
arterioles  and  restrain  the  inflammatory  process.  The  internal  ad- 
ministration of  the  iodide  of  potash  with  mercury  is  advocated.  Warm 
baths  are  grateful  to  the  patient,  and  produce  a  sedative  effect,  and  have 
seemed  to  me  to  be  of  greater  service  than  all  other  measures.  The  nour- 
ishment should  be  highly  nutritious  but  never  stimulating.  When  symp- 
toms of  heart  failure  or  asthenia  come  on,  stimulants  are  indicated. 
Careful  attention  to  the  condition  of  the  bladder  should  never  be  ne- 
glected. 

In  chronic  spinal  meningitis  counter-irritation  over  the  spine,  and  de- 
rivatives to  the  surface  are  to  be  employed  as  long  as  the  inflammatory  pro- 
cesses are  in  progress.'  Warm  douches  are  excellent  adjuvants,  and  in 
some  cases  are  followed  by  marked  benefit.  Iodide  of  potash  and  mercury 
— ^the  latter  both  internally  and  by  inunction — are  more  clearly  indicated 
in  chronic  than  in  acute  cases.  The  galvanic  current  is  often  of  service 
in  preventing  the  muscular  atrophy  and  contractions  which  are  sequelge 
of  the  paralyses. 

ACUTE  MYELITIS. 

Myelitis  is  an  inflammation  of  the  substance  of  the  spinal  cord,  and 
may  be  limited  to  the  gray  or  white  matter  ;  it  runs  an  acute  or  chronic 
course,  and  involves  the  whole  or  isolated  portions  of  the  cord. 

When  the  gray  m.atter  alone  is  involved,  it  is  called  central  myelitis  j 
when  the  white  matter  and  the  meninges  are  involved  it  is  called  cortical 
myelitis. 

When  once  established  the  disease  may  be  ascending,  descending,  or  trans- 
verse in  its  extension. 

1  Brown-Sequard  advises  sinapisms,  stimulating  ointments,  and  oils,  moxa,  and  in  severe  cases,  white' 
not  irons  to  the  spine. 


996 


DISEASES   OF   THE   NERVOUS   SYSTEM. 


Morbid  Anatomy. — In  acute  myelitis  the  portion  involved  is  softened  and 

discolored  to  an  extent 
corresponding  to  the 
amount  of  vascular  dila- 
tation and  transudation 
of  red  blood  cells. 
Hemorrhage  takes  place 
into  the  softened  spots, 
although  in  many  cases 
it  is  doubtful  whether 
the  hemorrhage  prece- 
ded or  followed  the  soft- 
In  most  cas6s 
,  and 
on  section,  blood  points 
and  spots  of  ecchymoses 
are  seen.  The  veins 
especially  are  distended 
and  surrounded  by  a 
layer  of  red  and  white 
blood  corpuscles. 

Microscopically  there 
will  be  found  swelling 
of  the  cells  of  the  neu- 
roglia, ampullge-like  di- 


enmg. 

the  cord  is  enlarged, 


Fig.  201. 

Acute  Myelitis. 

From  a  Section  through  the  Dorsal  Spinal  Cord,  including  portion  of 
the  Anterior  Gray  Cornu. 


A.  Patch  of  ecchymotic  tUsiie. 

B.  Nerve  fibres  ivith  swollen  axis-cylinder. 
C , ' Hype.rtrophied  and  'pigmented  ganglion  cells,  with  ampullar  latatioUS  of  the  a\is-CvL 

inders 


',  of  nerve  fibrils 

hypertrophy   of 

the  cells  in  the  anterior  horn  of  the  gray  substance,  and  an  albuminoid 
granular  degeneration  of  the  nerve  fibres.  The  nerve  cells  not  infre- 
quently show  pigment  degeneration,  and  the  ganglion  cells  are  clouded 
and  swollen. 

These  morbid  processes  result  in  entire  disappearance  of  the  normal  ana- 
tomical elements  of  the  cord.  The  adjacent  membranes  will  be  congested, 
thickened,  opaque,  and  adherent  to  the  cord,  while  collections  of  blood  or 
pus  underneath  the  membrane  may  cause  it  to  present  a  nodulated  appear- 
ance. These  changes  are  most  marked  in  the  gray  matter  of  the  dorsal  and 
lumbar  regions.  Acute  red  softening  soon  becomes  yellow  from  fatty  de- 
generation, from  changes  in  the  coloring  matter  of  the  blood,  and  from 
diminution  in  vascularity.  Later,  as  its  consistence  diminishes,  a  pale 
yellow  or  white  diffluent  mass  is  left.* 

Etiology. — Acute  myelitis  is  a  disease  of  children  and  young  adults.  In 
children  it  takes  the  form  of  acute  anterior  polio-myelitis  or  spinal  paral- 
ysis. Exposure  to  excessive  heat  or  cold,  intense  and  prolonged  muscular 
exertion,  and  excessive  venery  are  said  to  predispose  to  it ;  and  in  children, 
dentition  is  regarded  as  a  predisposing  cause.     Myelitis  may  be  excited  by 


1  Erb  states  that  this  softening  is  due  to  fluid  exudation  ft'om  the  vessels  and  destruction  of  the  nerve 
fibres. 


ACUTE    MlfELlTIS.  997 

traumatism,  lying  on  the  damp  ground,  and  expos^^re  to  sudden  chilling 
of  the  surface  when  overheated.  Whether  suppression  of  the  menses,  check- 
ing hemorrhoidal  fluxes,  or  profuse  perspiration  of  the  feet  can  cause  it  is 
uncertain.  Pressure  on  the  cord,  from  tumors  or  displacements  of  the 
bony  parts,  whether  occurring  suddenly  or  developing  slowly,  will  induce 
myelitis,  or  it  may  be  excited  by  extension  of  inflammation,  especially  from 
spinal  meningitis. 

Myelitis  also  arises  during  the  course  of  small-pox,  measles,  scarlet  and 
typhoid  fevers,  acute  articular  rheumatism,  malignant  pustule,  puerperal 
fever,  and  syphilis.  Continued  jarring  of  the  spine  from  travel  on  rail- 
ways will  induce  it. '  Visceral  disturbances — especially  of  the  genito-uri- 
nary  and  digestive  organs — and  diseases  of  the  joints  are  said  to  act  as 
reflex  causes.  In  many  cases  the  myelitis  comes  on  without  any  assignable 
cause. 

Symptoms. — Acute  myelitis  usually  commences  with  slight  febrile  symp- 
toms, pain  in  the  back,  a  peculiar  sensation  of  an  iron  band  around  the  waist, 
and  the  pulse  is  frequently  feeble  and  irregular.  Anorexia,  headache  and 
general  malaise  usually  precede  the  attack.  The  power  of  motion  in  the 
lower  extremities  is  rapidly  lost,  and  soon  complete  paralysis  occurs,  which 
is  usually  both  sensory  and  motor.  Patients  will  complain  of  a  sense  of 
numbness  in  the  feet ;  they  cannot  feel  the  ground  under  their  feet,  and 
they  have  a  sensation  as  if  something  was  crawling  over  their  legs.  Ee- 
tention  of  urine  and  fseces,  which  marks  the  onset,  gives  place  to  inconti- 
nence, from  paralysis  of  the  sphincters.  Tremulous  and  spasmodic  move- 
ments often  occur  in  the  limbs  that  are  subsequently  paralyzed ;  and  at  the 
commencement  of  the  paralysis  their  temperature  is  elevated.  Electro- 
muscular  contractility  is  diminished. 

The  pains  in  the  back  are  increased  by  pressure,  and  localized  at  certain 
vertebra.  The  application  of  lieat  or  cold  over  the  sensitive  spot  produces 
pain  ;  and  a  warm  or  cold  sponge  at  the  junction  of  the  normal  and  anges- 
thetic  parts  produces  a  burning  sensation,  felt  in  a  line  around  the  body. 
When  the  paraplegia  is  sudden  and  complete,  hemorrhage  into  the  softened 
focus  may  be  suspected.  The  paralysis  frequently  extends  rapidly  upward, 
and  when  the  cervical  cord  is  involved  paresis  and  anaesthesia  of  the  arms, 
irregularities  of  the  pupils,  dyspnoea  and  dysphagia  will  be  present  ;  the 
pain  in  these  cases  is  located  in  the  neck.  The  itching,  burning,  or  boring 
pains  in  the  limbs  and  the  sense  of  formication  that  precede  the  paraplegic 
symptoms  are  rarely  influenced  either  by  pressure  or  motion.  Reflex 
action  is  diminished  or  lost,  and  its  abolition  is  an  indication  of  the  extent 
to  which  the  gray  matter  is  involved. 

Trophic  or  vaso-motor  disturbances  appear  early,  causing  acute  bed-sores, 
oedema  of  the  paralyzed  limbs,  effusions  into  the  joints,  and  more  or  less 
muscular  atrophy.  The  urine  becomes  alkaline  and  often  bloody.  Reten- 
tion is  of  frequent  occurrence  and  results  in  cystitis  and  pyelitis  ;  uraemic 
symptoms  may  appear,  and  sepsis  often  occurs  from  the  bed-sores  and 
gangrenous   inflammation.       Among  the  later  manifestations  are  darting 

'  OUivier,  Hine  and  Leydeii  regard  mental  shock,  especially  from  fright  or  anj^'er,  as  a  cause. 


99.8  DISEASES   OP  THE   NERVOUS   SYSTEM. 

pains,  spasmodic  twitchings  and  contractions,  either  of  isolated  groups  or 
of  all  the  muscles  in  the  paralyzed  part/  Tliis  marks  its  passage  into  the 
chronic  stage.  In  some  few  cases  hemi-paraplegia  is  induced  by  myelitis. 
The  disease  is  always  progressive.  In  some  classes  the  paraplegia  may  be 
so  rapidly  developed  that  in  forty-eight  hours  the  patient  will  be  unable  to 
lift  or  move  his  legs. 

Differential  Diagnosis. — Acute  myelitis  may  be  confounded  with  acute 
spinal  menmgitis,  hysterical  paraplegia  and  paraplegia  from  reflex  urinary 
irritation. 

In  meningitis  there  is  acute  pain  on  motion,  with  rigidity  of  the  muscles 
of  the  back ;  in  myelitis  there  is  no  pain  on  motion  and  the  muscles  are 
flaccid  and  relaxed.  Paralysis  in  spinal  meningitis  is  incomplete,  but  para- 
plegia or  liemi-paraplegia  is  always  present  in  acute  myelitis.  Cutaneous 
and  muscular  hypersesthesia,  with  febrile  and  cerebral  symptoms,  exists  in 
meningitis,  but  is  absent  in  myelitis. 

Hysterical  paraplegia  is  diagnosticated  by  the  attendant  hysterical  symp- 
toms, globus  hystericus,  large  flow  of  limpid  urine,  Jactitation,  etc.  It  is 
not  a  true  paraplegia,  and  generally  occurs  in  young  women. 

In  paraplegia  from  reflex  irritation,  genito-urinary  troubles  y^'iW precede 
the  paraplegia  ;  in  myelitis  the  urinary  symptoms  follow  the  paraplegia. 
In  reflex  urinary  irritation  the  paraplegia  is  incomplete  and  does  not 
extend  upwards ;  in  myelitis  it  is  complete  and  increasing.  There  is  no 
paralysis  of  the  sphincters  in  reflex  irritation  ;  in  myelitis  it  is  an  early 
and  marked  symptom.  There  is  no  girdle  sensation,  no  formication,  or 
sense  of  swelling  and  heat  in  reflex  paraplegia ;  while  these  symptoms  are 
always  present  in  myelitis.  The  urine  is  acid  in  reflex,  and  alkaline  in 
myelitic  paraplegia.  The  muscles  are  atrophied  in  myelitis  ;  and  nor- 
mal in  reflex  paraplegia.  Myelitis  of  the  cervical  portion  of  the  cord  is 
attended  by  paralysis  of  all  the  extremities,  increase  in  reflex  irritability, 
dysphagia,  dyspnoea,  vomiting  and  impaired  speech.  When  the  whole 
cervical  region  is  involved  the  upper  extremities  are  first  implicated,  and 
they  lose  their  reflex  irritahility.  The  pharyngeal,  thoracic,  and  ocular 
symptoms  are  also  marked.     The  pulse  is  rapid  and  irregular. 

Prognosis. — In  acute  myelitis  death  may  occur  in  twelve  to  thirty  hours, 
or  be  delayed  two  or  three  weeks.  When  the  disease  is  protracted  a  month 
it  becomes  chronic.  Complete  recovery  is  rare  ;  incomplete  recovery  oc- 
curs quite  often.  Cervical  myelitis  is  the  most,  dorsal  the  least  unfavor- 
able. Bed-sores,  cystitis,  nephritis,  and  pyelitis,  or  high  fever  and  sud- 
den and  complete  paralysis,  render  the  prognosis  exceedingly  unfavorable. 

Treatment. — The  most  important  thing  in  the  treatment  of  acute  mye- 
litis is  absolute  rest.  Ergot  and  belladonna  have  been  highly  recommended, 
but  I  have  never  obtained  any  positive  results  from  their  use.  Blisters  and 
other  counter-irritants,  electricity  and  strychnia  are  contraindicated.  Spinal 
bags  filled  with  hot  water  have  seemed  to  me  to  give  the  greatest  relief  to 
this  class  of  patients.     Diuretics  and  mild  cathartics  should  be  given  ;  and 

'  The  siiinal  epilepsy  of  Brown-Sequard  is  a  spasm  of  all  the  muscles  of  the  lower  extremities  generally 
following  transverse  myelitis. 


CHRONIC   MYELITIS.  999 

catheterization  practised  from  the  outset.  If  the  myelitis  is  of  syphilitic 
origin,  iodide  of  potassium  may  be  of  service,  but  not  otherwise.  A  sup- 
porting, nourishing  plan  of  treatment  is  to  be  adopted  from  the  onset.  To 
prolong  life,  complications  must  be  prevented  as  far  as  possible.  Bed-sores 
must  be  prevented  by  great  cleanliness  and  the  daily  use  of  the  galvanic 
current ;  cystitis  may  be  avoided  by  the  frequent  use  of  the  catheter  and 
the  washing  out  of  the  bladder. 

CHEOlSriC    MYELITIS. 

Under  this  term  are  included  a  variety  of  changes  in  the  cord,  of  which 
white  softening  is  perhaps  the  most  frequent. 

Morbid  Anatomy. — When  chronic  myelitis  is  the  sequela  of  acute,  the 
change  to  white  softening  marks  the  entrance  into  the  chronic  stage.  In 
this  stage,  by  a  process  precisely  similar  to  that  which  occurs  in  the  brain, 
a  cyst  is  formed.  It  is  divided  by  numerous  septa  of  connective-tissue,  and 
contains  fluid  resembling  chalk  and  water.  After  absorption  the  cicatrix 
is  gray,  shrivelled,  and  pigmented.  Less  commonly,  though  by  no  means 
infrequently,  there  is  hyperplasia  of  the  neuroglia,  and  a  dense,  gTay,  scle- 
rosed focus  remains.  Large  cells  with  numerous  processes,  called  Deiter's 
cells,  are  seen  in  this  sclerosed  tissue,  and  the  ganglion  cells  are  found  at- 
rophied. Large  quantities  of  corpora  amylacea  are  formed.  Usually  the 
cord  is  hard  and  gray,  but  in  many  cases  it  appears  to  the  naked  eye  per- 
fectly normal,  while  the  microscope  reveals  chronic  myelitis.'  It  is  slightly 
diminished  in  volume,  and  the  atrophy  may  be  uniform,  or  irregular,  and  at 
scattered  points. 

Chronic  inflammation  of  the  meninges  with  progressive  atrophy  of  the 
roots  and  trunks  of  the  peripheral  nerves  is  met  with  in  chronic  myelitis. 
There  is  increase  in  the  connective-tissue  of  the  neuroglia,  and  degeneration 
of  the  nerve  fibres.  The  ganglion  cells  are  hard  and  pigmented,  and  large 
Deiter's  cells  are  abundant.  The  axis  cylinder  remains  intact  for  a  long 
time.^  Fat  cells  are  everywhere  present,  and  in  cases  of  very  long  standing 
large  excavations  in  the  substance  of  the  cord  may  occur. 

It  is  impossible  to  distinguish  interstitial  from  parenchymatous  my- 
elitis.' 

Etiology. — All  the  constitutional  causes  that  were  enumerated  as  causes 
of  acute  may  be  included  under  the  remote  causes  of  chronic  myelitis,  and 
of  these  chronic  alcoholismus,  sexual  excesses,  and  reflex  disturbances  are 
more  liable  to  result  in  chronic  than  acute  myelitis. 

Symptoms.— The  symptoms  of  chronic  myelitis  are  so  complex  that  Char- 
cot calls  it  a  "  polymorphous  "  disease.     It  is  usually  insidious  in  its  onset ; 

'  So-called  (iray  degeneration. 

*  Charcot  and  Leyden. 

3  Leyden,  in  the  Zeitschr.f.  Klin.  Med.,  Berlin,  1879,  No.  1,  p.  1-26,  recites  a  most  interesting  case,  where 
numerous  large  round  nucleated  cells  were  found  pushing  npart  nerve  fibres  in  the  posterior  dorsal  region 
of  the  cord  of  a  man  who  had  been  poisoned  in  a  caisson.  Recently  "  systems  "  have  been  described  in 
the  cord,  and  some  pathologists  huve  classified  diseases  of  the  cord  on  this  physiological  basis.  Leyden 
describes  two  forms  of  system  disease  of  the  cord,  where  chronic  myelitis  is  the  sole  lesion,  i.  «.,  tabes  dor- 
salifi,  and  atrophy  of  the  motor  parts  of  the  cord.  These  two  combined  give  a  combined  system  disease.  Re- 
generation of  destroyed  nerve  fibres  in  the  cord  is  possible  though  very  rare. 


1000  DISEASES    OF   THE   NERVOUS   SYSTEM. 

and  iu  its  development  disorders  of  sensation  precede  motor  disturbances. 
Pains  in  the  limbs  simulating  rheumatism  are  gradually  associated  with 
muscular  weakness ;  and  tingling,  formication,  numbness  of  the  limbs,  with 
the  girdle  sensation,  are  followed  by  an  unsteady  gait.  '  Local  anesthesia 
alternates  with  hypergesthesia.  Weakness  of  the  bladder  and  constiiDation 
are  both  the  result  of  muscular  weakness.  These  symptoms  are  followed 
by  paraplegia,  muscular  atrophy,  cystitis,  and  chronic  bed-sores.  Slight 
tremors  and  twitchings  of  the  muscles  are  not  uncommon.  Patients  with 
chronic  myelitis  always  complain  of  cold  feet.' 

There  is  usually  progressive  emaciation  and  cachexia.  Some  cases  remain 
stationary  for  months  and  even  years  ;  but  the  majority  reach  a  fatal  ter- 
mination through  successive  exacerbations  and  remissions. 

Differential  Diagnosis. — Chronic  myelitis  may  be  confounded  with  spinal 
apoplexy,  spinal  meningitis,  or  Ioco?notor  ataxia. 

It  is  distinguished  from  hemorrhage  by  the  sudden  advent  of  the  hemor- 
rhage, and  from  meningitis  by  the  absence  of  pain. 

In  locomotor  ataxia  the  double  heel-and-toe  tread,  the  neuralgic  pains, 
the  preservation  of  motor  power,  of  control  of  the  sphincters  and  sexual 
force,  all  stand  in  contrast  to  the  signs  of  chronic  myelitis. 

Prognosis. — The  prognosis  in  chronic  myelitis  is  always  unfavorable.  It 
may  continue  from  two  to  ten  years,  but  in  no  case  can  there  be  complete  re- 
covery. It  may  remain  stationary  also  ;  but  the  functions  are  never  restored. 
Death  results  from  cystitis  and  pyelitis,  bed-sores,  and  other  complications. 

Treatment. — Eest  is  the  most  important  remedial  agent.  When  a  cause — ■ 
such  as  lead  poisoning,  disease  of  bladder,  uterus,  etc. — can  be  reached  it 
must  be  removed.  Dry  cups  daily  to  the  spine  are  usually  of  service. 
Ergot,  belladonna,  nitrate  of  silver,  iodide  of  potash,  arsenic,  phosphorus, 
and  strychnia  have  all  been  recommended  and  benefit  claimed  for  them, 
as  may  be  said  of  hot  or  cold  baths  at  natural  springs.^  The  bladder  must 
be  emptied  twice  or  three  times  daily  and  the  bowels  kept  freely  open. 
The  galvanic  current  is  considered  beneficial,  or  at  least  harmless.  Fric- 
tion, shampooing,  and  massage  of  the  paralyzed  limbs  prevent  wasting  of 
the  muscles. 

NOlSr-IlSrFLAMMATORY    SOFTElSTHsTG. 

Our  knowledge  of  this  rare  condition  is  vague.  Indeed,  until  recently, 
its  existence  was  denied. 

Morbid  Anatomy. — The  site,  extent  and  limitation  of  non-inflammatory 
softening  are  the  same  as  in  myelitic  patches.  Myeline,  broken-down  nerve- 
tubes,  large  granulation  corpuscles,  are  all  found  in  the  patch.  Eadcliffe 
describes  white  softening  as  non-inflammatory  and  due  to  anaemia. 

Etiology. — Slowed  blood-current,  a  tendency  of  the  blood  to  spontaneous 
coagulation,  and  disease  of  the  walls  of  the  blood-vessels  are  regarded  as 
causes  of  non-inflammatory  spinal  softening/    It  is  sometimes  met  with 

1  Erb  states  that  catheterization  and  dressing;  the  bed-sores  produces  varied  movements  in  the  paralyzed 
lii^^o.  2  Erb,  Rosenthal  and  others. 

5  Dr.  Moxon  calls  attention  to  the  fact  that  the  blood  supply  at  the  lower  end  of  the  cord— where  soft- 
enings are  most  frequent — is  peculiar  and  easily  interfered  with..— Bnt.  Med.  Jour.,  vol.  i.  1881. 


ACUTE   BULBAK   PAEALYSIS.  1001 

within  the  month,  after  childbirth,  in  the  late  stages  of  syphilis,  after  great 
bodily  exertion,  sexual  excess,  and  exposure. 

Symptoms. — The  symptoms  of  non-inflammatory  softening  do  not  differ 
essentially  from  those  of  chronic  myelitis,  spinal  hemorrhage,  and  spinal 
tumors.  Its  invasion  is  generally  gradual,  and  the  complexity  of  symp- 
toms varies  according  as  the  foci  are  circumscribed  or  diffuse,  central,  lat- 
eral, or  completely  transverse.  If  the  softening  extends  completely  across 
the  cord,  there  is  complete  paralysis  of  the  lower  extremities  and  of  the 
abdominal  muscles.  The  limbs  are  cold  to  the  touch  and  their  tempera- 
ture is  sub-normal.  The  toes  are  turned  inward,  so  that  as  the  patient 
lies  in  bed  the  feet  form  a  cross.  The  skin  becomes  dry  and  rough,  and 
the  muscles  are  flabby  although  not  wasted.  There  is  almost  complete  abo- 
lition of  reflex  movement.  Early  in  the  disease  there  is  retention  of  urine, 
which  is  followed  by  incontinence  and  partial  retention,  and  the  usual 
sequelae  of  cystitis  and  possibly  pyelitis  or  ammongemia  ;  the  kidney  may 
become,  studded  with  minute  abscesses. 

Differential  Diagnosis. — Its  slow  onset  and  the  preyious  history  enable  us 
to  differentiate  between  non-inflammatory  softening  and  spinal  hemorrhage. 
tt  is  not  difficult  to  determine  the  extent  of  the  lesion  ;  but  to  determine 
(vhether  it  is  central  or  peripheral,  anterior  or  posterior,  is  always  difficult 
ftnd  often  impossible. 

Prognosis. — The  prognosis  is  always  unfavorable.  There  is  great  danger 
of  intercurrent  diseases,  especially  pneumonia,  local  or  general  meningitis, 
and  inflammation  of  the  genito-urinary  tract,  or  septicaemia.  In  rare  in- 
stances the  paralysis  may  gradually  disappear  and  partial  recovery  take  place. 

Treatment. — No  plan  of  treatment  is  successful.  The  bowels  and  blad- 
der must  be  attended  to,  and  the  latter  is  best  washed  out  with  a  one-half 
per  cent,  solution  of  chlorate  of  potash.  The  galvanic  and  Faradic  currents 
may  be  used. 

ACUTE   BULBAR   PAEALYSIS. 

While  acute  bulbar  paralysis  involves  a  nervous  distribution  similar  to 
that  of  the  chronic  form,  its  morbid  anatomy  is  very  different. 

Morbid  Anatomy. — At  the  autopsy  there  will  be  foci  of  softening  and  ex- 
travasation from  thrombosis  and  embolism.  Erb  states  that  there  is  an 
acute  bulbar  paralysis  not  due  to  these  causes,  but  which  is  in  reality  a 
primary  acute  myelitis  huTbi. 

Etiology. — The  etiology  of  acute  bulbar  myelitis  is  unknown,  aside  from 
the  causes  of  apoplexy,  embolism,  and  thrombosis  elsewhere  in  the  cerebro- 
spinal system. 

Symptoms. — Its  onset  is  very  sudden;  the  prominent  symptoms  are  head- 
ache, dizziness,  and  sometimes  loss  of  consciousness  (apoplectiform  variety). 
Cough,  dyspnoea,  and  hiccough  are  often  present,  and  sometimes  there  are 
convulsions  and  weakness  in  the  limbs  accompanied  by  tingling  sensations. 
In  other  cases  coma  and  asphyxia  precede  the  rapidly  fatal  issue.  In  oc- 
clusion of  the  basilar  artery  the  carotid  pulse  is  unusually  full.  Eosenthal 
states  that,  in  addition  to  dyspnoea,  Oheyne-Stokes'  respiration  often  ap- 


1002 


DISEASES   OF   THE    NERVOUS   SYSTEM. 


pears  as  a  characteristic  symptom  of  medullary  hemorrhage.'  When  the 
extravasations  extend  into  the  fourth  ventricle  polyuria  and  albuminuria 
are  observed.^  In  embolism  improvement  is  common,  but  in  hemorrhage 
it  is  rare ;  thrombosis  of  the  vertebral  arteries  pursues  a  more  chronic 
course,  but  with  similar  results. 

Prognosis. — If  the  patient  recovers  from  the  primary  effects  of  the  lesion, 
the  prognosis  of  the  paralysis  is  better  than  in  the  chronic  form.  The 
prognosis  is  better  when  the  disease  is  associated  with  or  due  to  syphilitic 
infection.  In  a  few  acute  cases  the  paralysis  is  permanent,  although  it  has 
no  tendency  to  increase.  In  sudden  and  complete  obstruction  of  the  basilar 
or  both  vertebrals  the  prognosis  is  exceedingly  bad.  Limited  or  capillary 
hemorrhages  render  the  prognosis  unfavorable. 

Treatment. — This  does  not  differ  from  the  treatment  of  similar  conditions 
elsewhere  in  the  brain,  which  has  been  considered  under  apoplexy  and  cere- 
bral softening. 

CHROETC    BULBAR   PARALYSIS. 

{Olosso-lcMo-laryngeal  Paralysis. ) 

This  is  a  progressive,  symmetrical  paralysis  of  the  lips,  adjacent  facial 
.  muscles,  tongue,  pharynx, 

and  sometimes  of  the 
larynx. 

Morbid  Anatomy. — The 
medulla  may  be  atrophied 
and  show  spots  of  gray 
discoloration  which  have  a 
sclerotic  feel.  There  is 
degenerative  atrophy  of 
the  gray  nuclei  in  the  floor 
of  the  fourth  ventricle ; 
with  atrophy  and  gray  dis- 
coloration of  the  nerve 
roots  from  the  medulla, 
especially  of  the  facial  and 
hypoglossal  nerves.^  The 
ganglion  cells  and  the 
nerve-nuclei  lose  their  stel- 
late form  and  become 
shrunken,  smaller,  and  of 
Morbid  condition  on  the  ^    dull    Ochre    color.      The 

prolongations  and  nuclei 
are  rudimentary  or  even 
completely  atrophied.  The 
cells   are   filled  with   pig- 


FiG.  202. 

Chronic  Bulbar  Paralysis. 

Transverse  section  qf  the  bulbus  on  a  level  with  the  middle  of 
the  nucleus  of  the  hypoglossus. 

AA'.  Line  dividing  the  section  centrally. 
left  hand. 

B.  ^Ganglion  cells  forming  nuclevs  of  hypoglossus. 

C.  A  vessel  forming  front  and  inner  boundary  of  B. 

D.  Floor  qf  fourth  veniricle. 

E.  Nucleus  'of  pnettmogastric. 

On  the  left  the  nuclei/.s  of  the  hypoglossus  is  nearly  obliterated, 
while  that  of  the  pneumog astric  is  'unaltered.     Charcot. 


1  See  also  accounts  by  Traube  in  the  Berlin.  Klin.  Wochen.,  1869  to  1874. 
^  Gazette  des  Hopitaux,  1862. 

3  Recent  physiological  investigations  show  that  the  lower  facial  nucleus  and  the  hypoglossal  nucleus 
are  closely  connected. 


CHRONIC    BULBAR   PARALYSIS. 


1003 


ment  and  granulcar  matter,  the  nucleus  and  nucleolus  present  a  vitreous, 
shining  appearance,'  and  are  separated  from  each  other  by  large  spaces. 
Atrophy  and  disappearance  of  the  motor  ganglion  cells  is  always  to  be 
noted.  It  may  be  the  sole  lesion  or  be  accompanied  by  increase  in  the 
neurolgia,  when  fat  and  granular  corpuscles,  numerous  corpora  amylacea, 
Gluge's  corpuscles,  and  spider-cells  will  be  found  in  the  newly-developed 
tissue.  The  walls  of  the  vessels  are  thick,  and  show  more  or  less  fatty 
change.  The  decrease  in  size  of  the  gray  nuclei  is  a  measure  of  the  inten- 
sity of  the  symptoms  that  existed  during  life. 

Similar  bilateral  lesions  may  be  found  in  the  nuclei  of  the  pneumogas- 
tric,  spinal -accessory,  glosso-pharyngeal,  facial,  trifacial,  motor  oculi,  and, 
very  rarely,  of  the  trigeminus.'^ 

The  muscles  are  j^ale  and  the  fibres  frequently  show  granular  degenera- 
tion ;  but  sometimes  fatty  tissue  is  in  excess.  The  fibres  may  be  thin,  and 
the  tissue  between  them  contain  the  pigment  products  of  degeneration,  so 
that  the  muscles,  though  degenerated,  will  preserve  their  normal  bulk. 


Fig.  203. 
Chronic  Bulbar  Paralysis. 

A.  Microscojncal  appearance  of  normal  viuscle  from  the  tongue, 

B.  Same  m,vscle  taken  from,  a  case  of  Glosno-ldhio-laryngeal 

C.  Fasciculi  of  muscular  fibres  in  transverse  section. 

D.  Atrophied  fibres  seen  longitudinally,     x  300. 


The  muscular  fibres  show  increase  in  their  nuclei  and  changes  precisely 
similar  to  those  in  progressive  muscular  atrophy. 

The  nerves  going  to  the  muscles  exhibit  sclerosis  of  the  neurilemma, 
slight  traces  only  of  the  axis-cylinders  remaining.  The  same  degenerative 
atrophy  is  found  in  the  nerve  roots  coming  from  the  bulb.  This  disease 
is  rare  before  the  fortieth  year  of  life  ;  it  is  essentially  a  disease  of  old  age. 
Males  are  more  subject  to  it  than  females. 


1  Yellow  degeneration  of  Charcot. 


2  Duchenne. 


1004  DISEASES   OF   THE    NERVOUS    SYSTEM. 

Etiology. — Its  etiology  is  always  obscure.  The  neuropathic  tendency 
seems  to  exercise  some  influence  in  certain  cases.  It  is  said  to  occur  with 
syphilis  and  rheumatism.  Bad  hygiene,  exposure  to  cold,  excessive  anxi- 
ety, close  mental  application,  and  prolonged  physical  exertion  are  all  ad- 
duced as  causes. 

Symptoms. — The  earliest  symptoms  of  bulbar  paralysis  are  imperfect  move- 
ments of  the  tongue  ;  the  speech  is  indistinct,  and  enunciation  of  the  pal- 
atal and  dental  sounds  is  imperfect.  Often  the  tongue  cannot  be  protruded 
as  far  as  normal,  nor  the  lips  brought  together  as  perfectly  or  separated  as 
promptly  as  in  health.  Whistling  and  whispering  are  impossible.  The 
lower  part  of  the  face  becomes  expressionless.  The  lips  remain  separated 
and  the  saliva  is  either  tenacious  or  dribbles  from  the  mouth,  which  is  so 
drawn  as  to  give  the  face  a  woe-begone  expression.  Speech  may  be  entirely 
lost. 

When  the  palate  muscles  are  involved,  deglutition  becomes  difficult, 
and  as  the  soft  palate  hangs  motionless,  not  closing  the  posterior  nares,  the 
food  regurgitates  through  the  nose,  or  lodges  in  the  u|)per  part  of  the  phar- 
ynx and  collects  between  the  cheeks  and  the  alveolar  arches  ;  portions  are 
also  apt  to  fall  into  the  larynx.  Another  effect  of  palatal  paresis  is  to  give 
a  nasal  twang  to  the  voice. 

If  the  laryngeal  muscles  become  weakened  and  closure  of  the  glottis  im- 
perfect, coughing  becomes  ineffective  and  phonation  is  interfered  with.  The 
muscles  of  mastication  are  rarely  involved  until  late  in  the  disease,  but  ex- 
haustion and  emaciation  from  insufficient  food  are  developed  early.  The 
muscles  atrophy,  and  tremblings  and  fibrillar  twitchings  occur.  When  the 
respiratory  centres  are  involved  there  is  a  sense  of  fulness  and  constriction 
in  the  chest  accompanied  by  attacks  of  dyspnoea. 

Lesions  in  the  cardio-inhibitory  centres  are  followed  by  attacks  of  syn- 
cope and  a  pulse  of  140  or  160  per  minute.  There  is  an  abnormal  amount 
of  saliva  secreted,  either  as  paralytic  saliva'  or  from  irritation  in  the  me- 
dulla.^ The  laryngoscope  reveals  paralysis  of  the  vocal  cords.  Should 
bronchitis  occur  expectoration  is  difficult,  and  if  pneumonia  or  any  other 
severe  pulmonary  affection  develops  it  almost  always  terminates  fatally. 
The  muscles  show  the  reaction  of  degeneration  ;  sensibility  is  unchanged, 
but  reflex  actions  are  greatly  diminished  or  destroyed.  Atrophy  of  the 
muscles  at  the  back  of  the  neck — the  trapezii  especially — is  not  infrequent. 
In  some  few  cases  the  paralytic  symptoms  may  be  preceded  by  dull  pains 
in  the  back  of  the  head  and  neck,  giddiness,  queer  sensations  in  speaking, 
and  loss  of  reflex  irritability  in  the  pharynx  and  larynx.' 

I  See  M.  Poster's  Physiology.    Art.  Sub-maxillary  Gland.  ^  Pfliiger's  Archiv,  Bd.  7. 

s  Kirchoff  reports  a  case  where  bulbar  paralj'sis  was  produced  by  a  uniialeral  lesion,  and  from  the  autop- 
sical  results  in  this  case  the  sj'mptoms  must  be  attributed  to  a  lesion  of  the  lenticular  nucleus.  A  new  and 
peculiar  variety  of  bulbar  paralysis  has  recently  been  described  by  Erb.  An  analysis  of  the  symptoms 
shows  that  the  parts  chiefly  involved  are  the  motor  oculi  communis,  the  motor  portion  of  the  trigeminus, 
the  spinal-accessory^,  and  the  upper  cervical  nerves  ;  and  those  more  slightly  affected  are  the  facial  (the 
upper  branches  to  the  face),  the  hypoglossal,  and  probably  also  the  glosso-pharyngeal  nerves.  The  nuclei 
of  origin  of  these  nerves  are  all  situated  in  the  floor  of  the  fourth  ventricle  and  in  its  immediate  neighbor- 
hood in  the  pons  Varolii.  Erb  supposes  that,  in  the  affection  under  consideration,  the  lesion  is  situated  in 
the  upper  half  of  the  fourth  ventricle  and  spreads  more  deeply  into  the  substance  of  the  medulla,  affecting 
nerve  fibres  as  they  pass  upward  from  the  nuclei  of  origin  in  the  fourth  ventricle. 


CHRONIC    BULBAR   PARALYSIS.  .1005 

DiiFerential  Diagnosis.— Progressive  bulbar  paralysis  may  be  mistaken  for 
tumors  in  the  medulla,  double  facial  palsy ,  embolism  and  thrombosis  of  the 
medulla,  medullary  apoplexy,  embolism  of  one  of  the  vertebral  arteries, 
progressive  muscular  atrophy  attacking  the  face,  Vind  getieral  paralysis  of 
the  insane. 

In  tumors  of  the  medulla,  we  find  neuralgia,  clonic  convulsions  of  the 
muscles  of  the  face  and  tongue,  disturbarfces  of  the  smell  and  hearing, 
headache,  vomiting,  dizziness,  and  epileptiform  attacks,  the  disease  being 
either  unilateral  or  decidedly  marked  only  on  one  side. 

In  double  facial  palsy ,  all  the  branches  of  the  facial  nerve  are  involved  ; 
movements  of  the  tongue  and  deglutition  are  normal. 

In  embolism  or  throrhbosis  of  the  medulla,  the  sudden  onset  of  the  symp- 
toms with  either  hemiplegia  or  paraplegia,  taken  in  connection  with  the 
age  of  the  patient  and  tlie  condition  of  the  arteries,  will  be  the  chief  points 
of  diagnosis.     In  embolism  improvement  is  possible. 

In  bulbar  hemorrhage,  loss  of  consciousness,  epileptiform  convulsions, 
vomiting,  prominence  of  unilateral  symptoms  are  combined  with  bulbar 
paralysis  of  sudden  advent.    The  previoiis  history  will  aid  in  the  diagnosis. 

Embolism  of  the  vertebral  arteries  is  accompanied  by  sudden  (apoplec- 
tiform) onset  of  the  symptoms  of  bulbar  paralysis,  hemiplegia,  anaesthesia, 
variations  in  the  paralyses,  and  co-existing  disorders  of  sight  and  hearing. 

Iw  progressive  muscular  atrophy,  paralysis /o/?ows  the  atrophy  ;  in  bulbar 
paralysis  it  is  the  reverse.  Moreover,  the  thenar  and  hypothenar  eminences 
are  involved  early,  even  should  muscular  atrophy  first  attack  the  tongue, 
lips  and  palate.^ 

In  general  paralysis  of  the  insane,  the  cerebral  disturbances  and  the  fact 
that  other  muscles  are  involved  besides  those  in  the  region  of  the  mouth 
and  palate,  will  establish  the  diagnosis. 

Prognosis. — The  prognosis  is  grave ;  although  a  temporary  arrest  may 
occur,  genuine  bulbar  paralysis  invariably  terminates  in  death.  The 
amount  of  dysphagia  and  dyspnoea  and  the  rapidity  of  development  will 
determine  the  relative  gravity  of  the  case.  Its  average  duration  is  about 
two  years.  Bulbar  j)ara]ysis  may  be  complicated  by  progressive  muscular 
atrophy,  amyotrophic  lateral  sclerosis  and  disseminated  sclerosis.  Death 
occurs  from  starvation,  paralysis  of  the  heart  or  respiratory  organs,  or  inter- 
current pulmonary  diseases.  Sometimes  coma  ends  the  scene,  and  there 
is  a  slight  rise  of  temperature. 

Treatment. — A  nutritious  diet  and  the  best  hygienic  surroundings,  with 
quinine,  arsenic  and  nitrate  of  silver  are  the  means  which  have  been  most 
extensively  employed.  The  German  physicians  condemn,  and  the  English 
advocate,  the  use  of  strychnine  and  phosphorus.  Ergot,  belladonna,  and 
iodide  of  potash  may  be  given.  Direct  galvanic  or  Faradic  currents  ap- 
plied to  the  paralyzed  parts  have  been  recommended.  In  some  cases  a 
stomach  tube  may  be  used  to  prolong  life,  and  perhaps  gastrostomy  may 
be  demanded. 

•  Duchenne. 


1006 


DISEASES   OF   THE   NERVOUS   SYSTEM. 


INFAISTTILE    SPIISTAL    PARALYSIS. 


Infantile  spinal  paralysis  or  acute  anterior  polio-myelitis  is  an  inflam- 
mation of  the  anterior  cornua  of  gray  matter  of  the  cord.  It  may  occur  in 
adults,  hut  is  almost  always  exclusively  confined  to  children. ' 

Morbid  Anatomy. — The  early  changes  are  those  of  inflammatory  soften- 


FiG.  204. 

Anterior  Gray  Cornu  of  Spinal  Cord  in 
Eaily  stage  of  Infantile  Spinal  Paral- 
ysis. 

A.  Large  mriltlpol'ir  ganglion  cdls. 

B.  Neuroglia  cells  in  a  state  of  active  pro- 

liferation.    X  300. 


Fig.  205. 

Anterior  Gray  Cornu  of  Spina  Cord 
after  establishment  of  the  Sclerotic 
Process  in  Infantile  Spinal  Paralysis. 

A.  Dense  nucleated  connective-tisfoie. 

B.  Large  masses  of  pigment— the   re- 

mains  of  ganglion  cells. 

C.  Corpora  dm'ylacea.     x  300. 


ing ;  medullary  hypergemia  and  vascular  exudations  are  the  incidental 
occurrences.^  Extensive  changes  may  exist,  and  yet  the  gross  appearance 
of  the  cord  be  unchanged. 

Microscopically  there  will  be  seen,  in  its  early  stage,  all  the  changes  of  acute 
interstitial  inflammation,  and  the  neuroglia  nuclei  are  in  active  prolifera- 
tion. Later  a  sclerotic  process  is  established,  and  new  connective-tissue 
developed,  in  which  are  multitudes  of  nuclei  and  corpora  amylacea.  Pig- 
mentation is  more  or  less  marked,  and  the  ganglion  cells,  that  have  lost 
their  processes,  may  remain  only  as  irregular  spherical  masses  of  pigment. 
Thickening  and  increase  of  neuroglia  in  the  anterior  columns  result  in 
more  or  less  atrophy  of  the  nerve  fibres.  The  antero-lateral  columns  of  the 
cord  may  be  invaded,  but  the  posterior  usually  escape.^    The  anterior  roots 

1  Niemeyer  calls  it  essential  palsy.  Erb  describes  it  as  a  more  or  less  diffuse  myelitis  of  the  anterior 
gray  substance,  which  reaches  its  greatest  intensity  in  the  lumbar  and  cervical  enlargements  of  the  cord, 
and,  as  a  rule,  leaves  no  permanent  and  irremediable  alteration  except  at  those  two  points. 

2  Rosenthal. 

3  The  most  careful  microscopical  examination  fails  to  decide  what  modern  pathology  is  still  earnestly 
discussing,  viz. :  whether  acute  polio-myelitis  is  an  interstitial  or  a  parenchj'matous  inflammation.  The 
majority  favor  the  latter  view,  the  ganglion  cells  being  its  supposed  starting-point. 


INFANTILE   SPINAL   PARALYSIS.  1007 

of  the  spinal  nerve  are  shrunken,  atrophied,  and  degenerated.  They  are 
gray  and  transhicent.  The  vessels  undergo  considerable  enlargement,  and 
their  walls  are  thickened.  The  motor  nerves  are  involved  secondarily  to 
the  cord  at  an  advanced  period  of  the  disease.  The  muscles  which  are  im- 
plicated rapidly  undergo  fibroid  changes  and  atrophy.  Their  transverse 
sfcrige  are  indistinct,  and  the  nuclei  become  abundant ;  the  muscular  fibres 
may  wholly  disappear.'  The  muscular  fibres  do  not  ahvays  suffer  this 
degeneration,  but  sometimes  they  undergo  fatty  degeneration,  or  the  mus- 
cles are  so  infiltrated  with  oil  globules  that  they  retain  their  normal  size, 
and  may  even  exceed  it  ;  this  is  a  pseudo-hypertrophy.'^  The  hones  are 
retarded  in  development,  somewhat  flexible,  and  contain  more  fat  than 
usual.  The  tendons  become  atrophied,  and  the  joints  lose  their  com- 
pactness. 

Etiology. — This  is  essentially  a  disease  of  the  first  three  years  of  life,  the 
usual  time  of  occurrence  being  between  the  sixth  and  fourteenth  months. 
It  attacks  equally  children  of  both  sexes,  the  robust  as  well  as  those  of 
feeble  and  cachectic  constitutions.  Cold,  dentition,  and  traumatism  are 
among  its  doubtful  causes.  It  has  occurred  in  two  or  more  offspring  of  the 
same  parents,  and  once  in  twins  '  after  an  attack  of  measles.  Many  regard 
acute  febrile  diseases  as  an  important  factor  in  its  causation.  It  is  devel- 
oped, if  at  all,  during  convalescence  from  such  fevers. 

Symptoms. — The  onset  of  infantile  spinal  paralysis  is  sudden.  A  child 
has  well-marked  febrile  movement  attended  by  dizziness,  headache,  restless- 
ness, nausea,  vomiting,  and  sometimes  delirium,  convulsions  and  coma. 
Accompanying  these  symptoms  there  is  more  or  less  pain  in  the  back.  In 
many  cases  the  febrile  symptoms  only  last  a  few  hours.  Following  a  con- 
Tulsion  or  attack  of  unconsciousness  the  child  becomes  paralyzed,  or  in 
some  cases  paralysis  may  come  on  suddenly  without  a  single  premonitory 
symptom  ;  the  child  goes  to  bed  perfectly  well  and  wakes  with  paraplegia. 
If  only  one  lower  limb  is  involved  at  first,  the  other  soon  becomes  so  ;  and 
it  is  not  unusual  for  all  four  extremities  to  be  affected  simultaneously.  The 
arms  alone  are  rarely  involved.  The  paralysis  is  not  accompanied  by  loss 
of  sensiUlity.  It  reaches  its  maximum  in  from  ten  hours  to  six  or  seven 
days,  and  begins  to  diminish  in  about  two  weeks  after  its  commencement. 
The  paralyzed  muscles  become  flaccid,  relaxed,  and  attenuated,  and  if  the 
paralysis  is  persistent  they  atrophy  and  undergo  degeneration.  The 
surface  of  the  body  is  cold  and  of  a  purplish  color.  The  limbs  may  pre- 
serve their  normal  contour  ;  but  they  are  soft  and  often  tender  to  pressure. 
The  tendon-reflexes  and  reflex  action  in  the  muscles  of  the  paralyzed  part 
are  entirely  lost,  and  they  fail  to  respond  to  the  Faradic  current.  These 
alterations  in  electrical  excitability  are  results  of  the  reactions  of  degener- 
ation. 

Paralysis  at  the  onset  is  general,  bat  later  it  is  localized  in  one  group  oi 
in  single  muscles.  The  muscles  on  the  back  of  the  forearm  and  front  of  the 
leg,  in  the  foot,  and  the  extensors  of  the  leg,  are  more  apt  to  be  affected, 

1  Erb  lays  great  Rtres-s  upon  the  replacement  of  muscle  tissue,  in  this  disease,  by  fat,  so  that  the 
muscleshave  tlie  faded-leaf  appearance  of  a  typhoid  heart. 

2  Erb.  ^  Moritz  Meyer. 


J.008  DISEASES    OF   THE    NEKVOUS    SYSTEM. 

but  the  paralysis  may  involve  only  the  deltoid,  tibialis  anticus,  sterno-clei- 
do-mastoid,  or  the  extensor  longus  digitorum.  The  joints  are  loosened,  and 
the  bones,  especially  the  long  ones,  are  smaller  and  shorter  than  those  in  the 
unafEected  limb.  The  temperature  of  the  paralyzed  parts  is  often  5°  or  8°  F. 
lower  than  normal.  The  deformities  and  unnatural  attitudes  that  result 
may  simulate  talipes  ;  and  all  varieties  of  contracture  occur  as  late  man- 
ifestations. The  epiphyses  atrophy  and  subluxations  sometimes  occur. 
The  general  health  of  the  patient  is  usually  good,  and  there  is  nothing  that 
interferes  with  long  life,  except  the  paralysis  and  deformity.  In  severe 
cases  there  is  at  the  onset  loss  of  control  of  bladder  and  rectum.  In  such 
cases  slight  vesical  weakness  usually  continues  during  life.  The  normal 
sensibility  of  the  skin  is  preserved  throughout. 

Differential  Diagnosis.— Infantile  spinal  paralysis  may  be  mistaken  for 
progressive  muscular  atrophy, pseudo-muscular  hypertrophy,  rachitis,  tem- 
porary infantile  paralysis,  myelitis,  and  hemiplegia. 

Progressive  muscular  atrophy  begins  insidiously  and  is  slowly  progres- 
sive ;  spinal  infantile  paralysis  begins  suddenly,  and  after  a  time  a  certain 
amount  of  improvement  occurs.  Progressive  muscular  atrophy  is  rare  in 
children  before  the  fifth  or  seventh  year  of  age.  It  commences  by  palsy 
about  the  lips  and  mouth,  and  the  electro-contractility  of  the  affected 
muscles  is  lost  only  in  proportion  to  their  atrophy  and  degeneration^  the 
uninvolved  fibres  rGspondi7ig  to  the  current.  This  fact  taken  in  connec- 
tion with  the  age  of  the  patient  will  usually  enable  one  to  make  a  diag- 
nosis. 

Pseudo-muscular  hypertrophy  begins  loithout  fever  ;  the  motor  power  at 
first  is  only  weakened,  and  the  trunk  and  extremities  are  involved  late 
in  the  disease.  The  electro-muscular  contractility  is  preserved,  and  there 
is  always  increase  in  the  volume  of  the  muscles.  In  walking  the  patient 
spreads  the  feet  far  apart,  and  there  is  a  peculiar  incurvation  of  the  verte- 
bral column  not  seen  in  infantile  spinal  paralysis. 

Bichets  is  attended  by  no  change  in  electro-muscular  contractility,  is 
preceded  by  no  cerebral  or  pyretic  phenomena,  and  there  coexist  develop- 
mental and  other  changes  that  cannot  fail  to  determine  the  character  of  the 
deformity. 

In  temporary  paralysis  there  are  no  signs  of  softening  or  atrophy  of 
muscles,  there  is  no  change  in  electro-muscular  contractility,  and  the  pa- 
ralysis is  recovered  from  in  twenty  to  thirty  days. 

In  myelitis,  trophic  disturbances  and  genito-urinary  complications  are 
sufficient  to  distinguish  it  from  infantile  spinal  paralysis. 

Hemiplegia  from  acute  cerebral  affections  in  childhood  can  generally  be 
distinguished  from  acute  anterior  polio-myelitis  by  loss  of  intelligence  and 
speech,  strabismus,  paralysis  of  half  the  face,  dilated  pupils,  and  normal 
electrical  contractility  in  connection  with  disturbances  in  sensation,  stiff- 
ness of  the  Joints,  spasmodic  contractures  with  absence  of  fever,  and  mus- 
cular atrophy. 

Prognosis. — There  is  little  or  no  danger  to  life  in  acute  anterior  polio- 
myelitis, even  when  the  attack  commences  with  very  active  symptoms.     A 


ACUTE   SPINAL   PAEALYSIS   OP   ADULTS.  1009 

mild,  or  even  a  severe,  onset  may  be  followed  by  complete  restoration  of  the 
function  and  power  of  the  paralyzed  muscles  : — so-called  temporary  spinal 
palsy.  Usually  the  improvement  is  such  that  the  function  of  the  few  mus- 
cles that  remain  permanently  paralyzed  and  atrophied  is  performed  by  the 
muscles  not  involved.  All  the  paralyzed  muscles  in  which  Faradic  irrita- 
bility is  not  completely  lost  are  restored. ' 

Treatment. — In  the  acute  stage  rest  in  the  recumbent  posture  is  the  most 
important  element  of  treatment.  Beyond  this  the  treatment  is  the  same 
as  for  acute  myelitis.  After  the  febrile  symptoms  have  subsided — usually 
by  the  fourth  week — measures  must  be  adopted  to  restore  the  function  of 
the  paralyzed  muscles.  The  early  and  persistent  use  of  the  galvanic  current 
hastens  the  recovery  in  those  muscles  whose  electric  contractility  is  but 
slightly  diminished,  and  will  often  arrest  the  wasting  and  restore  them  to 
a  normal  condition.  When  electric  contractility  is  entirely  lost  little  bene- 
fit can  be  expected.  The  longer  the  use  of  electricity  is  delayed  the  less 
the  chances  of  recovery.  Even  if  it  fails  to  cure  it  has  a  tendency  to  pre- 
vent deformity.  Saline  and  thermal  baths  and  the  water  treatment  of 
various  kinds  are  recommended.  Massage,  friction,  shampooing,  inunc- 
tions, etc.,  are  to  be  combmed  with  the  electric  and  hydropathic  plans  of 
treatment.  The  diet  must  be  such  as  to  bring  nutrition  to  its  highest 
point.  Minute  quantities  of  strychnia  injected  hypodermically  have  been 
found  beneficial.  Iron,  arsenic,  quinine  and  phosphorus  are  indicated — 
as  tonics — in  nearly  every  case. 


ACUTE    SPJlfAL   PARALYSIS    OF    ADULTS. 

Duchenne  and  Moritz  Meyer  first  observed  that  this  disease  not  infre- 
quently occurred  during  adult  life,  with  pathological  changes  identical 
with  those  of  the  disease  in  infancy. 

The  etiology  is  obscure  ;  cold.,  wet,  and  the  debility  found  in  conva- 
lescence from  fevers,  pneumonia,  malarial  poisoning,  etc.,  have  been  sug- 
gested as  causes. 

The  symptoms  at  the  onset  are  modified  by  the  greater  stability  of  the 
adult  nervous  system,  and  there  is  less  restlessness,  delirium,  fever,  etc. 
The  cerebral  symptoms  may  be  very  slight,  transient,  and  easily  overlooked 
and  followed  by  paralyses,  which  go  on  to  partial  recovery  as  in  the  infantile 
form.  There  are  no  bone  deformities  or  arrested  developments ;  and  the 
joints  do  not  become  lax.  Tingling,  numbness,  and  formication  occur  in 
adults  at  the  onset,  and  gastric  symptoms  are  more  frequent. 

Differential  Diagnosis. — Absence  of  spasms  and  of  trophic  disturbances, 
diminution  of  reflexes,  normal  sensibility,  non-interference  with  the  sphinc- 
ters, the  sudden  onset  and  the  subsequent  improvements  suffice  to  distin- 
guish this  disease  from  all  other  affections  of  the  cord. 

Chronic  atrophic  spinal  paralysis  resembles  it,  but  the  abrupt  invasion 

J  Seeligmiiller  records  two  cases  where  progressive  muscular  atrophy  occurred  late  in  life  In  those  who 
In  infancy  suffered  from  acute  anterior  polio-myelitis. 

64 


1010  DISEASES   OE   THE   NERVOUS   SYSTEM. 

of  anterior  polio-myelitis  is  absent  in  the  former  malady.     If  this  point  in 
the  history  be  wanting  a  differential  diagnosis  may  be  impossible. 
^hQ prognosis  and  treatment  are  the  same  as  in  children. 

CHEONIC    ANTEEIOR   POLIO-MYELITIS. 

Duchenne  was  the  first  to  describe  (1853)  this  disease  under  the  above 
name.  It  has  since  been  called  subacute  and  chronic  inflammation  of  the 
gray  anterior  horns,  chronic  atrophic  spinal  paralysis,  and  subacute  spinal 
paralysis. 

Morbid  Anatomy. — The  morbid  anatomy  of  this  disease  is  still  obscure. 
So  far  as  can  be  stated  from  the  few  recorded  autopsies  it  is  simply  a 
chronic  myelitis  of  the  anterior  cornua  ;  the  neuroglia  is  increased  ;  the 
blood-vessels  are  thickened,  the  anterior  nerve-roots  are  atrophied,  and 
there  is  an  abundance  of  granular  and  fat  cells  in  the  diseased  district. 
Eecently  vacuoles  have  been  found  in  the  ganglion  cells  of  the  anterior 
horns.  Almost  entire  disappearance  of  these  cells  was  the  chief  lesion  in 
one  case.* 

Etiology. — ^It  is  a  disease  of  adult  life  from  thirty  to  fifty,  and  excesses  of 
any  kind,  or  exposure  to  cold  and  wet,  are  said  to  exert  an  influence  on  its 
development  similar  to  that  in  other  spinal  affections.^ 

Symptoms. — In  some  subacute  cases  slight  fever  and  shooting  pains  in 
the  back  accompany  the  development  of  paralysis  of  the  lower  limbs.  In 
others  the  patient  first  notices  weakness  and  heaviness  in  his  legs,  followed 
by  paralysis  either  of  groups  of  muscles  or  of  the  whole  limb.  The  mus- 
cles become  flabby  and  progressively  waste  away.  They  are  sensitive  to  the 
galvanic  current,  but  respond  little,  if  at  all,  to  the  Faradic.  The  irreg- 
ular distribution  of  the  paralysis  is  characteristic.  As  the  muscles  are 
undergoing  atrophy,  fibrillary  twitchings  are  often  noticed.  Tendon- 
reflexes  and  skin-reflexes  are  both  abolished  ;  but  sensibility  is  unaffected. 
There  is  vaso-motorial  disturbance,  indicated  by  cold  and  blue  extremities. 
The  temperature  of  the  affected  limbs  is  lowered.  Later,  the  upper  limbs 
are  involved.  The  paralysis  first  attacks  the  flexors  or  extensors  on  the 
forearm,  and  gradually  involves  isolated  groups  of  muscles,  or  the  whole 
limb.  The  fingers  and  hand,  however,  suffer  most.  When  the  disease  has 
reached  this  stage  the  wasted  muscles  will  no  longer  respond  to  the  galvanic 
current.  The  rectum,  bladder,  and  sexual  power  are  undisturbed.  When 
the  process  extends  to  the  cervical  region  dyspnoea  is  present,  and  if  the  me- 
dulla becomes  involved  deglutition  and  articulation  are  affected,  and  great 
exhaustion  is  induced,  asphyxia  closing  the  scene.  The  general  health  re- 
mains good,  and  the  mental  faculties  are  unimpaired. 

Differential  Diagnosis. — Chronic  atrophic  spinal  paralysis  may  be  mis- 
taken iox  progressive  muscular  atrophy,  amyotropliic  lateral  sclerosis,  acute 
ascending  paralysis,  and  the  acute  spinal  paralysis  of  adults. 

In  progressive  muscular  atrophy  paralysis  follows  the  wasting ;  the  re- 

1  Arch,  de  Physiologle,  1876. 

2  Erb  suggests  that  its  co-esistence  with  chronic  lead  poisoning  is  the  result  of  an  inflammatory 
action  called  forth  by  the  saturnismus. 


PKOGRESSIVE   MUSCtJLAE   ATROPHY.  1011 

verse  is  the  case  in  polio-myelitis.  Portions  of  the  muscles  only  are  in- 
volved in  progressive  muscular  atrophy,  and  it  begins  in  the  muscles  of  the 
thumb.  Reflex  action  is  retained,  and  the  progress  is  much  slower  than  in 
chronic  polio-myelitis.  Moreover,  the  susceptibility  to  the  electrical  cur- 
rents is  never  wholly  lost  in  progressive  muscular  atrophy. 

In  amyotrophic  lateral  sclerosis,  though  the  upper  extremities  may  be 
wasted,  there  is  a  characteristically  different  combination  of  paralysis  ivitli- 
out  wasting,  and  with  more  or  less  rigidity  in  the  lower  extremities.  The 
reaction  of  degeneration  is  far  more  marked  in  chronic  anterior  polio- 
myelitis. Keflex  clonus  and  exaggerated  tendon-reflexes  are  absent  in 
chronic  polio-myelitis,  and  present  in  amyotrophic  lateral  sclerosis. 

In  acute  ascending  paralysis  the  atrophy  is  not  marked  ;  electrical  re- 
actions of  nerves  and  muscles  are  normal,  reflex  action  is  preserved  for  a 
long  time,  and  bulbar  symptoms  with  vesical  disturbances  are  not  uncom- 
mon. Acute  ascending  paralysis  is  of  short  duration  compared  with  chronic 
anterior  polio-myelitis. 

In  acute  spinal  paralysis  of  adults  the  paralysis,  which  is  sudden  in  its 
onset,  is  more  extensive,  and  after  a  short  time  there  is  improvement  in 
motor  power ;  while  in  chronic  atrophic  spinal  paralysis  there  is  a  dis- 
tinctly progressive  unremitting  spread  of  the  disease  from  part  to  part. 

Prognosis. — In  rapidly  progressive  cases  the  prognosis  is  bad,  but  in  those 
that  are  slowly  developed  and  partial  the  prognosis  is  better,  and  sometimes 
complete  recovery  may  take  place,  or  certain  muscles  or  groups  remain 
paralyzed  and  atrophied  while  others  improve.  After  a  long  time  the  dis- 
ease may  be  spontaneously  arrested  and  the  patient  remain  paralyzed  the 
remainder  of  life.  The  most  unfavorable  cases  are  those  in  which  the 
cervical  region  and  the  medulla  become  involved,  death  occurring  with 
symptoms  of  bulbar  paralysis.  The  usual  duration  is  from  a  few  months 
to  three  or  four  years. 

Treatment. — Electricity  and  a  nourishing  diet,  with  rest,  give  the  best  re- 
sults. Dr.  Bastian  suggests  that  counter-irritation  may  do  good  in  the 
early  stages.  Sulphur,  mineral,  and  brine  baths  and  the  cold  water  treat- 
ment are  advocated.  It  is  a  question  whether  either  iodide  of  potassium 
or  ergot  is  beneficial.  Modern  literature,  though  extremely  rich  in  theories, 
is  devoid  of  facts  which  can  aid  in  the  treatment. 

PEOGRESSIVE    MUSCULAR  ATROPHY. 

As  the  name  indicates,  this  disease  is  a  progressive  and  chronic  wasting 
and  atrophy  of  the  muscles,  and  results  from  trojjhic  changes  due  to  a  cen- 
tral nerve-lesion. 

Morbid  Anatomy. — The  morbid  anatomy  of  this  affection  differs  little 
from  that  in  spinal  paralysis  of  children.  Its  essential  lesion  is  atrophy  of 
certain  groups  of  nerve- cells  in  the  anterior  cornua  of  the  cord.  Some- 
times atrophy  of  the  anterior  horns  is  associated  with  a  sclerotic  condition 
of  the  lateral  columns.  The  general  changes  are  the  same  as  in  the  late 
stage  of  anterior  polio-myelitis.     The  central  canal  of  the  cord  is  some^ 


1012 


DISEASES    OF   THE   NERVOUS   SYSTEM. 


times  dilated  and  filled  with  fluid.  On  microscopic  examination  the 
ganglion  cells  show  pigmentation  to  a  marked  degree,  with  more  or  less 
atrophy.     They  are  surrounded  by  indurated  tissue.     The   blood-vessels 

are  often  dilated,  and  sur- 
rounding them  is  a  zone 
of  granular  disintegrated 
or  diffluent  material,  the 
so-called  mixed  exuda- 
tion. All  these  changes, 
may  be  found  in  both 
gray  and  white  matter. 
The  anterior  roots  of  the 
spinal  nerves  are  atro- 
phied, and  show  more  or 
less  gray  degeneration. 
Sometimes  all  except  the 
neurilemma  has  disap- 
peared. The  muscles  over 
the  body  are  not  equally 
involved ;  indeed,  bundles 
of  fibrillse  in  the  same 
muscle  are  affected  in  dif- 
ferent degrees.  This  un- 
even character  of  the  atro- 
phy is  'peculiar  to  this 
The      muscles 


Fig.  200. 


Teased  Fibres  from  the  Abductor  Pollicis  in  a  case  of  Progressive 
Muscular  Atrophy. 

A.  Fibres  from  a  normal  bundle. 

B.  Fibres  from  a  fasciculus  adjoining  A,  atrophied  and  showing  dlSCaSC. 
fatty  degeneration,     x  300.  .        ,  ^    , 

Simply  waste,  and  become 
pale  or  of  a  faintly  yellow  hue.  They  are  harder  and  firmer  than  normal. 
The  strise  disappear  only  after  great  reduction  in  size.  The  interstitial 
structure  is  increased  and  filled  with  numerous  lymphoid  cells.  Fatty  and 
granular  degeneration  may  occur  later,  with  fatty  infiltration,  and  if  the 
fat-globules  are  present  in  large  quantity  the  muscle  may  not  he  reduced 
in  size.  Granular  disintegration  is  soon  followed  by  transformation  of  the 
muscular  tissue  into  fine  fat-granules. 

In  some  cases  progressive  muscular  atrophy  has  occurred  without  ap- 
preciable changes  in  the  cord,  and  given  rise  to  the  belief  that  such  changes- 
were  secondary  to  the  muscular  atrophy.  It  is  very  generally  accepted, 
however,  that  the  central  lesion  is  the  primary  and  characteristic  change.' 

Etiology. — Progressive  muscular  atrophy  is  chiefly  met  with  in  adult 
males  in  middle  life.  Heredity  and  consanguinous  influence  can  no  longer 
be  doubted.^  Excessive  physical  labor,  exposure  to  cold  and  wet,  are  said 
to  excite  it.  Those  who  habitually  use  one  set  of  muscles  are  perhaps  pre- 
disposed to  the  disease.   Injury  to  the  spine  is  an  important  causative  factor. 

1  Virchow  calls  fat  in  the  fibres  parenchymatous,  and  fat  in  the  interfibrillary  tissue  the  interstitial 
form  of  degeneration. 

5  Leyden  states  that  in  hereditary  cases  the  lumbar  muscles  and  those  of  the  lower  limbs  are  first  at- 
tacked ;  that  it  may  appear  in  childhood,  and  that  several  members  of  the  same  family  may  be  simulta- 
neously afEected. 


PROGEESSIVE   MUSCULAR   ATROPHY. 


1013 


Symptoms. — The  invasion  of  progressive  muscular  atrophy  is  irregular 
and  variable.  It  usually  comes  on  insidiously,  the  first  indication  of  its 
presence  being  a  wasting  and  loss  of  power  of  some  muscles  or  group  of 
muscles.  When  regular  in  its  course  the  wasting  begins  in  the  muscles  of 
the  hand  ;  first  the  ball  of  the  thumb  of 
the  right  hand,  then  the  hypothenar 
eminence  and  the  interossei  are  at- 
tacked, in  the  order  named.  Marked 
atrojohy  of  the  interossei  causes  the  hand 
to  have  the  characteristic  bird-claw  look. 
The  left  hand  is  soon  involved,  and  the 
wasting  then  slowly  ascends,  attacking  the 
muscles  of  forearms,  arms,  shoulders,  the 
pectorals,  and  latissimus  dorsi,  with  sym- 
metrical alternation.  The  arms  may  be 
reduced  to  skeletons  of  limbs,  and  the 
wing-shoulder  is  not  uncommonly  seen. 

When  the  muscles  of  the  trunk  are  in- 
volved, those  of  respiration  and  deglu- 
tition are  very  likely  to  become  im]3lica- 
ted  early.  Sometimes  the  starting-point 
is  in  the  thoracic  muscles.  Although  the 
legs  become  extensively  involved  later, 
the  wasting  seldom  begins  there.  These 
atrophic  changes  advance  very  slowly, 
and  the  patient  will  remember  that  he  had  for  weeks  or  months  a  feeling  of 
slight  numbness  or  formication,  and  that  his  fingers  have  seemed  clumsy. 
They  also  may  complain — just  before  atrophy  begins— of  a  sensation  of 
cold  air  being  blown  on  them  ;  the  hand  and  arm  are  very  easily  fatigued, 
and  wandering  pains  not  infrequently  precede  the  wasting  of  the  muscles. 
The  parts  to  be  attacked  or  those  just  involved  are  colder  than  normal.  A 
peculiar  fibrillary  tremor — transient  oscillatory  movements  in  the  fibres 
of  the  affected  muscles — is  present  early.  It  occurs  unknown  to  the 
patient,  and  may  be  excited  by  gently  blowing  or  tapping  on  the  skin. 
When  the  atrophy  becomes  extensive  this  ceases.  The  muscles  respond 
promptly  to  the  Faradic  and  voltaic  currents,  with  a  force  in  proportion 
to  their  bulk.  The  wasting  in  the  muscles  produces  very  different  ap- 
pearances according  to  the  group  involved  ;  should  those  of  the  face  be- 
come implicated,  as  frequently  happens  in  children,  the  expression  is 
stolid,  grave,  and  unchangeable.  Often,  the  head  falls  forward,  and  the 
saliva  dribbles  from  the  mouth.  The  speech  may  be  faltering  ;  and  the 
tongue  small  and  shrivelled.  Mastication  and  deglutition  may  become 
difficult,  and  as  the  muscles  of  respiration  are  involved  dyspnoea  is  urgent 
and  asphyxia  or  pulmonary  complications  result  fatally.  Many  state  that 
the  pupil  on  the  affected  side  is  much  smaller  than  its  fellow,  and  re- 
acts to  light  but  slightly.' 

1  Rosenthal,  Schneemann,  Voisin,  Menjaud  and  Bergmann. 


Fig.  20r. 
Sketch  of  a  Hand  in  Progressive  Muscn]ar 
Atrophy.- 


-Charcot. 


]014  DISEASES   OF  THE   NEEVOUS   SYSTEM. 

In  a  certain  number  of  cases  agonizing  pain  along  the  nerves  leading  to 
the  affected  muscles  occurs  and  is  a  promineat  symptom  throughout. 
Late  in  the  disease  atrophy  of  muscles  proceeds  so  far  that  absolute  im- 
mobility of  a  member  is  the  result. '  The  general  health  is  unimpaired, 
and  the  intellect  is  clear. 

Differential  Diagnosis. — Progressive  muscular  atrophy  may  be  mistaken 
for  acute  anterior  polio-myelitis,  for  j)cdsy  due  to  injury  of  a  nerve,  lead 
palsy,  malarial  paralysis,  post-paralytic  atrophy  of  muscles,  and  sclerosis 
of  the  lateral  columns. 

In  injury  of  a  nerve  the  atrophy  is  confined  to  the  muscles  supjalied  by 
that  nerve,  and  is  not  progressive.  In  injuries  of  mixed  nerves,  sensation 
will  also  be  lost. 

In  lead  palsy  the  history  of  exposure,  the  blue  line  about  the  gums,  and 
the  colic,  with  the  fact  that  the  extensor  muscles  of  the  hand,  rather  than 
those  of  the  thenar  and  hypothenar  eminences,  are  first  atrophied,  caus- 
ing the  drop-wrist  instead  of  a  claw  hand,  and  that  their  electric  con- 
tractility is  greatly  diminished,  are  sufficient  for  a  differential  diagnosis. 

In  malarial  palsy  there  is  no  muscular  wasting,  no  tremor,  and  there 
are  the  attendant  well-known  malarial  symptoms. 

Muscular  atrophy  sometimes  ioWow^ paralysis.  But  this  fact  alone,  when 
the  muscles  do  not  respond  to  Faradization,  excludes  progressive  muscular 
atrophy. 

Symmetrical  sclerosis  of  the  lateral  columns — amyotrophic  lateral 
sclerosis — is,  according  to  Charcot,  distinguished  by  its  rapid  course,  the 
ultimate  affection  of  all  the  limbs,  and  the  almost  constant  extension  to  the 
bulbar  nuclei,  by  the  prolonged  preservation  of  electro-muscular  contrac- 
tility, and  by  permanent  spasmodic  contractures  of  the  paralyzed  and 
atrophied  limbs.  The  symptoms  of  muscular  atrophy  are  preceded  in 
amyotrophic  sclerosis  by  paralysis,  and  accompanied  by  rigidity  ;  this  does 
not  occur  in  muscular  atrophy. 

Prognosis.— Progressive  muscular  atrophy  is  always  a  grave  disease.  Its 
course  is  slow  and  irregular  ;  it  may  appear  in  the  muscles  of  the  hand,  and 
years  elapse  before  it  extends.  There  is  little  hope  of  checking  its  advance, 
even  if  the  treatment  is  commenced  at  its  onset.  The  disease  is  arrested 
spontaneously  in  a  few  instances  within  two  or  three  years.  Complete  re- 
covery is  rare.  One  year  is  the  average  duration,  when  recovery  takes 
place.  Its  average  duration  is  five  years.'  An  hereditary  element  in  the 
etiology  renders  the  prognosis  unfavorable,  and  when  the  disease  is  pro- 
longed several  years,  or  the  muscles  of  respiration  and  deglutition  become 
involved,  a  fatal  termination  is  rarely  long  delayed.  Inanition,  bronchitis, 
pneumonia,  and  hypostatic  congestion  are  the  causes  of  death. 

Treatment. — In  the  cases  that  have  come  under  my  observation  no  plan 
of  treatment  has  had  any  beneficial  effect.  If  an  exciting  or  predisposing 
cause  can  be  reached  it  should  at  once  be  removed.     Damp,  cold,  and  over- 

1  Herpes  has  been  observed  along  the  line  of  a  nerve  going  to  an  atrophied  muscle,  and  Rosenthal 
mentions  hj'pertrophy  of  the  bones  with  concentric  osseous  atrophj%  arthropathies,  and  bed-sores  as  rare 
trophic  disturbances. 

*  Roberts,  in  Reynolds  System  of  Medicine. 


CEEEBRO-SPINAL   SCLEEOSIS. 


1015 


exertion  should  be  avoided,  and  if  syphilis  be  suspected,  an  anti-syphilitic 
treatment  is  indicated  ;  and  cod-liver  oil,  phosphorus,  arsenic,  and  the 
mineral  tonics  are  to  be  given  with  a  highly  nutritious  diet.  The  body  is 
to  be  warmly  clothed  in  flannel  ;  friction,  moderate  exercise,  shampooing, 
massage,  and  inunctions  are  undoubtedly  beneficial,  if  persevered  in. 
Warm  baths  at  natural  springs  are  strongly  recommended.  Galvanism, 
however,  is  probably  the  most  efficient  remedy.  The  current  should  be 
applied  along  the  spine,  especially  in  the  cervical  region,  and  directly  to 
the  affected  muscles.  Faradization  alternating  with  the  constant  current 
often  leads  to  improvement  and  a  temporary  arrest  of  the  disease/  The 
cramps  and  neuralgic  pains  are  best  controlled  by  hypodermic  injections  of 
morphine.^ 

CEEEBRO-SPIIirAL  SCLEEOSIS. 


Morbid  Anatomy. — On  opening  the  spinal  canal  the  cord  is  seen  to  be 
studded  with  well-defined  nodules  of  sclerotic  tissue  which  have  given  it 
the  name  of  nodular  sclerosis. 
These  nodules  are  distributed  ir- 
regularly throughout  both  the 
gray  and  white  matter.  They 
vary  in  number,  and  range  in  size 
from  minute  microscopical  objects 
to  the  size  of  a  walnut.  They 
present  a  yellowish  red,  glistening 
appearance,  are  slightly  elevated, 
semi-transparent,  of  a  jelly-like  or 
cartilaginous  feel,  and  are  marked 
by  fine  white  lines.  The  meninges 
over  the  nodules  are  thickened  and 
opaque,  but  seldom  adherent  to 
the  substance  of  the  cord.  The 
sclerosed  patches  are  well  defined 
and  easily  distinguished  from  the 
normal  tissue  in  which  they  are 
imbedded ;  still  there  is  no  ab- 
rupt transition  from  healthy  to 
diseased  tissue. 

A  microscopical  examination 
shows  the  centre  of  the  nodules  to 
be  a  dense  mass  of  very  fine  fibril- 
lated  connective-tissue,  containing 
fat  granules,  corpora  amylacea,  Bel- 
ter's cells  and  small  axis-cylinders 
which  are  glossy  and  brittle.  The 
persistence  of  the  axis-cylinders  is  regarded  by  Charcot  as  peculiar  to  dissem- 

1  Remak  recommends  galvanization  of  the  fibres  of  the  sympathetic  nerve. 

2  Loclthart  Clarlt  hints  that  blietering  and  other  forms  of  counter-irritation  to  the  spine,  laU  in  the  dis- 
ease, deserve  further  trial. 


Fio.  208. 

Cerebro-Spinal  Sclerosis. 

Nodvles  of  sclerotic  tissue  on  the  surface  of  the  cord. 

A.  Dura  mater  divided. 

B.  Pia  mater  showing  sclerotic  patches. 

C.  Pia  mater  reflected. 

D.  Sclerotic  nodules  on  the  cord. 


1016  DISEASES    OP   THE   NEEVOUS    SYSTEM. 

inated  sclerosis.  ISTear  the  periphery  the  nerve  tubes  are  surrounded  by 
connective-tissue  fibrillae  running  parallel  with  the  inclosed  nerves,  and 
there  is  commencing  hyperplasia  of  the  neuroglia,  proliferation  advancing 
more  or  less  rapidly  according  to  the  age  of  the  nodule.  The  walls  of  the 
vessels  are  thickened  and  infiltrated  with  numerous  fat  and  lymphoid  cells, 
but  their  lumen  is  notably  diminished. '  The  nerve  cells  in  the  gray  cor- 
nua  are  either  primarily  or  secondarily  involved  and  undergo  cloudy  swell- 
ing, followed  by  pigmentation  or  granulo-fatty  degeneration, — the  yellow 
degeneration. 

Thus  it  appears  that  sclerosis  is  a  primary  and  multilocular  chronic  in- 
terstitial myelitis  or  encephalitis  a  secondary  condition. 

Etiology, — The  recognized  exciting  causes  of  multiple  cerebro-spinal 
sclerosis  are  damp  and  cold,  sudden  chilling  of  the  body,  traumatism,  and 
severe,  long-continued  brain  work  or  physical  exercise.  Continued  jar- 
ring of  the  body  is  also  thought  to  produce  the  disease,  and  it  is  said  to  oc- 
cur in  nervous  people,  with  hysteria  and  after  acute  febrile  diseases.  It  is 
essentially  a  disease  of  earl}^  life,  few  cases  occurring  outside  the  limits  of 
fifteen  and  thirty-five.  Heredity  is  said  to  play  an  important  part  in  its 
etiology.  Quite  recently  cases  are  reported  as  occurring  in  very  young  chil- 
dren. 

Symptoms. — Charcot  makes  three  varieties  of  this  disease,  according  as  it 
is  confined  to  the  brain,  or  cord,  or  involves  both.  The  latter  is  the  more 
common ;  it  may  come  on  insidiously  or  be  sudden  in  its  development.  If  it 
is  insidious  in  its  advent  the  patient  complains  vaguely  of  headache,  ver- 
tigo, muscular  weakness,  mental  disturbances,  and  queer  feelings  as  for- 
mications, itchings,  burnings,  etc.,  in  the  limbs.  The  symptoms  which 
are  referable  to  the  sympathetic  system  are  nausea,  vomiting,  and  cardial- 
gia.  The  patient  notices  very  soon  a  loss  of  co-ordinating  power  ;  he  can- 
not control  his  hands  in  writing  or  his  feet  and  limbs  in  walking.  There 
is  also  impairment  of  the  special  senses.  If  the  spinal  element  is  promi- 
nent, there  is  more  or  less  paresis  of  all  the  extremities,  with  contractures 
of  the  muscles.  As  soon  as  an  attempt  is  made  to  use  the  paretic  limbs, 
they  become  tremulous  and  contracted.  This  tremor  is  peculiar  in  not  oc- 
curring until  an  attempt  is  made  at  voluntary  motions,  and  at  once  ceas- 
ing when  the  parts  are  allowed  to  rest.  It  is  called  the  shaking  tremor. 
The  more  powerful  the  mental  efPort  the  more  marked  is  the  tremor.  Even 
tlie  head  participates  in  it. 

In  some  cases  the  patient  becomes  childish  or  morose,  and  the  cerebral 
symptoms  in  such  cases  are  identical  with  those  of  cerebral  softening.  Dur- 
ing prolonged  fits  of  yawning,  sobbing,  or  laughing  the  respirations  ie- 
come  stridulous,  and  in  the  advanced  stages  the  voice  is  changed.  The 
patient  talks  in  a  low  monotone  or  whisper,  dividing  his  words  into  sylla- 
bles, and  emphasizing  them  as  when  scanning  a  line  of  poetry.  If  the 
sensory  nerves  are  involved  there  are  pains  in  the  course  of  the  affected 
nerves,  and  a  girdle  pain  is   felt  about  the  abdomen.     Amblyopia,   nys- 

1  Charcot,  Cornil  and  Ranvier  maintain  that  in  tiie  sclerotic  islands  nerve-elements  are  always  present. 
Frommannand  Erb  hold  the  reverse.— Ziewi.  Cycl.,  vol.  siii. 


CEKEB HO- SPINAL  SCLEKOSIS.  101? 

tagmus,  diplojoia,  and  inequality  of  the  jDupils  evidence  invasion  of  the 
base  of  the  brain  and  optic  tracts.  In  the  advanced  stage  vesical  symp- 
toms, acute  bed-sores,  and  loss  of  sexual  power  and  control  of  the  sphinc- 
ters become  marked  symptoms.  Sometimes  a  sudden  apoplectiform  attack 
followed  by  paretic  symptoms  ushers  in  the  disease.  The  course  of  the 
disease  is  peculiar.  As  its  development  is  by  stages,  it  may  gradually 
progress  for  several  years,  and  then  remain  stationary  for  a  long  period. 

Differential  Diagnosis. — Disseminated  sclerosis  of  the  brain  and  cord  may 
be  mistaken  for  paralysis  agitans,  or  locomotor  ataxia,  and  when  ushered 
in  by  apoplectiform  symptoms  may  be  mistaken  for  cerebral  hemorrhage. 

In  paralysis  agitans  the  fine  tremor  exists  when  the  patient  is  at  rest, 
and  is  not  accompanied  by  shaking  of  the  head  ;  while  in  the  shaking  of 
disseminated  sclerosis  the  head  is  always  involved,  the  symptom  ceasing  as 
soon  as  the  patient  is  at  rest.  Paralysis  agitans  is  rare  before  forty  ;  mul- 
tiple sclerosis  is  rare  after  thirty-five.  Changes  in  the  voice  and  speech  and 
ocular  symptoms  are  present  in  disseminated  sclerosis  and  absent  in  jDaraly- 
sis  agitans. 

In  locomotor  ataxia  the  peculiar  tremor,  impairment  of  voice  and  speech, 
and  nystagmus  that  belong  to  disseminated  sclerosis  are  absent.  In  the 
former  disease  we  notice  the  peculiar  iron-band  sensation,  vesical  symptoms, 
the  Meniere's  vertigo,  the  very  slow  and  late  appearance  of  paretic  symp- 
toms, the  lightning-like  and  agonizing  neuralgic  pains,  and  the  peculiar 
double  beat  in  walking,  the  heel  being  put  down  first,  all  of  which  are  in 
marked  contrast  to  the  symptoms  of  multiple  cerebro-spinal  sclerosis. 

When  disseminated  multiple  sclerosis  is  ushered  in  by  loss  of  conscious- 
ness which  rapidly  deepens  into  coma,  with  marked  hemiplegic  symptoms,, 
it  may  be  mistaken  iov  cerebral  hemorrhage  ;  but  in  sclerosis  the  tempera- 
ture is  very  high  during  these  peculiar  attacks— 104°  or  105°  F. — the  hemi- 
plegia passes  off  as  the  patient  returns  to  consciousness  or  in  a  few  days 
after,  and  the  temperature  rapidly  falls  to  normal. 

Prognosis.— ^This  disease  is  usually  of  long  duration,  five  to  ten  years  be- 
ing its  average.  It  is  rare  for  death  to  occur  in  coma.  There  is  no  well- 
authenticated  instance  where  recovery  has  occurred.  During  the  stage  of 
its  development  and  greatest  activity  deceptive  remissions  occur  ;  but  after 
six  or  seven  years  emaciation  sets  in,  a  marasmus  is  developed,  and  the  pa- 
tient is  apt  to  die  from  intei'current  disease. 

Treatment. — The  best  method  of  treatment  yet  proposed  is  the  restora- 
tive ;  the  object  is  to  improve  nutrition.  Among  the  drugs  that  have  been 
used,  especially  by  Charcot  and  his  followers,  are  chloride  of  gold,  phos- 
phate of  zinc,  nitrate  of  silver,  chloride  of  barium,  potassium  iodide  and 
bromide,  arsenic,  belladonna,  calabar  bean,  and  ergot.  The  galvanic  cur- 
rent is  the  best  means  of  administering  electricity.  Opinion  is  divided  as 
to  the  benefit  obtained  from  hot  or  cold  baths  and  thermal  springs,  or  in- 
unctions and  massage.  Pain  not  infrequently  becomes  so  severe  as  to  de- 
mand hypodermic  injections  of  morphine. ' 

'  Leyden  reports  a  case  of  almost  complete  cure  from  galvanism  and  the  baths  of  Kehme. — Beit.  z.  acute 
u.  chron.  Myelitis.    Zeitsch.fiir  klin.  Med.    Berlin,  1879,  i.,  p.  126. 


1018 


DISEASES   OF   THE   KERVOUS    SYSTEM. 


LOCOMOTOR    ATAXIA, 

Locomotor  ataxia '  is  one  of  the  most  frequent  diseases  of  the  spinal 
cord. 
Morbid  Anatomy. — Its  principal  pathological  lesion  is  an  increase  in  the 


J>03ierior. 


Pig.  209. 
Diagram  illustrating  the  Regions  of  Degenerative  Changes  in  the  Spinal  Cord. 

A.  Pyramidal  tracts. 

B.  Anterior  columns. 

C.  Haddon  and  Goiuer^s  lateral  sensory  tract. 

D.  Mixed  zone  of  lateral  columns. 

E.  Processus  reiic^ilaris. 

F.  Crossed  pyramidal  tracts. 

G.  Bi7'ect  cerebellar  tracts. 
p.  Postero-external  columns. 

I.  Postero-internal  columns. 


Columns  of  Goll. 


After  Flechsig. 


interstitial  connective-tissue  of  the  spinal  cord.  As  the  cord  is  removed 
from  the  spinal  canal  there  will  be  noticed  a  grayish  discoloration  on  both 
sides  of  the  posterior  median  fissure.  The  pia  and  dura  mater  will  be 
more  or  less  firmly  adherent  to  each  other  ;  and  the  dura  mater  may  be 
thickened,  pigmented,  opaque  and  studded  with  osseous  plaques  ;  the  pia 
mater  may  be  congested  and  there  may  be  an  exudation  into  its  meshes. 
The  posterior  aspect  of  the  cord  may  appear  atrophied,  and  have  a  firm, 
hard  feel.     In  advanced  cases  the  whole  cord  is  smaller  than  normal. 

A  cross  section  will  show  an  increase  in  the  cephalo-rachidian  fluid,  and 
the  posterior  columns  will  be  shrunken,  gray,  cartilaginous  and  shining  in 
appearance.  Not  infrequently  the  sclerosis  will  extend  to  the  lateral 
columns  and  forward  to  the  margin  of  the  anterior  columns.  These 
changes  usually  begin  in  the  lateral  part  of  the  posterior  column  in  the 

1  Duchenne  was  the  first  to  give  an  accurate  description  of  this  disease.  Trousseau  and  others  have 
called  it  Duchenne's  Disease.  It  is  also  known  as  posterior  spinal  sclerosis,  tabes  dorsalis,  gray  degeneration 
of  the  posterior  columns  and  leuJco-myelitis  posterior  chronica.  It  is  often  called  progressive  locomotor 
ataxia. 


LOCOMOTOR   ATAXIA. 


1019 


Fig   310 

Locomotor  Ataxia. 

Section  of  Spinal  Cord  in  tlie  Cenical  Region. 

A  A.  Sclerosis  of  the  columns  of  Goll. 


upper  lumbar  and  lower  dorsal  regions,  and  extend  upward  and  down- 
ward. It  is  possible  in  long  stand- 
ing cases  for  the  medulla  and  the 
second,  third,  sixth  and  eighth  cra- 
nial nerves  to  be  involved,  and  for 
the  entire  cross  section  of  the  cord, 
at  various  points,  to  be  shrunken, 
hard  and  gray. 

As  a  rule,  the  sclerosis  ceases  at 
the  restifo7"m  bodies.^  If  GoU's 
columns  are  involved  it  is  a  second- 
ary degeneration.  The  posterior 
roots  of  the  spinal  nerves  show  gray 
degeneration  and  atrophy  to  the 
naked  eye.^  On  microscopical  ex- 
amination there  will  be  found  evi- 
dences of  a  large  amount  of  dense 
and  delicate  connective-tissue  con- 
taining nuclei,  granular  and  amy- 
loid corpuscles,  in  which   are  very 

few  atrophied  nerve  fibres,  which  have  lost  their  medullary  sheaths.' 
Large  spider  cells  are  found  throughout  the  sclerotic  tissue.  The  j^os- 
terior  columns  are  seen  fused  together  by  connective-tissue  in  the  pia 
mater  which  dips  down  into  the  fissure.  The  walls  of  the  capillaries  and 
small  vessels  are  thickened  and  rigid,  and  their  calibre  is  diminished. 
Their  sheaths  are  filled  with  oil  globules.  They  are  also  markedly  pig- 
mented.* The  sclerosis  travels  from  the  cord  to  the  posterior  roots  of 
the  spinal  nerves,  which  show  atrophy.  The  sciatic,  crural,  and  brachial 
nerves  have  been  found  sclerosed  and  atrophied.* 

Etiology. — Locomotor  ataxia  is  more  frequently  met  with  in  men  than  in 
women,  the  proportion  being  six  to  one.  It  occurs  oftenest  between  the 
ages  of  twenty  and  fifty.  In  a  neuropathic  predisposition  it  may  be  in- 
duced by  anything  that  seriously  depresses  the  nervous  system.  Cold  and 
wet,  bad  hygienic  surroundings,  excessive  mental  or  bodily  exertions, — 
onanism,  excesses  in  venery,  etc.,  especially, — depression  of  spirits,  an  in- 
sufficient or  improper  diet,  the  impoverished  blood  states  that  occur  with 
or  follow  wasting  acute  or  chronic  maladies,  prolonged  lactation,  syphilis,* 
and,  according  to  some,  excessive  use  of  tobacco, — are  among  its  predis- 
posing causes.      Blows  on  the  spine,  the  suppression  of  menses  or  old 

1  Charcot  describes  the  external  bands  :— two  bands  near  the  posterior  cornua  in  the  outer  part  of  the 
posterior  columns.    They  run  parallel  with  the  posterior  horns  of  gray  matter. 

2  Charcot  has  drawn  attention  to  the  condition  of  the  joints  in  some  cases  of  locomotor  ataxia.  "  Snr 
quelques  arthropathies,"  eic.—A7rhiv.  de  Fhysiologie,  i.,  1868,  p.  161. 

3  Cornil  and  Ranvier  insist  that  the  axis-cylinder  always  exists,  but  that  it  requires  a  peculiar  mode  of 
preparation  to  demonstrate  this. 

*  Lockhart  Clark  states  that  he  has  sometimes  found  the  extremities  of  the  posterior  cornua,  and  even 
the  central  gray  substance,  more  or  less  damaged  by  disintegration.  The  question  has  been  raised  whether 
the  initial  lesion  may  not  be  in  these  cornua. 

6  Friedreich. —  V>rchoiu''s  Archiv.,  Bde  26,  27. 

«  Erb  found  a,  syphilitic  history  in  twenty-seven  out  of  forty-four  cases. 


1030  DISEASES    OF   THE   NERVOUS    SYSTEM'. 

hemorrhoidal  fluxes  may  excite  it.  It  is  a  question,  when  it  follows  pneu- 
monia, rheumatic  fever,  or  diphtheria,  if  there  is  any  causal  relationship 
between  them.'  Its  hereditary  tendency  is  shown  by  its  attacking  two  or 
more  members  of  the  same  family,  other  members  suffering  from  some 
other  form  of  nervous  disease.  This  is  an  example  of  the  "  neuropathic 
tendency."*     In  a  large  proportion  of  cases  there  is  no  assignable  cause. 

Symptoms. — The  symptoms  of  locomotor  ataxia  may  be  divided  into  three 
periods  :  a  period  characterized  by  disturbances  of  sensation,  a  period  in 
which  there  is  loss  of  coordinating  power,  and  a  period  of  paralysis.  Dur- 
ing the  first  period  there  are  sharp,  tearing,  lightning  pains  in  the  lower 
limbs,  dysuria,  incontinence,  spermatorrhoea,  nocturnal  pollutions,  excite- 
ment of,  or  loss  of  sexual  desire,  a  sense  of  weariness  in  the  limbs,  and  nausea 
and  vomiting  attended  by  severe  and  paroxysmal  aching  in  the  stomach. 
A  sense  of  numbness  and  formication  in  the  limbs  is  not  uncommon  in  this 
period.  There  maybe  a  girdle  sensation,  not  only  about  the  waist,  but  also 
in  the  limbs — chiefly  about  the  knee  and  ankle.  In  some  cases  there  will 
be  evidence  of  arthropathies  and  symptoms  much  resembling  those  of  active 
cerebral  hypersemia.  Eectal  and  urethral  colics,  bronchial  spasms,  and 
nephritic  symptoms  resembling  those  of  renal  colic,  are  not  infrequent.  The 
pains  during  this  period  are  usually  in  the  feet  and  legs ;  but  they  may 
have  their  seat  in  the  back,  stomach,  intestines,  or  bladder.  If  they  are 
situated  in  the  internal  viscera,  the  functions  of  those  viscera  are  disturbed. 
Wherever  they  may  be  seated,  at  first  they  do  not  come  on  often,  and  are 
of  short  duration  ;  but  as  the  disease  advances,  the  attacks  become  more 
frequent  and  are  of  longer  duration.  The  muscles  of  the  eyes  may  be  af- 
fected, causing  double  vision  or  strabismus,  which  may  last  a  few  days  or 
weeks  and  then  disappear  ;  or  changes  may  occur  in  other  nerves  which 
lead  to  loss  of  sight.  There  may  be  temporary  or  permanent  dilatation  of 
one  or  both  pupils. 

The  destructions  of  surface  sensation  are  manifold  ;  sometimes  the  pa- 
tient will  complain  of  a  sense  of  numbness  in  the  hips,  sometimes  a  prick- 
ing sensation,  or  a  sensation  of  some  soft  substance  between  the  feet  and 
the  ground  ;  one  portion  of  the  surface  may  be  anaesthetic,  another  hyper- 
aesthetic.  After  a  varying  period,  the  ataxic  symptoms  appear,  and  the 
muscles  are  no  longer  moved  in  their  natural  way.  The  gait  becomes  un- 
steady, the  patient  walks  like  one  intoxicated  ;  there  is  a  sense  of  heaviness 
in  the  limbs,  and  if  the  feet  are  brought  close  together,  and  the  eyes  closed, 
the  body  sways  to  and  fro  and  sometimes  falls.  After  a  time  the  patient  is 
compelled  to  watch  his  feet  while  walking.  Later  on  he  throws  out  his 
feet  and  legs  in  the  most  grotesque  manner ;  for  when  the  will  acts  the 
muscles  contract  far  more  than  the  patient  intends.  If  the  upper  extrem- 
ities are  involved,  he  is  unable  to  dress  himself ;  he  cannot  pick  up  a  pin, 
button  his  garments,  or  hold  anything  in  his  fingers.     The  movements  of 

1  The  most  recent  theory  of  its  causation  is  that  of  Kahler  and  Pick,  who  regard  those  cases  whicti  fol- 
low acute  infectious  diseases  as  the  result  of  the  accumulation  of  fungi  in  the  central  nervous  system 
producing  nutritive  disturbances. 

2  Carre  records  eighteen  cases  of  tabes  in  the  same  family  in  three  generations.— J/.  Carre,  These. 
Paris,  1862. 


LOCOMOTOR   ATAXIA.  1021 

his  liancls  and  arms  are  forcible,  irregular,  and  jerking.  The  gait  during 
this  period  is  peculiar ;  the  heel  is  brought  down  first,  then  the  toe  :  there 
IS  a  double  beat  to  the  step.  Quiet  or  steady  movements  are  impossible. 
At  times  the  loss  of  coordination  is  so  great  that  for  days  the  patient  is  un- 
able to  walk,  and  then  the  coordinating  power  is  partially  restored.  One 
extremity  maybe  involved  after  the  other,  or  both  be  attacked  at  the  same 
time.  During  this  period  there  is  a  marked  loss  of  sensation,  especially  in 
the  feet  and  legs ;  these  patients  are  often  unable  to  tell  when  their  feet 
touch  the  floor.  Sensitiveness  to  pain  is  diminished,  and  it  may  be  several 
mmiites  before  the  prick  of  a  pin  is  felt.  The  sensation  disturbances  of  the 
first  period  are  increased,  and  the  sight  is  more  imjDaired.  In  this  period 
there  is  less  loss  of  the  reflex  action  of  the  muscles  of  the  lower  extremi- 
ties, especially  the  muscles  of  the  calf  of  the  leg.  The  abolition  of  the  pa- 
tellar tend  on- reflex  is  one  of  the  diagnostic  signs  of  the  disease.  Loss  of 
the  sense  of  temperature,  a  greater  or  less  loss  in  electro-muscular  contrac- 
tility, and,  in  the  irritative  forms,  increase  in  galvanic  excitability  are  not 
uncommon.  During  this  period  there  may  be  developed  a  peculiar  affec- 
tion of  the  joints  ;  the  Joints  mpst  frequently  affected  are  the  knee,  hip, 
shoulder,  and  elbow.  The  joint  rapidly  swells  and  the  synovial  sac  fills  with 
fluid  ;  after  a  time  disorganization  of  the  articular  surfaces  takes  place  and 
may  be  followed  by  the  destruction  of  the  ends  of  the  bones.  In  some  in- 
stances the  swelling  suddenly  disappears  and  the  joint  is  not  disabled.'  De- 
generative changes  in  the  anterior  horns  are  thought  to  be  the  cause  of 
these  joint  symptoms.  In  a  few  cases  skin  eruptions  of  various  kinds  make 
their  appearance.^  In  the  last  period  paralysis  occurs,  and  then  are  devel- 
oped muscular  atrophy,  bed-sores,  and  those  vesical  and  renal  symptoms  that 
are  so  apt  to  lead  to  death. 

Nearly  all  the  symptoms  of  locomotor  ataxia  appear  intermittently,  and 
the  progress  of  the  disease  is  rarely  continuous.  During  the  third  period 
there  is  always  complete  impotence.  In  some  cases  the  face  has  a  pale 
yellow  color,  which  is  most  marked  during  cold  weather.^  During  this 
last  period  sensation  about  the  rectum  is  lost ;  hence  the  patient  is  apt  to 
become  exceedingly  filthy  unless  great  care  is  exercised.  This  condition  is 
accompanied  by  almost  constant  dribbling  of  the  urine.  Intelligence, 
memory,  and  the  higher  cerebral  functions  are  rarely,  if  at  all,  impaired. 
In  a  few  cases  of  locomotor  ataxia  the  patients  become  color-blind.  Loco- 
motor ataxia  is  a  non-febrile  disease,  but  during  the  initial  period  febrile 
symptoms  may  occur,  and  are  then  especially  important  as  indicating  a 
rapid  progress  in  the  disease."  The  former  is  neither  an  early  nor  a  late 
symptom.  Pierret  says  that  all  possible  nervous  disturbances  of  hearing 
may  precede  ataxia.     After  reaching  the  second  period,  the  disease  may  for 


*  Blum  states  that  the  great  friability  of  the  bones  that  results  in  spontaneous  fracture  is  due  to  raxeij- 
mgostitis.—Des.  Arth.  iVori.  nen.  Thhe.    Paris,  1875. 

*  Chfircot  says  that  they  follow  the  track  of  nerves  that  have  been  the  seat  of  pain. 

8  Eulenberg  attributes  dicrotism  of  the  pulse  in  ataxics  to  loss  of  vascular  tone  of  spinal  origin.— Ber- 
lin. Klin.  Wochen. 

*  Among  the  most  recent  contributions  to  this  disease  is  Erb's  paper,  wherein  he  ascribes  great  im- 
portance as  a  symptom  to  spinal  myosis,  i.  «.,  reflex  immobility  of  the  pupil. 


1022  DISEASES    OF   THE   KERVOUS   SYSTEM. 

along  time  remain  stationary,  or  it  may  temporarily  improve,  but  com- 
plete recovery  is  rarely,  if  ever,  reached.  In  the  long  and  slowly  progres- 
sive cases  fluctuations  always  occur,  with  improvement  in  summer  and 
exacerbations  'in  winter. 

Differential  Diagnosis. — Locomotor  ataxia  may  be  confounded  with  joara- 
plegia,  multiple  cerebro-sinnal  sclerosis,  cerebellar  lesions,  chronic  myelitis, 
hysterical  ataxia,  and  chronic  spinal  meningitis. 

Paraplegia  is  a  true  paralysis  ;  ataxia  is  not,  and  it  is  readily  proved  that 
in  the  latter  disease  muscular  force  is  not  diminished.  In  paraplegia  the 
limbs  are  not  thrown  about  in  walking, — they  are  merely  dragged.  In 
paraplegia  there  is  little  or  no  resistance  to  artificial  movement,  while  in 
ataxia  there  is  great  resistance  in  bending  the  limbs  against  the  will  of  the 
patient.  The  nutrition  of  the  muscles  is  markedly  impaired  in  paraplegia, 
and  normal  in  ataxia.  Neuralgic  pains  are  absent  in  paraplegia  and  present 
in  ataxia.  Strabismus,  ptosis,  etc.,  are  present  in  ataxia  and  absent  in 
paraplegia. 

The  diiferential  diagnosis  between  multiple  sclerosis  and  ataxia  has  been 
given. 

Cerebellar  disease  has  for  its  characteristic  symptom  vertigo  ;  this  is  rare 
in  ataxia.  A  patient  with  cerebellar  disease  can  stand  and  walk  better  with 
his  eyes  shut  than  open,  has  unimpaired  cutaneous  sensibility,  and  the 
movements,  while  uncertain,  are  not  so  abrupt,  vehement,  and  Jerky  as  in 
ataxia ;  they  resemble  rather  the  stupid  movements  of  a  drunken  man. 
The  absence  of  neuralgic  pains,  of  vesical  and  sexual  weakness,  and  the 
prominence  of  headache,  vomiting,  and  convulsions  in  cerebellar  disease 
will  be  sufl&cient  for  the  diagnosis. 

In  chronic  myelitis  there  are  no  disorders  of  coordination.  The  patient 
sufEers  paresis,  or  even  complete  paralysis  of  the  lower  extremities,  while 
in  ataxia  there  is  no  paralysis,  muscular  power  being  undiminished.  The 
limbs  are  dragged  simply  in  chronic  myelitis  ;  they  are  thrown  forcibly 
about  in  ataxia.  Ocular  symptoms  are  absent  in  chronic  myelitis,  present 
in  ataxia.  Contractures,  spasms,  paralysis  of  the  bladder,  cystitis,  and  the 
early  formation  of  bed-sores,  together  with  the  absence  of  intense  neuralgic 
pains,  will  also  serve  to  distinguish  chronic  myelitis  from  ataxia. 

In  hysterical  ataxia  the  history,  and  the  occurrence  of  the  disease  in  a 
female,  with  the  subsequent  course  of  the  disease,  will  enable  one  to  dis- 
tinguish it  from  ataxia. 

In  meningitis  there  is  pain, — increased  on  pressure, — slight  paralysis  but 
no  incoordination,  no  flinging  of  the  limbs  in  walking  or  moving,  no  aboli- 
tion of  tendon  reflexes,  and  no  ocular  symptoms  such  as  are  present  in 
ataxia. 

Prognosis. — The  usual  course  of  locomotor  ataxia  is  progressive. 

The  prognosis  as  to  its  duration  is  uncertain.  The  disease  sometimes 
ceases  of  itself,  leaving  the  patient  in  a  disabled  condition,  but  still  giving 
him  years  of  life.  The  slower  the  development  the  longer  the  duration. 
The  prognosis  is  more  unfavorable  when  it  occurs  with  a  history  of  nervous 
disease  in  the  family,  when  the  early  symptoms  are  serious  and  constant. 


SPASMODIC   TABES   DOESALIS.  1023 

and  when  constitutional  symptoms  (especially  emaciation)  become  marked. 
Complications -likewise  render  the  prognosis  unfavorable.  Comi^lete  re- 
covery is  possible  but  not  jjrobable.  The  duration  of  the  disease  varies 
from  six  months  to  as  many  years. 

Treatment. — The  efficacy  of  treatment  depends  upon  the  stage  at  which  it 
is  commenced.  Undoubtedly,  if  the  disease  can  be  early  recognized,  its 
advance  can  in  many  cases  be  cliecked. 

Of  the  drugs  recommended,  nitrate  of  silver  is  perhaps  the  one  most  ex- 
tensively used.  It  should  be  given  cautiously  ;  about  one  grain  a  day  in 
divided  doses.  The  galvanic  current  is  nearly  always  of  service.  Some 
cases  will  be  benefited  by  the  iodides,  others  by  the  bromides.  Strychnia, 
phosphorus,  arsenic,  the  chlorides  of  gold,  sodium,  and  bariam,  the  phos- 
phide of  zinc,  belladonna  and  ergot  all  have  been  recommended.'  The 
diet  and  mode  of  life  should  be  such  as  to  conduce  to  the  highest  degree  of 
health  and  nutrition.  Cod-liver  oil  and  ]ohosphorus  may  be  given  as  ad- 
juvants to  a  nutiitious  diet. 

The  patient  should  remain  at  rest  as  much  as  possible.  Under  no  cir- 
cumstances should  he  be  allowed  to  expose  himself  to  cold  or  wet  or  to  sud- 
den changes  in  temperature.  Flannel  should  be  constantly  worn  next  the 
skin.  Simple  thermal  baths  seem  to  do  harm,  but  saline  thermal  baths 
sometimes  give  good  results.  Sulphur,  clialybeate  and  mud  baths  have 
been  recommended.  Erb  recommends,  as  better  than  all,  the  cold  water 
cure.  He  advocates  the  wet  pack  for  the  neuralgic  pains.  Bleeding  or 
depletion  of  any  sort  is  contraindicated,  even  in  the  initial  stages.  For  the 
gastric  derangement  bismuth  will  generally  be  found  efficacious.  Consti- 
pation must  be  overcome  by  mild  cathartics.  For  the  vesical  weakness  or 
for  incontinence,  Faradization  of  the  bladder,  bromide  of  potash,  camphor, 
and  lupulin  are  advocated.  In  order  to  preserve  the  nerve  force  and  pre- 
vent exhaustion,  crutches  are  very  useful,  as  they  prevent  the  muscles  from 
being  constantly  overtaxed. 

m 
SPASMODIC   TABES   DOESALIS. 

Under  this  name  Charcot  has  described  what  Erb  calls  spastic  spinal 
paralysis.     It  has  also  been  called  tetanoid  pseudo-paraplegia. 

Morbid  Anatomy. — As  far  as  can  be  stated  there  is  symmetrical  sclerosis 
of  the  lateral  columns,  chiefly  of  their  posterior  portions.  The  induration 
shades  off  imperceptibly  into  the  normal  tissue  of  the  columns. 

This  degeneration  does  not  differ  microscopically  from  that  seen  in  scle- 
rosis of  the  cord  ;  it  often  extends  in  varying  degrees  the  entire  length  of 
the  cord.  Anterior  polio-myelitis  and  posterior  sclerosis  are  frequently 
associated. 

Etiology. — Spasmodic  spinal  paralysis  is  more  common  in  males  than  in 
females,  and  is  rare  except  between  the  ages  of  twenty  and  fifty  ;  it  rarely 

1  Lockhart  Clark  recommends  morphine,  cannabis  indicaand  belladonna  ivitli  silver  nitrate  when  the  lat 
ter  irritates  the  bowels  or  bladder. 


1024  DISEASES   OE   THE   KERVOUS   SYSTEM'. 

occurs  in  children.  Traumatism  and  exposure  to  wet  and  cold  are  named 
as  its  causes. 

Beyond  this  its  etiology  is  obscure. 

Symptoms. — Beginning  very  insidiously,  the  first  symptoms  noticed  are 
weakness  and  paresis  of  the  lower — rarely  of  the  upper— extremities. 
These  patients  drag  their  limbs.  This  is  followed  by  twitchings  and  stiff- 
ness of  the  muscles,  and  later  there  is  so  much  muscular  rigidity  that  loco- 
motion is  embarrassed  or  rendered  impossible.  Exaggeration  of  the  tendon- 
reflexes  is  an  early  and  important  symptom,  and  is  associated  with  marked 
ankle-clonus,  in  which  the  muscles  of  the  calf  or  the  whole  limb  are  put  in 
a  state  of  tremor  when  the  foot  is  flexed,  or  when  the  patient  puts  his  toes 
to  the  ground.  As  the  muscular  rigidity  increases  these  signs  diminish. 
Later,  general  muscular  tremors  or  shiverings  unaccompanied  by  tempera- 
ture changes  may  occur,  in  which  all  the  muscles  partake.  They  may  be 
excited  by  cold  or  follow  excitation  of  ankle-clonus  when  they  do  not  occur 
spontaneously.  If  the  patient  is  able  to  walk,  he  has  the  typical  spastic 
gait ;  the  adductors  keep  the  thighs  close  together,  the  toes  are  dragged, 
and  as  the  heel  is  brought  down  the  extensors  of  the  foot  contract  spas- 
modically and  may  throw  the  patient  forward,  lifting  him  on  his  toes. 
Sensibility  and  skin-reflexes  remain  normal. 

Electric  reaction  of  the  muscles  is  unchanged ;  while  that  of  the  nerves 
is  lowered  to  loth  currents.  In  the  advanced  stage  of  the  disease  the 
muscles  of  the  abdomen,  back,  or  upper  limbs  may  become  involved.  In 
the  latter  case  the  fingers  and  hand  are  strongly  flexed  ;  the  forearm  is  pro- 
nated  and  semiflexed,  and  the  arm  is  fixed  to  the  side.  After  a  varying 
period  paralysis  of  the  affected  parts  occurs,  and  the  contractures  become 
more  marked ;  the  legs  are  permanently  extended,  and  the  foot  assumes 
an  equino-varus  position.  Pain  rarely  accompanies  the  contractures,'  and 
the  nutrition  of  the  affected  muscles  is  not  impaired,^ 

DiiFerential  Diagnosis. — Spastic  paralysis  may  be  confounded  with  tabes 
dorsalis,  chronic  anterior  jjolio-myelitis,  multiple  sclerosis,  peripheral  paral- 
ysis, and  transverse  m.yelitis. 

In  locomotor  ataxia  the  ataxic  symptoms,  the  double  beat  and  stamp 
of  the  walk,  the  absence  of  tendon-reflexes,  the  general  pains,  the  bladder 
symptoms,  and  the  absence  of  paralysis  and  contractures  are  in  direct  con- 
trast to  the  symptoms  of  primary  lateral  sclerosis. 

In  chronic  anterior  polio-myelitis  atrophy  follows  the  paresis  and  the 
muscles  lose  electric  excitability.  Tendon-reflexes  are  absent.  In  spastic 
paralysis  rigidity  follows  paresis,  and  tendon-reflex  and  electric  excitability 
are  exaggerated. 

Multi2Jle  sclerosis,  when  it  is  located  in  the  lateral  column  at  the  onset, 
is  practically  spastic  tabes.  "When  the  sclerotic  process  attacks  other 
portions  of  the  cord,  or  when  cerebral  disturbances  occur,  it  assumes  its 
distinctive  characteristics. 

1  Erb  states  that  pain  in  the  back  and  limbs  attended  by  formication  and  other  paraesthesiae  not  un- 
commonly precedes  the  motor  wealiness  at  the  beginning  of  the  disease. — Virchmv''s  ArcMv.,  b.  70.    1877. 

^  Recently,  Stumpell  calls  attention  to  the  relaxation  of  the  muscles  which  occurs  in  spastic  paralysis 
when  the  legs  are  not  irritated  by  their  own  weight. 


AMYOTROPHIC    LATERAL   SCLEROSIS.  1025 

In  peripheral  paralysis  there  are  disturbances  of  sensation  and  nu- 
trition ;  the  disease  develops  unsymmetrically ,  and  reflex  excitability  and 
electro-muscular  contractility  are  rapidly  lost. 

In  tranverse  myelitis  trophic  disturbances,  vesical  derangements,  and 
alterations  in  sensation  are  early  and  marked  symptoms.  They  do  not  oc- 
cur in  spastic  paralysis. 

Prognosis. — In  uncomplicated  spastic  paralysis  the  prognosis  is  good. 
Some  claim  that  complete  recovery  is  possible,  and  in  most  instances  the 
symptoms  can  be  ameliorated.  The  disease  may  progress  slowly  for  years, 
and  then  remain  stationary  indefinitely ;  or  it  may  become  complicated  by 
bulbar  or  glosso-labio-laryngeal  paralysis,  and  prove  rapidly  fatal. 

Treatment. — In  addition  to  the  treatment  proposed  for  chronic  myelitis  the 
galvanic  current  is  most  useful.  Iodide  of  potash,  arsenic  and  cod-liver  oil 
in  small  doses,  with  careful  attention  to  rest  and  diet,  are  to  be  recommended. 
Shampooing,  rubbing  and  massage  afford  great  comfort,  and  calabar  beaq 
may  be  given  for  the  cramps.     Nerve  stretching  has  also  been  employed, 

AMYOTEOPHIC    LATERAL    SCLEROSIS. 
{Spastic  Paralysis.) 

Charcot  calls  this  disease  the  deuteropathic  form  of  progressive  muscular 
atrophy.  Pathologically  and  clinically  it  is  a  complex  of  progressive  mus- 
cular atrophy  and  spasmodic  spinal  paralysis. 

Morbid  Anatomy. — The  sclerotic  process  begins  in  the  cervical  region, 
and  although  at  first  it  is  limited  to  the  lateral  columns,  it  soon  attacks  the 
anterior  cornua  and  leads  to  destruction  and  atrophy  of  the  large  ganglion 
cells.  It  also  extends  downwards  into  the  dorsal  and  lumbar  lateral  columns, 
and  almost  invariably  upwards  so  as  to  involve  the  medulla,  when  the  signs 
of  bulbar  paralysis  are  induced  and  followed  by  a  fatal  issue.  This  process 
has  its  seat  in  the  same  portions  of  the  cord  as  the  secondary  descending 
degeneration  of  Tiirck,  and  new  bands  of  dense  connective-tissue  join  the 
degenerated  lateral  columns  with  those  portions  of  the  anterior  horns  that 
are  involved. '  In  the  floor  of  the  fourth  ventricle  the  cells  of  the  nucleus 
of  the  spinal-accessory,  facial,  and  hypoglossal  nerves  are  degenerated.  The 
anterior  roots  and  peripheral  nerves  are  atrophied.  Trophic  changes  in  the 
muscles  are  identical  with  those  of  progressive  muscular  atrophy.^ 

It  is  stated  that  interstitial  growth  of  neuroglia  is  sometimes  found  with- 
out marked  degeneration  or  atrophy  of  the  nerve  fibres,  but  that  the  whole 
system  of  fibres  and  ganglion  cells  which  unite  the  motor  centres  iji  the 
cortex  with  the  muscles  is  involved.^ 

Etiology.- — Nothing  more  can  be  said  regarding  its  etiology  than  lias  al- 
ready been  stated  concerning  the  origin  of  the  two  diseases  of  which  it  is; 
a  compound. 

»  Archiv.  de  Phys.  Nor.  et  Path.  1879. 

2  Rosenthal  states  that  their  inflammatory  character  is  more  marlced  in  amyotrophic  lateral  sclerosis^. 
and  that  hyperplasia  of  the  perimysium  is  more  pronounced. 

3  Flichsig  and  Pick  state  that  the  whole  system  of  nerve  fibres  and  ganglion  cells  which  unite  the  motot 
centres  in  the  centres  of  the  brain  with  the  muscles  are  affected  in  amyotrophic  lateral  sclerosis. 

65 


1026  DISEASES   OF   THE   IsTERVOUS    SYSTEM. 

Symptoms. — The  disease  begins  with  weakness,  paresis,  and  then  actual 
paralysis  in  tho  upper  extremities,  associated  with  muscular  atrophy,  which 
is  usually  diffuse  and  rapidly  progressive.  Fibrillary  spasms  and  twitch- 
ings  of  the  affected  muscles  are  well  marked  ;  but  electrical  contractility- 
is  preserved.  Sensibility  is  not  impaired,  but  the  muscles  become  rigid 
and  contracted  with  the  arms  flexed.'  In  a  few  months  the  lower  limbs  are 
involved  in  the  paralysis  and  rigidity,  with  exaggerated  tendon-reflexes  and 
contractures.  Subsequently  the  muscles  atrophy  and  show  the  reaction 
of  degeneration  and  fibrillary  spasm,  while  the  contractures  diminish. 
This  is  followed  by  the  symptoms  of  bulbar  paralysis. 

Differential  Diagnosis. — Amyotrophic  lateral  sclerosis  maybe  mistaken  for 
progressive  muscular  atrophy.  But  in  the  latter  disease  the  slow  course, 
absence  of  bulbar  paralysis,  and  partial  affection  of  certain  groups  of 
muscles,  are  in  marked  contrast  to  the  symptoms  of  the  former.  More- 
over, in  amyotrophic  lateral  sclerosis  the  atrophy  is  preceded  by  paralysis. 

Prognosis.— The  prognosis  is  decidedly  unfavorable ;  death  results  in 
from  one  to  three  years  from  bulbar  paralysis.  It  is  not,  however,  pre- 
ceded by  paralyzed  sphincters,  vesical  troubles,  bed-sores,  or  other  trophic 
lesions. 

Treatment. — Eesidence  in  the  open  air  at  a  high  altitude  and  strict  at- 
tention to  the  genera]  health  are  of  first  importance.  Beyond  this  the 
treatment  is  identical  with  that  of  other  forms  of  spinal  sclerosis. 

Mitchell  recommends  cod-liver  oil,  iron,  strychnia,  and  dry  cupping 
along  the  spine,  with  massage. 

PSEIJDO-HYPERTEOPHIC     PAEALYSIS. 

This  is  a  progressive  muscular  paralysis  occurring  chiefly  in  boys. 

Morbid  Anatomy. — The  German  pathologists  generally  regard  this  dis- 
-ease  as  a  chronic  myositis  with  hyperplasia  of  interstitial  connective-tissue. 
Gowers,  however,  in  a  recent  monograph,  describes  the  substance  with 
which  the  muscle  is  filled  and  its  fibres  replaced  as  a  new  growth.  Fat 
:accumulates  in  the  new  growth  to  such  an  extent  as  to  induce  atrophy,  and 
the  muscles  undergo  granular  and  fatty  metamorphosis. 

As  a  final  stage  Charcot  mentions  waxy  degeneration  of  the  muscular 
elements.  If  a  portion  of  the  affected  muscle  is  examined  it  will  be 
found  of  a  pale  red  or  yellow  color,  according  to  the  date  of  the  disease.^ 

Etiology. — Age  and  sex  are  the  most  constant  predisposing  causes,  over 
eighty-eight  per  cent,  of  the  recorded  cases  occurring  before  the  tenth 
year.  Hereditary  influence  appears  most  powerfully  on  the  mother's  side. 
The  neuropathic  tendency  is  more  marked  than  in  any  other  nervous  dis- 
ease. The  recognized  exciting  causes  are  cold,  falls,  and  convalescence 
from  acute  febrile  disorders. 

1  Erb  states  that  as  atrophy  of  the  muscles  progresses  they  may  undergo  simultaneous  lipomatous 
hypertrophy. 

2  Charcot,  Cohnheim  and  Eulenberg  found  no  changes  in  the  cord.  Others  have  found  spots  of  sclerosis 
and  atrophy  of  the  ganglion  cells  in  the  anterior  horns.  Lockhart  Clark  and  Gowers  have  discovered  ex- 
tensive disintegration  of  the  gray  matter  at  the  centre  of  each  lateral  half  of  the  cord  and  of  the  anterior 
commissui-e. 


PSEUDO-HYPERTROPHIC    PARALYSIS.  1027 

Symptoms, — M.  Duclienne  makes  three  stages  :  first,  a  stage  of  weakness 
without  increase  in  the  size  of  the  muscles ;  the  muscles  chiefly  affected  are 
those  of  the  legs,  especially  the  gastrocnemii,  lower  part  of  the  back,  and 
the  erectores  spinas.  Second,  a  stage  in  which  hypertrophy  appears  and 
weakness  extends  to  the  u])per  extremities.  During  this  stage  for  a  year 
or  more  the  child  may  evince  no  symptoms  beyond  a  progressive  weakness. 
He  is  easily  and  quickly  tired,  raises  himself  with  increasing  difficulty,  and 
when  erect  does  not  stand  firmly.  He  soon  begins  to  show  a  peculiarity  of 
gait  and  attitude.  He  walks  with  a  swaying,  unsteady  step,  and  as  he 
stands  the  shoulders  are  thrown  backward  and  the  spine  is  sharply  bent  in 
the  lumbar  region.  The  hyperplastic  and  degenerative  changes  in  this  stage 
produce  the  pseudo-hypertrophy  of  the  muscles,  which  become  firm  and 
hard  with  increased  loss  of  function.  When  the  child  is  j)laced  in  an 
erect  position  the  increase  in  size  becomes  very  marked.  In  the  supine 
position  the  soles  of  the  feet  are  approximated  and  the  joints  of  the  lower 
extremities  are  flexed.  Similar  hypertrophy  sometimes  affects  the  muscles 
of  the  upper  half  of  the  body ;  but  more  commonly  they  are  wasted,  and 
thus  the  protuberant  belly  and  the  thick,  firm  calf  and  thigh  afford  a  strik- 
ing contrast  to  the  emaciated  muscles  above  the  diaphragm.  The  children 
walk  only  with  the  greatest  difficulty,  or  possibly  they  cannot  stand  without 
support,  and  the  act  of  sitting  or  rising  becomes  difficult.  Sometimes  it  is 
impossible  for  them  to  maintain  even  a  sitting  posture.  The  antero-pos- 
terior  curvature  of  the  spine  and  the  displacement  of  the  shoulders  are  much 
exaggerated,  and  the  toes  often  undergo  a  claw-like  deformity. 

Gradually  some  muscles  become  soft  and  fatty  while  others  remain  firm 
and  hard,  and  the  child  passes  into  a  stage  of  complete  jaaralysis  of  the 
trunk  and  upper  extremities  in  which  all  the  muscles  that  were  hypertro- 
phied  atrophy,  and  the  patient  becomes  completely  helpless.  Formication 
is  not  uncommon  at  first,  but  neither  anaesthesia  nor  hyperesthesia  is  pres- 
ent at  any  time.  Electro-contractility  of  the  muscles  is  unimpaired  until 
the  advanced  stages  of  the  disease.  The  upper  extremities  seldom  suffer 
pseudo-hypertrophy,  but  may  exhibit  true  progressive  muscular  atrophy. 
The  deltoid  and  triceps  are  usually  the  only  muscles  enlarged.  In  nearly 
all  cases  the  disease  progresses  symmetrically.  The  skin  of  the  affected 
parts  is  sometimes  bluish,  dry,  and  thinned.  The  tongue  and  the  muscles 
of  the  face  may  become  enlarged,,  and  some  consider  the  cardiac  hyper- 
trophy that  is  often  present  as  of  similar  origin. 

In  a  number  of  cases  the  mental  faculties  have  been  impaired,  but  the 
general  health  is  usually  good,  and  the  sphincters  are  never  involved. 

Prognosis. — The  prognosis  is  unfavorable,  and  when  progressive  muscular 
atrophy  is  superadded  it  is  especially  so.  Cases  of- recovery  have  been  re- 
ported. Its  duration  varies  from  a  few  months  to  several  years.  Intercur- 
rent disease  is  generally  the  direct  cause  of  death. 

Treatment. — Duchenne's  treatment  is  regarded  as  the  most  efficient.  Lo- 
cal electricity,  shampooing,  and  massage,  if  employed  before  the  hyper- 
trophic changes  occur,  may  arrest  its  development. 


1028  DISEASES   OF   THE    NERVOUS   SYSTEM. 


ACUTE    ASCENDING    PARALYSIS. 

This  peculiar  disease  has  no  well  recognized  anatomical  lesions,  but  is 
regarded  by  most  observers  as  a  purely  functional  disease,' 

Etiology. — Acute  ascending  paralysis  is  a  disease  of  adult  life,  more  com- 
mon in  'men  than  in  women.  Exposure  to  cold,  emotional  influences, 
venereal  excesses,  syphilis,  acute  febrile  disease,  and  poisoning  from  corro- 
sive sublimate'  have  each  been  followed  by  it. 

Symptoms, —For  the  first  few  days  there  is  possibly  a  slight  fever,  accom- 
panied by  a  sense  of  weariness  and  numbness  and  darting  pains  in  the 
limbs,  chiefly  in  the  feet  and  in  the  tips  of  the  fingers.  This  is  followed  by 
paresis,  then  actual  paralysis  of  the  distal  portions  of  the  lower  extremities. 
The  paralysis  gradually  extends  upward,  until  in  a  few  days  paralysis  of 
the  lower  extremities  is  complete.  Soon  the  trunk  muscles  are  implica- 
ted ;  the  patient  can  neither  turn  nor  sit  up  in  bed.  The  upper  extrem- 
ities are  then  involved,  the  paralysis  extending  from  the  finger  tips  to  the 
shoulder  joint.  Sometimes  there  is  a  distinct  interval  between  the  paraly- 
sis of  the  trunk  and  the  upper  extremities.  In  about  seventy  per  cent,  of 
cases  the  muscles  of  the  neck  and  the  diaphragm  are  involved,  and  finally 
bulbar  paralysis  is  superadded. 

In  some  cases  the  disease  pursues  a  reverse  course,  palsy  of  the  extremities 
following  the  symptoms  of  bulbar  paralysis.  The  paralyzed  limbs  are  lax 
and  the  muscles  flaccid  ;  but  they  do  not  undergo  atrophy,  and  the  electri- 
cal reactions  of  nerves  and  muscles  continue  perfectly  normal.  Sensibility 
is  little  if  at  all  affected,  the  sphincters  are  not  involved,  cutaneous  nu- 
trition is  unimpaired,  and  there  are  few,  if  any,  vaso-motor  or  trophic  dis- 
turbances. Eeflex  action  diminishes  after  the  first  two  or  three  days.  There 
is  usually  constipation  and  difficult  defecation,  on  account  of  the  paralysis 
of  the  abdominal  muscles.  The  intellect  is  never  disturbed.  In  over  thirty 
per  cent,  of  the  cases,  when,  or  before,  the  arms  are  implicated,  the  disease 
is  arrested,  and  soon  recovery  of  power  begins  to  manifest  itself,  the  parts 
first  paralyzed  being  last  restored.  It  is  said  that  recovery  has  taken  place 
even  after  the  paralysis  has  reached  the  nerves  of  the  bulb.  As  a  rule  there 
are  no  pains  complained  of  in  the  paralyzed  parts. 

DifFerental  Diagnosis. — Acute  ascending  paralysis  may  be  confounded  with 
acute  myelitis,  acute  spinal  paralysis  of  adults,  and,  when  slowly  evolved, 
with  chronic  spinal  paralysis. 

Acute  ascending  paralysis  is  differentiated  from  acute  ascending  mye- 
litis by  the  slight  disturbances  of  sensation  which  attend  it,  by  the  preser- 
vation of  electrical  excitability,  and  by  the  absence  of  motor  irritation  and 
trophic  disturbances. 

Acute  ascending  paralysis  differs  from  acute  spinal  paralysis  of  adults 

1  Dejerine  claims  to  have  found  in  two  cases  an  alteration  in  certain  fibres  of  the  anterior  roots  (parenchy- 
matous neuritis;.  The  myeline  was  brolien  up  into  fragments.  Multiplication  of  the  nuclei  in  the  white 
substance  of  Schwann,  and  disappearance  of  the  axis-cylinders  were  noted.  The  majority  of  the  fibres 
were  unaltered.    The  same  lesions  were  found  in  the  intramuscular  nerves  of  the  affected  members. 

2  Ketly  in  the  Pester  Med.  Chir.  Fres.  Nos.  8-9.    1878. 


SPINAL   APOPLEXY. 


1029 


in  the  absence  of  atrophy  of  the  paralyzed  muscles  ;  the  electrical  reactions 
remain  normal,  and  it  is  more  rapidly  progressive.  The  medulla  is  not 
involved  in  acute  spinal  jjaralysis,  whereas  about  seventy  per  cent,  of  cases 
of  ascending  paralysis  end  in  bulbar  symptoms. 

Kapid  atroj^hy  of  the  muscles  and  the  reaction  of  degeneration  are 
prominent  symptoms  of  chronic  spinal  paralysis,  which  are  absent  in  acute 
ascending  paralysis.  In  the  latter  disease  there  is  persistence  of  reflex 
actions  and  a  far  greater  tendency  to  extend  to  the  medulla. 

Prognosis. — Acute  ascending  paralysis  is  generally  fatal.  It  may  last 
several  weeks  ;  but  its  average  duration  "is  from  ten  to  fifteen  days.  The 
more  rapid  its  progress,  and  the  earlier  the  medulla  is  involved,  the  more 
unfavorable  the  prognosis.  Improvement  may  take  place  even  in  the  most 
acute  cases.     Death  occurs  from  the  same  causes  as  in  bulbar  paralysis. 

Treatment. — All  that  can  be  done  in  this  disease  is  to  maintain  the 
nutrition.  Electrical  currents  may  be  ajDplied  to  the  affected  muscles. 
Sulphur  baths,  iron,  arsenic,  strychnine,  and  iodide  of  potash  are  recom- 
mended for  the  more  slowly  progressive  forms,  but  clinical  experience 
does  not  sustain  the  claim  of  beneficial  results  which  have  been  obtained 
by  their  use. 

SPinSTAL    APOPLEXY. 


Spinal  apoplexy  is  not  of  frequent  occurrence,  except  when  due  to  trau- 
matism or  to  some  pre-existing  disease  of  the  cord. 

Morbid  Anatomy. — A  meningeal  hemorrhage  may  extend  the  entire 
length  of  the  cord ;  primary 
hemorrhage,  however,  usually  j- 
occurs  into  the  gray  matter, 
and  if  slight,  may  only  involve 
one  side.  The  white  matter 
is  never  alone  involved,  but 
about  fifty  per  cent,  of  spinal 
hemorrhages  are  circumscribed. 
In  a  few  cases  punctate  capil- 
lary hemorrhages  are  found 
studding  the  gray  substance. 
A  clot  of  varying  size,  one- 
fourth  to  one  inch  in  diameter, 
is  found  in  the  central  portion 
of  the  cord  containing  debris  of 
nerve-tissue,  corpora  amylacea, 
fat'  granules,  and  pigment.  This 
blood  sac  commonly  lies  with 
its  long  axis  parallel  with  the 
cord.  The  centre  may  have  undergone  softening,  and  the  wall  is  formed 
of  ragged  nerve- tissue.  About  a  clot  in  the  white  substance,  the  tissue  is 
always  more  or  less  deeply  tinged  with  blood.  When  the  extravasation  in- 
volves the  periphery  of  the  cord  there  will  be  hypersemia  of  the  adjacent 


Fie.  211. 
Spinal  Apoplexy. 
Section  of  the  Cervical  Spinal  Cord,  shoiving  a  small  clot  in 
the  region  of  the  anterior  cornu  of  the  left  side. 

A.  Clot. 

B.  Meninges  adjacent  to  the  clot  shoioing  hypercEmia. 


1030  DISEASES  OE  THE   NERVOUS  SYSTEM. 

membranes.  Capillary  aneurisms  have  usually  been  found  in  the  spinal 
vessels  at  the  seat  of  the  apoplexy  ;  and  Liouville  has  found  ampullary  dila- 
tation of  the  large  vessels,  thickening  of  their  walls,  and  proliferation  of 
their  nuclei.  Charcot  states  that  there  is  swelling  of  the  nerve  cells  and 
axis  cylinders.  The  clot  may  undergo  retrogressive  changes  and  result  in 
softening,  abscess,  or  a  cicatrix.  Erb  describes  softening  of  the  gray  sub- 
stance as  a  not  infrequent  sequela  of  spinal  apoplexy.  White  softening 
accompanied  by  gelatinous  oedema  surrounds  the  blood  tumor  and  merges 
imperceptibly  into  healthy  cord  substance.  Ch.  Bastian  states  that  inflam- 
matory softening  may  start  from  the  clot  and  extend  up  or  down  the 
cord. ' 

Etiology. — Spinal  hemorrhage  is  most  commonly  the  result  of  trauma- 
tism, and  especially  of  severe  concussion."  It  may  result  from  rupture  of 
vessels  in  or  near  neoplasia,  in  foci  of  myelitic  or  other  softening,  or  in 
any  chronic  spinal  disease.  Small  hemorrhages  may  occur  with  scorbutus, 
purpura,  and  in  the  hemorrhagic  diathesis.  Atheromatous,  fibroid,  and 
fatty  degeneration  of  the  blood-vessels,  nuclear  proliferation,  and  minute 
aneurismal  dilatations  predispose  to  spinal  hemorrhage.  Age  and  sex  are 
also  predisposing  factors,  as  it  is  most  frequently  met  with  in  men  between 
the  ages  of  fifteen  and  forty.  Anything  that  induces  or  predisposes  to  ac- 
tive hypersemia  acts  as  a  predisposing  cause.  ^ 

Symptoms. — Sometimes  the  symptoms  of  myelitis,  spinal  irritation,  or 
active  spinal  hypersemia  precede  the  extravasation,  but  usually  it  com.es  on 
suddenly  and  causes  complete  paralysis  of  both  motion  and  sensation  be- 
low the  site  of  the  hemorrhage,  without  loss  of  consciousness.  It  is  at- 
tended by  severe  pain  in  the  back,  that  may  be  localized  or  extend  the 
entire  length  of  the  spine.  This  sometimes  disappears  when  the  paralysis 
becomes  complete.  Pressure  does  not  increase  it.  At  the  onset  spasmodic 
twitchings  may  occur  in  the  paralyzed  parts  ;  and  all  reflex  motion  is 
abolished — the  muscles  being  completely  relaxed.  Priapism  and  dyspnoea 
may  occur  when  the  clot  is  high  up.  When  hemorrhage  occurs  in  the 
dorsal  or  lower  cervical  region,  the  temperature  of  the  paralyzed  limb 
— which  at  first  is  sub-normal — rises  2°  to  3°  F.  higher  than  the  axillary 
as  a  result  of  vaso-motor  paralysis.  The  bladder  is  at  first  paralyzed,  but 
when  the  sphincters  are  also  involved  the  urine  passes  involuntarily.  Cys- 
titis is  soon  developed  and  pyelitis  rapidly  follows.  The  faeces  are  passed 
involuntarily  and  bed-sores  appear  early.  The  paralyzed  parts  begin  to 
undergo  atrophy,  and  while  so  doing  exhibit  the  electrical  reaction  of 
degeneration.  If  a  clot  occupies  one-half  the  gray  matter  at  any  point, 
Jiemi-paraplegia  is  developed  in  the  limb  of  the  same  side  as  the  lesion. 
Should  it  implicate  the  root  of  the  phrenic  nerve,  intense  dyspnoea  and  per- 
haps instantaneous  death  may  result. 

Differential  Diagnosis. — Apoplexy  of  the  cord  may  be  confounded  with 

'  Charcot  and  Hayem  regard  this  lesion  as  always  consecutive  to  myelitis. 

2  Sir  William  Gull  relates  a  ease  where  small  extravasations  were  found  on  the  anterior  and  posterior 
comua  as  well  as  in  the  posterior  columns  of  the  cord.    The  case  was  the  result  of  a  fall. 

'  Erb  claims  that  variola  hemorrhagica,  typhoid,  yellow,  and  malarial  fevers  are  causes  of  spinal  hemor- 
rhage. 


TUMOKS   OF   THE   SPINAL   CORD.  1031 

meningeal  apoplexy  and  tliromhotic  soflenlng.  In  meningeal  apoplexy  sen- 
sory paralysis  is  absent  or  but  sliglitly  marked  ;  after  the  initial  motor 
paralysis,  improvement  is  marked  and  speedy  ;  pain,  hypergestliesia,  and 
irritation  symptoms  are  prominent ;  and  bed-sores,  cystitis,  and  pyelitis 
do  not  occur.  All  these  are  in  distinct  contrast  with  the  symptoms  of 
spinal  or  intramedullary  apoplexy,  Vaso-motor  disturbances  are  absent 
in  meningeal,  but  present  in  spinal  hemorrhages. 

Thrombotic  softening  produces  incomplete  paraplegia,  without  loss  of 
sensation.  The  absence  of  sensory  and  motor  excitement  is  regarded  as 
diagnostic.  Hemorrhage  not  infrequently  occurs  in  a  spot  of  myelitic  soft- 
ening, but  in  such  cases  the  paraplegia /oZ/o2^s  irritation,  pain  on  pressure, 
fever,  vesical  symptoms,  and  the  girdle  sensation.  In  apoplexy  paraplegia 
is  i\\Q  first  symptom,  the  other  symptoms  coming  on  at  greater  or  less  in- 
tervals. 

Prognosis. — Charcot  states  that  a  true  spinal  apoplexy  is  always  fatal. 
The  prognosis  is  certainly  exceedingly  unfavorable  when  the  onset  is  severe 
or  when  the  thoracic  and  respiratory  muscles  are  implicated.  Death 
may  occur  in  six  hours.  Incomplete  recovery  is  possible,  with  paralysis 
and  atrophy  of  the  muscles  of  the  lower  extremities.  Septic  fever,  cystitis, 
and  pyelitis  are  its  complications  ;  and  death  may  occur  from  exhaustion 
and  marasmus.  The  chief  danger,  if  life  is  prolonged  a  few  weeks,  is  from 
myelitis  and  extensive  softening. 

Treatment. — Absolute  rest  in  the  prone  (not  supine)  position,  is  most  im- 
portant. Blood-letting,  purgatives,  or  revulsives  are  not  allowable.  Ice-bags 
should  be  applied  along  the  spine.  Bromides  and  oj)iates  may  be  employed 
to  insure  rest.  Attention  to  the  bladder  is  an  important  element  of  treat- 
ment. The  treatment  is  the  same  as  for  cerebral  apoplexy  with  transfer- 
ence of  local  measures  from  the  head  to  the  spine. 

TUMOES    OF    THE    SPINAL    CORD. 

As  tumors  in  the  spinal  canal  arise  from  the  same  causes  and  present  the 
same  anatomical  appearances  as  similar  growths  in  the  brain,  it  is  only 
necessary  to  consider  their  clinical  phenomena. 

Symptoms. — These  will  vary  greatly  in  their  nature  and  in  the  order  of 
their  development,  with  the  seat  of  the  tumor,  its  extension,  and  the 
amount  of  intercurrent  changes  in  the  adjacent  tissues. 

I.  Tumors  which  primarily  involve  the  substance  of  the  cord  are  more 
common  in  the  gray  matter,  and  are  attended  by  a  gradual  abolition  of 
function.  The  changes  are  due  more  to  pressure  than  inflammation,  so 
that  pain  is  a  less  common  and  prominent  accompaniment.  The  earlier 
symptoms  are  those  of  paresis.,  either  with  hemiplegia  or  paraplegia  of  the 
parts  below  the  tumor,  according  as  the  growth  involves  a  lateral  half  or 
the  entire  substance  of  the  cord.  When  the  lesion  is  lateral,  the  paralysis 
may  be  crossed  or  mixed  ;  motor  paralysis  of  one  side  may  be  attended 
by  anesthesia  of  the  other.  The  paralysis  is  rarely  complete  at  first,  but 
is  progressive,  though  liable  to  remarkable  remissions,  and  eventually  be- 


1032  DISEASES   OF   THE   NERVOUS   SYSTEM. 

comes  complete.  As  these  tumors  extend  and  involve  the  meninges  and  roots 
of  the  nerves  and  are  attended  by  inflammation,  peripheral  pains  and  mus- 
cular spasms  may  develop,  while  the  edematous  softening  or  ascending  and 
descending  degenerative  changes  may  cause  atrophy  and  wasting  of  the 
muscles.  Tumors  of  the  substance  of  the  cord  may  thus  resemble  muscu- 
lar atrophy,  tabes  dorsalis,  or  other  forms  of  sclerosis. 

II.  Meningeal  growths  and  tumors  developed  exterior  to  the  membranes 
pursue  a  less  latent  course.  They  involve  the  roots  of  the  nerves  early,  and 
are  productive  of  more  marked  inflammatory  changes.  Hence  the  early 
symptoms  are  those  of  both  sensory  and  motor  irritation.  There  are  burn- 
ing, lancinating,  and  crushing  pains,  which  are  irregular  and  liable  to 
severe  exacerbations,  which  may  be  attended  by  hyperaesthesia  and  cuta- 
neous eruptions.  There  are  muscular  twitchings  and  spasms  which,  as  the 
nerves  are  more  seriously  affected  or  the  cord  becomes  compressed,  pass  on 
to  paresis  or  complete  paralysis  with  muscular  ati'ophy  and  wasting.  The 
sensory  symptoms  at  the  same  time  give  place  to  numbness  and  anaes- 
thesia. 

Spinal  tumors  of  all  forms  produce  more  or  less  myelitis,  and  with  this 
the  reflex  excitability  is  greatly  increased  and  may  cause  contraction  and 
rigidity.'  Trophic  changes  are  late  symptoms.  In  all  forms  of  spinal 
growths  the  symptoms  are  liable  to  sudden  and  marked  changes  either 
favorable  or  unfavorable.  A  sudden  a3dema  or  hemorrhage  may  cause  ex- 
tensive paralysis,  which  may  be  permanent  or  slowly  recovered  from.  Or 
a  rapid  and  marked  improvement  may  be  speedily  followed  by  a  more  com- 
plete and  widespread  paralysis.  When  the  new  growth  involves  the  verte- 
brae and  results  in  destructive  changes,  as  frequently  occurs  with  cancer, 
the  early  symptoms  of  pain  and  hyperaesthesia  are  usually  severe  and  the 
paralysis  rapidly  becomes  complete. 

DiiFerential  Diagnosis. — Inflam^nation,  hemorrhage,  and  softening  of  the 
cord  are  excluded  by  their  abrupt  onset,  and  the  fact  that  their  symp- 
toms are  more  general  and  uniform  in  their  development  than  those  of  a 
tumor. 

The  nature  of  a  tumor  can  seldom  be  determined,  and  the  diagnosis  rests 
almost  entirely  upon  the  history  and  the  presence  of  some  adventitious 
growth  in  other  organs. 

Prognosis. — Complete  or  even  partial  recovery  is  not  to  be  expected.  The 
paralysis  and  muscular  atrophy  are  progressive.  No  estimate  of  their 
duration  can  be  made. 

Treatment. — Every  tumor  should  be  treated  as  syphilitic,  as  this  is  the 
only  kind  amenable  to  treatment.  When  the  vertebras  are  involved,  sup- 
porting appliances  are  indicated.  Beyond  this  the  treatment  is  purely 
symptomatic. 

•  Schiippel  claims  that  the  spine  is  always  curved  towards  the  side  upon  which  the  tumor  is  situated, 
and  that  the  combination  of  irritative  and  paralytic  symptoms  of  striMng  inconstancy  is  diagnostic  of 
tumor. 


SPIHA-BIFIDA.  1033 


SPIJSrA-BIFIDA. 


Spina-bifida  is  a  congenital  malformation  due  to  arrested  development 
of  some  portion  of  the  spinal  column.  It  is  usually  associated  with  dropsy 
of  the  spinal  cord,  or  hydrorachis.  Internal  hydrorachis  is  a  collection  of 
serum  in  the  central  canal,  causing  atrophy  or  destruction  of  the  spinal 
medulla.  External  hydrorachis  is  an  effusion  into  the  subarachnoid  space. 
If  the  spinal  canal  closes,  it  is  called  H.  incolumis  ;  if  not,  H.  deldscens. 

Morbid  Anatomy. — Usually  two  or  three  spinous  processes  and  laminai  are 
deficient,  the  rudimentary  portions  of  the  vertebral  arches  are  spread  out 
and  irregularly  expanded,  and  the  membranes  protrude  through  the  aper- 
ture as  a  hernial  sac.  The  tumor,  which  is  oval  or  spherical  and  at  birth 
about  one  inch  in  diameter,  occurs  almost  invariably  in  the  lumbar  or 
lumbo-sacral  region.  It  is  tense  and  fluctuant,  being  tilled  with  cerebro- 
spinal fluid.  Pressure  on  the  tumor  increases  the  tension,  and  may  produce 
symptoms  of  cerebral  pressure.  The  skin  over  the  tumor,  although  some- 
times normal,  is  usually  thin  and  transparent.  The  nerve-trunks  forming 
the  Cauda  equina  often  traverse  the  interior  of  the  sac.  The  skin  at  the 
apex  of  the  tumor  is  sometimes  destroyed  and  the  sac  exposed.  The  point 
is  excoriated  or  covered  with  pus  and  granulations,  and  the  ulceration  may 
go  on  to  perforation.     The  dura  mater  always  forms  one  layer  of  the  sac. 

Etiology. — Nothing  is  known  concerning  the  etiology  of  the  hydrorachis 
which  accompanies  spina-bifida. 

Symptoms. — The  symptoms  of  hydrorachis  are  obscure.  It  may  cause 
pressure  on  various  parts  of  the  cord  and  cause  paresis  or  absolute  paralysis 
and  wasting  of  the  muscles.  When  associated  with  spina-bifida,  the  tumor 
is  the  diagnostic  symptom.  If  the  effusion  is  in  the  central  canal  and  the 
cord  is  thus  implicated,  the  lower  limbs  are  usually  paralyzed  as  well  as  the 
bladder  and  the  lower  bowel.  Convulsions,  spinal  inflammation,  or  rupture 
of  the  sac  with  escape  of  its  contents,  usually  precede  death,  which  usually 
occurs  within  a  few  weeks  after  birth.  When  the  fluid  oozes  away  gradu- 
ally, relief  follows ;  spontaneous  and  complete  cure  may  then  occur,  the 
tumor  contracting  to  a  small  nodule,  and  the  aperture  in  the  canal  closing 
more  or  less  completely.  When  the  dropsy  is  external  to  the  cord  and  the 
skin  thick,  the  tumor  may  increase  in  size  without  causing  serious  disturb- 
ance, and  may  even  reach  the  size  of  a  child's  head,  and  life  be  prolonged 
twenty  or  thirty  years. 

Other  forms  of  arrested  development  often  accompany  spina-bifida. 

Prognosis. — It  is  very  rare  for  patients  with  spina-bifida  to  reach  puberty. 
The  majority  of  cases  terminate  fatally  a  few  days  or  weeks  after  birth. 
The  prognosis  is  favorable  when  the  base  of  the  tumor  is  narrow,  the  skin 
over  it  thick  and  normal,  and  when  it  is  situated  in  the  sacral  region. 

Treatment. — The  process  of  spontaneous  cure  has  been  successfully  imi- 
tated by  small  tappings,  frequently  repeated,  and  followed  by  light  com- 
pression. Only  a  small  portion  of  the  fluid  should  be  withdrawn  at  any 
operation,  and  the  puncture  should  always  be  made  at  the  side  of  the 


1034  DISEASES   OF  THE   NERVOUS   SYSTEM. 

tumor  so  as  to  avoid  injury  to  nerve-trunks.     Cases  have  been  successfully 
treated  by  the  injection  of  small  quantities  of  iodine. 

Other  opersitive  measures,  such  as  compression  of  the  neck  of  the  tumor 
by  means  of  a  clamp  or  ligature,  and  excision,  have  occasionally  been  em- 
ployed with  success  ;  but  no  such  attempt  should  be  made  except  when  the 
tumor  has  a  very  narrow  base,  and  is  situated  over  the  sacrum, 

FUN^OTIONAL  DISEASES  OE  THE  NEKVOUS  SYSTEM. 

I  shall  consider  under  this  head — 

I.  Epilepsy.  XI,  Paralysis  Agitans. 

II,  Hysteria.  XII.  Localized  Spasm  and  Paralysis. 

III.  Hystero-Epilepsy,  XIII,    Chronic  Lead  Poisoning. 

IV,  Catalepsy.  XIV.    Chronic  Mercurialism. 
V,  Neurasthenia.  XV,    Vertigo. 

VI.    Chorea.  XVI,   Neuralgia. 

VII.  Sunstrohe.  XVII,   Megrim. 

VIII.  Spinal  Irritation.  XVIII,   Eclampsia  and  Infantile  Coti' 

IX.   Tetanus.  vulsions. 

X,  Facial  Paralysis.  XIX,  Sea-sickness. 

EPILEPSY. 

Epilepsy  is  a  chronic  functional  disease  of  the  nervons  centres  marked  by 
sudden  signs  of  temporary  loss  of  consciousness  or  some  other  mental  dis- 
turbance, accompanied  by  tonic  or  clonic  convulsions,^ 

In  its, typical  and  fully  developed  form  the  disease  has  received  the  name 
epilepsia  gravior,  or  le  haul  mal,  and  when  mild  and  incomplete  is  called 
epilepsia  mitior,  le  petit  mal,  or  epileptic  vertigo. 

Morbid  Anatomy. — Diiferent  portions  of  the  nervous  system  have  been  re- 
garded as  the  seat  of  lesions  which  may  cause  epileptic  seizures.  Some  have 
located  these  lesions  in  the  convolutions  of  the  hemispheres,  the  ganglia 
at  the  base,  or  the  pons  and  medulla  oblongata.  Others  have  claimed  that 
all  the  nervous  centres  are  involved.  Death  has  occurred  in  some  cases  dur- 
ing an  epileptic  seizure  in  which  no  change  was  discovered  at  the  autopsy 
except  cerebral  hypergemia.  Many  pathologists  claim  that  the  vaso-motor 
centre  in  epileptics  is  so  easily  excited  that  slight  impressions  result  in  ar- 
terial spasm  producing  angemia  of  the  brain,  Brown-Sequard  states  that 
the  true  seat  of  epilepsy  is  in  nerve  cells  having  the  power  of  producing 
muscular  contractions,  and  that  these  cells  are  located  chiefly  at  the  base 
of  the  brain.  Experiments  on  animals  show  that  epileptiform  convulsions 
may  be  produced  by  irritation  of  the  skin  after  the  removal  of  the  brain 
and  cerebellum. 

The  pathology  of  epilepsy  is  still  obscure,  and  no  uniform,  constantly 

1  In  ionic  convulsions  the  muscles  involved  remain  in  continuous  contraction;  in  clonic  the  spasmodic 
movements  are  of  short  duration,  alternating  with  periods  of  relaxation. 


EPILEPSY.  1035 

recurring  histological  changes  have  as  yet  been  discovered.     Russell  Rey- 
nolds sums  up  its  pathology  as  follows  : 

I.  The  seat  of  primary  derangement  is  the  medulla  oblongata,  upper  por- 
tion of  the  spinal  cord,  and  vaso-motor  system  of  nerves. 

II.  This  derangement  consists  in  an  increased  and  perverted  readiness  of 
action  in  these  organs  ;'  the  result  of  such  action  being  the  induction  of 
spasm  in  the  contractile  fibres  of  the  vessels  supplying  the  brain,  and.  in 
those  of  the  muscles  of  the  face,  pharynx,  larynx,  respiratory  apparatus, 
and  limbs  generally.  By  contraction  of  the  vessels,  the  brain  is  deprived 
of  blood,  and.  consciousness  is  arrested  ;  the  face  is,  or  may  become,  pale  by 
being  deprived  of  blood. ;  from  contraction  of  the  muscles  mentioned  there 
is  arrest  of  respiration,  the  chest  walls  are  fixed,  and  the  other  phenomena 
of  the  first  stage  of  the  attack  are  brought  about. 

III.  The  arrest  of  breathing  leads  to  the  special  convulsions  of  asphyxia, 
which  are  in  direct  proportion  to  the  completeness  and  continuance  of  the 
asphyxia. 

IV.  The  subsequent  phenomena  are  those  of  poisoned  blood,  i.  c,  of 
blood  poisoned  by  the  retention  of  carbonic  acid,  and  altered  by  the  absence 
of  a  due  amount  of  oxygen. 

V.  The  primary  nutrition  change  which  is  the  starting-point  of  epilepsy 
may  exist  alone,  and  epilepsy  be  an  idiopathic  disease. 

■VI.   This  change  may  be  transmitted  hereditarily. 

VII.  It  may  be  induced  by  conditions  acting  upon  the  nervous  centres 
directly,  such  as  mechanical  injuries,  overwork,  insolation,  emotional  dis- 
turbances, excessive  venery,  etc. 

VIII.  The  nutrition  change  of  epilepsy  may  be  a  part  of  some  general 
metamorphosis,  such  as  that  present  in  the  several  cachexiae,  rheumatism, 
gout,  syphilis,  scrofula,  and  the  like  ;  and  further,  it  may  often  be  asso- 
ciated with  change  in  the  cortical  substance  of  the  cerebral  hemispheres. 

IX.  It  may  be  induced  by  unknown  circumstances  determining  a  rela- 
tive excess  of  change  in  the  medulla  during  the  general  excess  and  per-^ 
version  of  organic  change  occurring  at  the  periods  of  puberty,  pregnancy, 
and  dentition. 

X.  It  may  be  due  to  diseased  action  extending  from  contiguous  portions- 
of  the  nervous  centres  or  their  appendages. 

XI.  The  so-called  epileptic  aura  is  a  condition  of  sensation  or  of  motion 
dependent  upon  some  change  in  the  central  nervous  system,  and,  like  the 
paroxysm,  is  a  peripheral  expression  of  the  disease  ;  not  its  cause.  Paraly- 
sis of  the  cerebral  blood-vessels  and  resultant  hyperasmia  of  the  medulla  is 
a  constant  change  in  a  severe  epileptic  seizure. 

Etiology. — Thirty  per  cent,  of  epileptics  give  a  history  of  an  inherited 
tendency,  either  to  epilepsy  or  some  neurosis  ;  and  children  of  consanguin- 
eous marriages  are  often  epileptics.  It  most  frequently  develops  between 
the  ages  of  ten  and  twenty.     The  next  most  frequent  period  is  between  the 


'  Gowers  thinks  that  loss  of  inhibitory  function  of  the  nerve  cell  is  far  more  likely  than  increased  irri- 
tability. For  a  complete  and  exhaustive  summary  concerning  pathology  and  pathogenesis,  vide  Hugh- 
lings- Jackson,  Medical  Times  and  Gazette,  1879,  vol.  i.,  p.  233. 


1036  DISEASES    OF   THE    NEEVOUS   SYSTEM. 

second  and  the  tenth  year.  In  a  small  number  of  cases  it  exists  at,  oi  de- 
velops immediately  after  birth.'  Sex  appears  to  have  no  influence,  except 
in  hereditary  epilepsy,  which  develops  earlier  among  girls  than  boys.^  That 
puberty  is  an  exciting  cause  of  epilepsy  is  a  fact  accepted  by  the  majority 
of  authorities.  Irritation  of  some  portion  of  the  nervous  system  is  its  fre- 
quent exciting  cause,  such  as  injury  to  peripheral  nerves,  the  skull  or 
meninges,  and  diseases  of  the  brain  substance.^  Sunstroke  has  induced  it. 
Epileptiform  seizures  are  not  infrequent  symptoms  of  disease  of  different 
portions  of  the  nervous  system.  Among  its  nervous  causes,  excesses  in 
venery  and  onanism  have  undoubtedly  been  over-estimated. 

Among  its  psychical  causes  are  great  anxiety,  grief,  mental  overwork, 
and  long-continued  depressing  emotions.  Sympathetic  epilepsy  is  claimed 
to  arise  in  children  from  dentition  and  intestinal  irritation.  It  may  arise 
from  irritation  of  the  genitals,  anomalies  of  menstruation,  and  phimosis. 
Blood  changes  are  also  enumerated  as  among  its  causes.* 

Symptoms. — The  phenomena  of  epileptic  seizures  differ  so  widely  that  it 
is  impossible  to  give  a  description  which  will  answer  for  all  cases.  Epilep- 
sia gravior  may  or  may  not  be  preceded  by  premonitory  symptoms.  If 
present,  these  warnings  may  precede  the  seizure  for  a  day  or  only  for  two 
or  three  minutes.  The  epileptic  aura  of  Galen,  the  sense  of  a  mist  or  va- 
por rising  from  the  feet,  occurs  only  in  rare  instances.  Under  the  head  of 
prodromata  are  included  changes  indisposition,  moroseness and  irritability, 
cold  feet,  spasm  of  certain  muscles,  epistaxis,  headache,  vertigo,  a  marked 
increase  or  decrease  in  the  sexual  appetite,  optical  illusions,  hallucinations, 
involuntary  discharge  of  urine  and  faeces,  great  somnolence  or  insomnia, 
darkening  of  the  skin,  changes  in  the  appetite,  cardiac  palpitation,  cardi- 
algia,  vomiting,  abundant  flow  of  tears,  and  excessive  secretion  of  saliva. 
Sometimes  the  attack  is  preceded  by  a  definite  sensation  referred  to  the 
head,  stomach,  or  limbs.  Drawing  the  head  toward  one  shoulder  is  some- 
times a  warning  of  an  epileptic  seizure.  In  the  majority  of  cases  prodro- 
mata are  absent,  and  the  onset  of  the  fit  in  a  typical  attack  is  sudden  and 
attended  by  complete  loss  of  consciousness.  Uttering  a  loud,  sharp  cry, 
the  epileptic  falls  heavily,  or  sinks  to  the  ground.  The  face  is  extremely 
pale  immediately  before  and  at  the  time  of  the  seizure,  and  there  may  be 
tonic  spasm  of  the  muscles  of  the  eye  and  face.  The  pupil  is  invariably 
dilated  at  the  onset.  Tonic  spasm  of  all  the  muscles  immediately  occurs  ; 
the  eyes  are  fixed  and  staring,  and  the  muscles  of  the  face,  trunk,  and  ex- 
tremities are  rigid.  Opisthotonos  or  emprosthotonos  may  occur,  or  the 
body  may  be  bent  sidewise.  The  face  soon  becomes  dark,  the  veins  tur- 
gid, and  though  the  carotid  pulsates  strongly  the  radial  pulse  is  weak. 
Respiration  is  impeded  and  asphyxia  rapidly  develops,  until  after  a  few 
seconds — rarely  over  a  minute — clonic  convulsions  succeed  the  tonic  spasms, 

1  Reynolds  and  Echeverria  state  that  hereditary  epilepsy  does  not  develop  later  than  the  twentieth 
year. 

2  Brown-Sequard  states  that  after  the  twenty-fifth  year  women  are  attacked  oftener  than  men. 

3  Wostphal  {Berlin.  Kiin.  Wochen.)  has  shown  that  in  guinea-pigs  blows  on  the  head  may  immediately 
give  rise  to  epileptiform  attacks  ;  and  that  on  pinching  the  skin  of  the  epileptogenic  zone  several  weeks 
after,  convulsions  will  occur. 

■*  Gowers  states  that  rickets  causes  it,  through  defective  nutrition  of  the  nervous  system. 


EPILEPSY.  1037 

which,  though  general,  are  usually  best  marked  upon  one  side.  Sensation 
is  usually  wholly  lost,  and  onJy  in  rare  cases  can  reflex  action  be  excited. 
The  unconsciousness  still  continues.  The  muscles  contracting  and  relaxing 
in  quick  succession  induce  the  most  violent  contortions.  The  tongue  is 
thrust  between  the  teeth,  which,  closing  ujion  it,  cause  deep  indentations 
or  lacerations  of  its  edges.  The  teeth  are  sometimes  In-oken  ;  bones  may  be 
fractured  or  dislocated,  and  muscles  torn- from  their  attachments.  The 
patient  froths  at  the  mouth,  and,  from  the  injuries  to  the  tongue,  the  sal- 
iva is  often  bloody.  The  body  is  bathed  in  a  profuse  (sometimes  very 
fetid)  sweat,  and  frequently  the  contents  of  the  bladder,  bowels  and  vesic- 
ulaB  seminales  are  forcibly  ejected.  All  secretions  are  abnormally  increased. 
The  breathing  is  forcible,  irregular,  and  rapid,  and  the  auxiliary  muscles 
are  called  into  play ;  the  face  is  turgid  and  distorted,  the  eyes  protrude, 
the  pupils  are  alternately  dilated  and  contracted,  inspiration  is  accompanied 
by  loud  gurgling  noises,  the  pulse  becomes  full  and  labored,  and  when  the 
cyanosis  reaches  its  maximum  the  paroxysm,  which  seldom  lasts  longer 
than  one  or  two  minutes,  begins  to  abate. 

The  fit  may  terminate  suddenly  or  gradually.  If  it  subsides  gradually 
the  spasms  become  less  violent  and  frequent,  the  respiration  quieter  and  more 
regular,  and  the  jDatient  passes  into  a  comatose  state.  Consciousness  grad- 
ually returns,  and  the  patient  appears  as  if  waked  out  of  a  deep  sleep.  He 
recovers  rapidly  or  remains  confused,  delirious,  or  maniacal  for  hours.  A 
day  may  elapse  before  complete  recovery  is  reached.  The  patient  has  no 
recollection  of  the  attack.  The  degree  and  duration  of  stupor  after  an  at- 
tack have  no  relation  to  the  duration  of  the  convulsive  period.  A_  slight 
seizure  may  be  followed  by  great  mental  disturbance,  and  vice  versa. 
Marked  dicrotism  of  the  pulse  often  occurs  as  the  patient  is  recovering  c-on- 
sciousness  ;  and  for  twenty-four  hours  the  ophthalmoscope  shows  hyperse- 
mia  of  the  fundus  oculi.  The  urine  after  the'  attack  is  increased  in  quan- 
tity and  contains  an  excess  of  urea  and  phosphates. 

Brown-S6quard  gives  the  accompanying  table  of  the  causes  and  effects  of 
an  epileptic  attack: 

Cause.  Effect. 

T.  Excitation  of  certain  parts  of        I.  Contraction  of  blood-vessels  of 

the  excito-motor  organs  of  the  nerv-  the  brain  and  face  ;  tonic  spasm  of 

ous  centre.  the  muscles  of  the  eye  and  face. 

II.  Contraction  of  the  facial  blood-        II.  Facial  paleness, 
vessels. 

III.  Contraction  of  the  blood-ves-  III.  Loss  of  consciousness,  con- 
sels  of  the  cerebral  lobes.  gestion  of  the  base  of  the  brain  and 

the  spinal  cord. 

IV.  Extension  of  the  excitation  IV.  Tonic  contraction  of  the 
in  the  excito-motory  organs  of  the  laryngeal,  cervical  and  some  respira- 
nervous  centre.  tory  muscles  (laryngismus  and  trach- 

elismus). 


1038 


DISEASES   OF  THE   iSERVOUS   SYSTEM. 


Cause. 

Y.  Tonic  contraction  of  some  re- 
spiratory and  vocal  muscles. 

VI.  Further  extension  of  the  ex- 
citation in  the  excito-motory  organs. 

VII.  Loss  of  consciousness  alone, 
or  with  tonic  spasm  in  trunk  and 
limbs. 

VIII.  Laryngismus,  trachelismus 
and  rigid  spasm  of  some  respiratory 
muscles. 

IX.  InsuflBcient  breathing,  rapid 
consumption  of  oxygen,  and  deten- 
tion of  venous  blood  in  the  encepha- 
lon. 

X.  Asphyxia  and  perhaps  pressure 
by  accumulated  venous  blood  in  the 
base  of  the  brain. 

XI.  Exhaustion  of  the  nervous 
power  generally,  and  of  the  reflex 
excitability,  especially  return  of  reg- 
ular respiratory  movements. 


Effect. 

V.  Epileptic  cry. 

VI.  Tonic  contraction  reaching 
most  muscles  of  trunk  and  limbs. 

VII.  Fall  or  precipitation,  forward 
or  backward,  to  the  ground. 

VIII.  Insufficient  breathing ;  ob- 
stacle to  entrance  of  blood  into  the 
chest  and  to  its  issue  from  the  cra- 
nio-spinal  cavity. 

IX.  Increasing  asphyxia. 


X.  Clonic  convulsions  everywhere: 
contractions  of  the  bowels,  the  blad- 
der, the  womb,  increase  of  secretions, 
efforts  to  inspire. 

XI.  Cessation  of  the  fit,  coma,  or 
fatigue,  headache  and  sleep. 


Le  petit  mal,  or  epilepsia  mitior,  is  a  momentary  loss  of  consciousness;  the 
patient  while  about  his  usual  avocations  suddenly  stops,  or  drops  whatever 
he  may  hold,  has  a  fixed  gaze  for  a  second  or  two,  and  upon  coming  out  of 
such  a  faint  or  blank  proceeds  as  if  nothing  had  happened.  Sometimes 
these  blanks  may  be  accompanied  by  vertigo,  and  then  the  patient  will 
stagger  slightly.  In  rare  cases  he  proceeds  mechanically  with  what- 
ever is  occupying  him  during  the  paroxysm.  He  often  pales  for  a 
few  minutes  and  then  grows  red  in  the  face.  The  pupils  are  somewhat 
dilated.  The  mind  may  be  distinctly  confused  for  a  long  period  after  such 
an  attack.  Sometimes  momentary  spasmodic  contractions  occur  in  the 
muscles  of  the  face,  tongue,  throat,  eyes  and  neck.  The  head  is  turned 
slightly  to  one  side  and  the  face  is  pale.  Clonic  spasms  never  occur. 
There  may  be  slight  cyanosis  when  the  diaphragm  and  respiratory  muscles 
are  involved.  Sometimes  certain  fingers,  or  part  of  one  extremity,  suffer 
transient  spasm. 

The  variations  from  the  typical  phenomena  of  an  epileptic  seizure  are  so 
numerous  that  it  is  impossible  to  give  them  in  detail ;  I  shall  only  refer  to 
those  which  are  of  common  occurrence. 

Sudden  tonic  spasm  of  the  facial  and  thoracic  muscles  may  be  followed 
by  a  clonic  convulsion  without  any  loss  of  consciousness.  An  attack  may 
be  marked  by  such  motor  activity  that  the  patient  runs  or  walks  rapidly 


EPILEPSY.  1039 

during  a  period  of  complete  unconsciousness.  Sometimes  maniacal  excite- 
ment talies  the  })]ace  of  the  fit.'  In  this  delirium  lu  epileptic  may  be 
haroiless  and  wanders  around  in  a  dazed  condition  ;  or  be  exceedingly- 
dangerous  to  those  about  him.  Kleptomania  and  dipsomania  are  said  to 
be  exhibitions  of  epileptic  delirium.  Brown-Sequard  describes  nocturnal 
attacks  of  epilepsy  that  not  infrequently  occur  without  the  knowledge  of 
the  person  so  affected.  In  such  cases  the  individual  on  wakmg  is  tired 
and  exhausted;  he  has  pains  in  the  limbs,  back  and  head,  his  mind  is  con- 
fused and  his  memory  enfeebled  ;  he  is  disinclined  to  exert  himself,  and 
remains  during  the  day  in  a  confused  state.  His  tongue  shows  the  indents 
of  the  teeth,  and  the  pillow  may  be  blood-stained.  More  rarely  it  is  found 
that  an  involuntary  discharge  of  urine  has  occurred.  Such  attacks,  al- 
though frequent  and  violent,  may  remain  altogether  unknown  and  unsus- 
pected by  the  patient  or  his  friends. 

Between  the  paroxysms  the  condition  of  epileptics  varies  greatly.  In 
the  majority  there  is  no  impairment  of  mental  or  physical  condition  ;  not 
infrequently,  however,  there  is  depression  of  nervous  vitality  and  mental 
activity.  Of  all  the  abnormalities  met  with,  sub-normal  temperature  is  the 
most  common.'^  Of  the  mental  faculties,  memory  is  most  often  impaired. 
Women  show  mental  disturbances  more  frequently  than  men.  The  earlier 
epilepsy  commences  the  less  liable  are  mental  changes  to  occur  ;  and  the 
mental  deterioration  is  in  inverse  ratio  to  that  of  muscular  disturbance. 
The  most  remarkable  mental  phenomena  are  those  which  constitute  the 
so-called  epileptic  mania.  Epileptics  are  frequently  gloomy,  capricious 
and  irritable,  all  the  finer  psychical  functions  are  dull,  acquisition  of  new 
ideas  is  difficult,  and  hypochondria,  melancholia  and  imbecility  may  occur 
as  late  exhibitions  of  the  disease.  Motor  disturbances,  such  as  tremors 
and  clonic  or  tonic  spasms,  ai'e  not  infrequent  between  the  paroxysms. 
Epilepsia  major  is  more  common  than  epilepsia  mitior,  and  hereditary  ten- 
dencies seem  to  predispose  more  to  the  former  than  to  the  latter. 

As  regards  frequency  of  attack  there  is  the  widest  range  :  the  first  fit  may 
also  be  the  last ;  they  may  occur  once  a  year,  or  two  or  three  times  in  the 
twenty-four  hours.  In  "women  it  sometimes  seems  to  be  connected  with  the 
menstrual  epoch.  Eighty  per  cent,  of  all  epileptics  are  attacked  oftener 
than  once  a  month  ;  sometimes  paroxysms  occur  on  days  that  are  multi- 
ples of  seven.  Often  three  or  four  fits  occur  in  a  day,  and  then  ensues  a 
period  of  immunity.  When  the  seizures  follow  one  another  so  closely  as 
to  leave  no  rest,^  we  have  the  status  epilepticus,  in  which  the  temperature 
may  rise  to  108°  F.,  or  higher  as  death  approaches.  If  the  patient  re- 
covers, bed-sores  are  liable  to  be  formed.  Pneumonia  and  pulmonary 
oidema  are  apt  to  occur  in  this  condition.  Seizures  of  petit  mal  are  usually 
verj  xVtr^fUtJkt.     All  the  different  forms  may  occur  in  the  same  individual. 

Differential   Diagnosis. — An  epileptic  seizure  may  be  confounded   with 

1  Delirium  epilepticum. 

2  Brown-Sequard,  in  Quairi's  Dictionary,  states  that  the  health  is  very  poor,  an. opinion  antagonistic  to 
all  other  anthorities. 

3  In  Delasianre's  case  there  were  twenty-five  hundred  attacks  in  one  month  in  a.boy  of  fifteen. — Traite 
de  V Ejnlepsie,  Paris,  1854. 


1040  DISEASES   OF   THE   NERVOUS   SYSTEM. 

cerebral  apoplexy  and  hysteria.  It  is  often  difficult  to  distinguish  le  petit 
mal  from  an  attack  of  syncope. 

Convulsions  from  urmmia,  opium  poisoning,  or  alcohoUsmus  are  at- 
tended by  coma  as  the  chief  event,  and  are,  each  of  them,  accompanied 
by  such  peculiar  signs,  or  urinary  conditions,  and  give  such  a  definite 
previous  history,  that  they  will  not  long  be  mistaken  for  an  epileptic 
seizure. 

In  the  convulsions  of  children  caused  by  dentition,  falls,  and  gastric 
disturbances  there  is  not  complete  loss  of  consciousness  ;  the  fit  is  of 
shorter  duration  than  an  epileptic  paroxysm,  is  longer  in  coming  on,  and 
IS  not  followed  by  stupor.  The  discovery  of  a  cause  of  the  seizure  is  an 
argument  against  epilepsy. 

Convulsions  from  organic  brain-disease,  tumors,  chronic  softening,  men- 
ingitis, and  sclerotic  processes  are  distinguished  by  the  attendant  inter- 
paroxysmal  symptoms,  viz.  :  pain,  mental  aberration  of  various  kinds, 
paresis  or  paralysis,  and  disorders  of  special  senses.  In  other  words,  a  con- 
vulsion is  a  part  only,  and  not  the  chief  part,  of  the  symptoms  ;  whereas  a 
paroxysm  is  the  prime  event  in  epilepsy.  Moreover,  the  previous  history, 
the  slowness  of  invasion,  and  the  absence  of  subsequent  stupor  in  organic 
brain  disease  will  confirm  the  diagnosis. 

Hysterical  convulsions  are  always  preceded  by  hysterical  symptoms  ;  voli- 
tional power  is  diminished,  the  fits  come  on  gradually,  the  pupils  are  not 
dilated,  there  is  no  frothing  at  the  mouth,  loss  of  consciousness  is  not  com- 
plete, tonic  and  clonic  spasms  alternate,  stupor  does  not  follow,  and  the 
subsequent  hysterical  mania  has  its  own  peculiarities.  The  attack  is  always 
followed  by  a  profuse  flow  of  pale,  limpid  urine. 

Syncope  differs  from  le  petit  mal  in  that  the  loss  of  consciousness  is  not 
sudden,  is  always  preceded  by  a  weak,  faint,  sickening  sensation,  recovery 
is  slow,  and  the  patient  recollects  the  details  of  the  syncope.  Loss  of  con- 
sciousness is  usually  longer  in  syncope   than  in  epilepsia  mitior. 

Malingerers  overact  their  part,  the  conjunctivae  retain  their  sensibility, 
and  the  size  of  the  pupils  and  the  color  of  the  face  are  both  normal. 

Prognosis. — Epilepsy  rarely  directly  causes  death.  But  its  long  duration 
and  the  suddenness  of  its  onset  make  it  a  dreaded  disease.  About  two  to 
five  per  cent,  undergo  spontaneous  cure.'  The  curability  of  the  disease 
diminishes  with  its  duration.  Inherited  epilepsy  is  rarely  recovered  from. 
Epilepsy  beginning  before  the  twentieth  and  after  the  fiftieth  year  fur- 
nishes the  best  prognosis.  Reynolds  states  that  the  more  obscure  the 
origin  the  worse  the  outlook.  Alcoholismus  always  renders  the  prognosis 
worse. 

Treatment. ^The  two  things  to  be  accomplished  in  the  treatment  of 
epilepsy  are,  if  possible,  to  remove  the  cause  or  render  it  inoperative ;  and 
to  diminish  the  number,  length  and  severity  of  the  paroxysms. 

When  aurcB  exist  it  may  be  possible  to  abort  the  fit  by  tying  a  hand- 
kerchief around  a  limb,  pinching  or  rubbing  the  surface,  irritating  it  by 
means  of  cold  or  galvanism,  and  pricking  it  with  needles.    When  muscular 

i  Nothnagel. 


EPILEPSY.  1041 

contraction  precedes  a  Qt,  forciblt/ axcitmg  the  contracting  muscles  or  a 
blow  on  them  will  sometimes  prevent  the  convulsions.  When  disturbances 
of  respiration  precede  a  paroxysm,  inhalation  of  ether,  chloroform,  or  amyl 
nitrite  may  abort  it.  An  emetic,  purge,  a  hypodermic  of  morphia  and. 
atropia,  ice  to  the  nape  of  the  neck,  hot  water  to  the  extremities,  valerian, 
belladonna,  a  large  dose  of  chloral  hydrate,  breathing  very  fast,  running, 
reading  very  rapidly  and  loudly  have  all  been  found  in  some  instances  to 
abort  epileptic  paroxysms.  Reynolds  advocates  the  administration  of  dif- 
fusible stimulants.  When  an  epileptic  fit  is  once  established  there  is  little 
to  be  done  but  to  prevent  the  patient  from  injuring  himself.  The  chest 
and  neck  should  be  freed  from  close-fitting  garments,  and  if  possible  a 
piece  of  rubber  or  cloth  should  be  inserted  between  the  teeth. 

The  measures  employed  for  the  cure  of  epilepsy  are  innumerable.  Tre- 
phining over  cranial  depressions,  operations  for  phimosis,  excisions  of 
cicatrices,  removal  of  neuromata,  opening  of  abscesses,  ligating  the  caro- 
tids, application  of  caustics  to  the  throat,  and  tracheotomy  have  all  been 
undertaken  for  its  cure.  Since  epilepsy  is  a  neurosis,  different  drugs  must 
not  only  be  employed  with  different  individuals,  but  the  doses  must  be 
varied  in  different  cases.  The  bromides  have  the  most  extensive  reputa- 
tion, and  at  the  present  time  are  more  used  than  any  other  remedy.  They 
should  be  given  in  large  doses  and  continuously  for  a  long  period,  and  only 
discontinued  temporarily  when  the  symptoms  of  bromism  appear.  Sixty 
grains  of  bromide  of  potassium  a  day  in  divided  doses  is  the  usual  amount 
to  commence  with;  it  may  be  gradually  increased  until  one  hundred  grains 
a  day  is  administered.  It  is  best  to  commence  with  the  bromide  of  potash, 
the  bromide  of  ammonium,  iodide  and  bicarbonate  of  potash  in  a  strong, 
bitter  infusion — I  prefer  hops.  With  the  bromides  the  oxide  of  zinc, 
strychnine,  arsenic  or  atropia  may  be  given.'  Oxide  of  zinc  (one  and 
one-half  grains  a  day  at  first,  increasing  to  five  grains  per  diem),  especially 
with  valerian  root,  or  belladonna,  or  hyoscyamus,  is  regarded  as  next  in 
efficacy  to  the  bromides.  Atropine  and  ammoniated  sulphate  of  copper 
are  regarded  by  Brown-Sequard  as  forming  a  most  powerful  comjDOund  in 
idiopathic  epilepsy.  The  same  authority  ranks  next  in  order  the  cotyledon 
umMlicus,  silver  nitrate  and  bromide  of  zinc.  Whenever  there  is  a  weak 
pulse,  the  sesquicarbonate  of  ammonia  must  be  substituted  for  the  bromide 
of  the  same  salt  in  the  combination  treatment." 

In  mild  epilepsy,  or  le  petit  mal,  large  doses  of  bromide  of  ammonium 
should  be  administered  until  a  condition  of  bromism  is  reached.  Cod-liver 
oil  is  especially  useful  in  this  form  of  epilepsy.  Iron  is  only  to  be  used — and 
then  as  the  citrate — in  the  anaemic  or  cholorotic.  Manganese  is  often  ser- 
viceable here.  External  applications  such  as  setons,  issues,  inunctions, 
croton  oil,  blisters,  or  the  actual  cautery  to  the  nuchal  region,  have  been 
extensively  used  without  satisfactory  results.     Galvanization  of  the  sympa- 

1  Echeverria  recommends  conium,  and  Clonston  the  Indian  hemp. 

2  Belladonna  Is  recommended  by  Trousseau  is  one-fifth  grain  of  the  extract  daily  for  the  first  month 
to  be  gradually  increased  until  from  one  to  two  grains  are  taken  daily. 


1042  DISEASES   OF   THE   NERVOUS   SYSTEM. 

thetic  is  strongly  recommended  by  some.'     Epileptics  should  lead  a  life 
free  from  mental  excitement  or  physical  excess.  '^ 

HYSTEEIA. 

Hysteria  is  a  functional  disorder  of  the  nervous  centres,  affecting  pri- 
marily the  psychical  faculties,  especially  the  will,  reason,  imagination  and 
the  emotions  ;  and  secondarily  both  the  motor  and  sensory  tracts,  in  which 
the  protean  manifestations  at  different  times  indicate  abolition,  exaltation, 
and  perversion  of  functional  activity  of  the  nervous  centres. 

Morbid  Anatomy. — Hysteria  has  no  pathological  changes  or  morbid 
anatomy.  The  special  functional  disturbance  is  generally  considered  to  be 
an  exalted  irritability  of  sensory  centres  and  peripheral  expansion,  which 
results  in  an  acquired,  or  is  associated  with  a  congenital,  neurasthenia, 
most  marked  in  the  higher  centres,  but  extending  to  those  controliing  auto- 
matic movements,  and  characterized  by  partial  or  complete  suspension  of 
inhibitory  influence.^  It  is  quite  possible  that  in  many  cases  the  centric 
neurasthenia  may  be  the  primary  condition  and  the  cause  of  the  exalted 
irritability.* 

Etiology. — Hysteria  affects  females  principally ;  usually  making  its  ap- 
pearance between  the  ages  of  puberty  and  thirty  years.  Over  one-fourth 
of  the  cases  occur  between  the  ages  of  twenty  and  thirty  ;  a  little  less  than 
one-fourth  between  the  ages  of  fifteen  and  twenty  ;  and  about  one-sixth  be- 
tween the  ages  of  ten  and  fifteen.  It  is  rarely  developed  after  the  meno- 
pause, although  it  frequently  occurs  jast  at  the  climacteric.  It  is  most 
liable  to  occur  in  women  of  a  neuropathic  tendency  and  in  members  of 
families  in  which  epilepsy,  chorea,  catalepsy,  and  insanity  have  occurred. 
Anything  which  affects  the  emotions  powerfully,  such  as  fright,  anger, 
jealousy,  grief,  and  disappointment,  predisposes  to  its  development,  and 
secret  nursing  of  imagined  wrong  or  anxiety  is  especially  liable  to  induce  it. 
Sexual  abuse,  masturbation,  onanism  and  premature  cessation  of  ovulation 
;are  at  times  exciting  causes  of  hysteria.  Its  relation  to  uterine  and  ovarian 
disease  is  direct  and  well  established,^  but  is  by  no  means  constant,  as  many 
patients  with  severe  ovarian  disturbances  remain  entirely  exempt  from  hys- 
terical phenomena.  Hysteria  is  undoubtedly  oftener  met  with  in  the  single 
than  in  the  married,  and  is  intensified  by  the  menstrual  epoch.  Occupa- 
tion and  position  in  life  have  much  to  do  with  its  production.  Women 
who  lead  a  life  of  continual  excitement  are  more  prone  to  hysteria  than  any 

1  Nothnagel  recommends  methodical  hydrotherapeia  for  three  or  four  months,  especially  in  cases  that 
are  not  inveterate. 

2  Reynolds  advocates  quinine,  but  Brown-Sequard  considers  it'  highly  injurious,  stating  that  malarial 
disease  in  epileptics  is  better  treated  by  arsenic.  Recently  Lepine  has  had  success  from  bleeding  and 
depletion.  Kunze  reports  radical  cures  from  subcutaneous  injection  of  curare  ;  Vallender  from  apomor- 
phia.  Govcers,  in  Gulstonian  Lectures.,  says  borax  deserves  a  trial  when  bromide  fails.  Very  recently 
picrotoxine  and  cocculus  indicus  have  been  tried  and  found  to  produce — especially  the  former — most  bene- 
ficial effects. 

3  Jolly  and  Buzzard. 

*  Rosenthal  states  that  the  vaso-motor  system  is  also  involved,  and  that  spasm  of  the  cerebral  arteriee 
and  consequent  anaemia  are  often  present  in  hysterical  paroxysms. 

fi  Charcot  claims  that  hysterical  fits  can  be  produced  by  firm  pressure  over  the  ovaries. 


HYSTERIA.  1043 

other  class.  Among  savage  nations  and  hard-working  women  it  is  unknown 
or  rare.  It  is  said  that  since  the  blacks  have  been  freed  and  their  education 
and  condition  bettered,  hysteria,  previously  unknown,  has  appeared  among 
them. 

It  not  infrequently  becomes  epidemic,  and  is  apparently  contagious. 

Symptoms. — The  symptoms  of  hysteria  are  manifest  through  all  the 
nervous  phenomena,  and  may  be  grouped  as  psychical,  motor,  sensory  and 
sympathetic. 

I.  In  many  cases  mental  and  moral  disturbances  appear  only  during  the 
attack,  and  the  patient  has  full  control  of  the  mental  powers  in  the  inter- 
vals. More  frequently,  and  when  the  condition  has  become  chronic,  the 
patients  are  constantly  irritable  and  excessively  emotional.  As  a  rule  their 
judgment,  energy,  and  concentration  are  enfeebled,  and  although  their 
memory  is  not  aHected  the  will-power  is  greatly  impaired.  During  their  hys- 
terical paroxysms  they  always  want  an  audience  ;  they  crave  attention  and 
sympathy,  and  will  at  all  times  deceive  and  practise  most  dishonest  meas- 
ures to  obtain  them.  Their  emotions  pass  beyond  their  control,  tears  and 
laughter  being  apparently  always  at  their  command.  Hallucinations  and 
various  kinds  of  fancies  and  delusions  are  common. 

After  a  violent  fit  of  hysteria,  patients  often  become  dangerously  un- 
manageable, mischievous,  and  highly  abusive  or  blasphemous.  The  coma 
that  follows  an  attack  is  like  a  deep  sleep,  and  may  last  for  hours  or  days. 
More  or  less  analgesia  is  present,  but  complete  unconsciousness  never  oc- 
curs. Probably  a  so-called  ''trance"  is  but  prolonged  hysterical  coma. 
Ecstasy  and  somnambulism,  temporary  catalejDsy  and  trance,  are  all 
reckoned  by  some  among  chronic  hysterical  psychoses.' 

II.  The  motor  symptoms  of  hysteria  are  very  varied.  Globus  hysteri- 
cus is  the  most  common  ;  the  patient  imagines  that  a  lump  rises  from  the 
epigastric  region  into  the  throat  and  remains  there  causing  a  sensation  of 
choking.  Spasm  of  the  respiratory  muscles  produces  peculiar,  harsh, 
rasping,  expiratory  sounds,  and  the  inspirations  are  prolonged,  rapid,  and 
whooping  in  character,  accompanied  by  yawning,  hiccough,  laughing, 
crying,  and  sneezing.  There  is  a  loud,  barking,  brassy  cough  (the  hyster- 
ical cough),  but  no  expectoration.  The  patients  claim  that  all  voluntary 
movements  are  impossible  ;  they  cannot  rise  or  move  from  their  beds — yet 
they  gesticulate  wildly  and  perform  irrational  movements  in  excess.  The 
facial  muscles  are  in  constant  action.  Reflex  action  is  so  exaggerated  that 
the  slightest  irritation  produces  spasms.  Clonic  spasms  of  muscles  of  the 
face  and  cervical  region  and  of  the  muscles  of  the  thigh  are  common.* 
Tonic  muscular  spasms  in  the  limbs  are  frequent,  often  lasting  for  months; 
they  may  suddenly  disappear,  but  these  contractions  resist  the  influence 
of  chloroform  and  persist  during  sleep.  Abdominal  phantom  tumors  are 
thus  produced,  but  long-continued  Faradization  will  reduce  them.  When 
the  tonic  spasms  affect,  as  they  may,  portions  of  the  alimentary  canal, 

1  Griesinger  and  Briquet. 

'  Rhythmical  contraction  of  the  thigh  muscles  induces  an  apparent  pulsation  which  may  be  mistaken  for 
that  of  aneurism. 


1044  DISEASES    OF   THE   NERVOUS   SYSTEM. 

vomiting,  griping  pains,  borborygmi,  eructations,  diarrlicea  or  constipa- 
tion, and  dysphagia  occur.  Ketention  of  urine  and  great  distention  of  the 
bladder  may  happen.  In  rare  instances  the  secretion  of  urine  is  almost 
entirely  suppressed. '  In  hysterical  hemiplegia  the  face  and  tongue  are  not 
involved.  While  walking,  hysterical  patients  look  about,  whereas  a  true 
paralytic  keeps  his  eye  on  his  feet.  The  paraplegia  may  be  complete  and 
the  patients  unable  to  walk,  but  their  limbs  are  perfectly  well  nourished 
and  they  can  regain  the  upright  position  loithout  assistance.  Hysterical 
is  distinguished  from  organic  aphasia  by  the  fact  that  the  patient  is  able 
to  write  his  wishes  with  the  greatest  readiness.  Hysterical  aphonia  comes 
on  abruptly,  and  as  abruptly  disappears.  When  an  hysterical  patient  has 
a  convulsive  seizure  the  globus  hystericus  precedes  the  fall,  which  always 
takes  place  where  there  is  no  chance  of  injury.  The  patients  often  talk 
continuously  and  incoherently  during  their  convulsive  seizure,  and  throw 
themselves  into  the  most  grotesque  attitudes.  Complete  loss  of  conscious- 
ness rarely  if  ever  occurs.  The  pupils  are  not  dilated,  and  no  respiratory 
symptoms  are  present  sufficient  to  cause  asphyxia.^ 

III.  Derangements  of  sensibility  form  one  of  the  most  common  exhibi- 
tions of  this  disease.  Local  or  general  hypersesthesia  is  never  entirely 
absent  ;  it  is  sometimes  evinced  by  increased  acuteness  of  the  senses. 
Photophobia  is  common.  The  sense  of  touch  is  so  exaggerated  that  hys- 
terical women  will  recognize  individuals  by  the  touch  ;  the  olfactory  sense 
is  also  exceedingly  acute,  and  patients  are  disturbed  by  the  slightest  noise 
and  can  recognize  friends  by  their  step  at  a  long  distance.  Muscse  voli- 
tantes,  tinnitus  aurium,  pains  and  neuralgias  in  various  parts  are  all  com- 
mon. The  pains  complained  of  are  greatly  in  excess  of  any  discoverable 
cause,  and  cease  when  the  attention  of  the  patient  is  diverted.  The  pain 
often  simulates  left  intercostal  neuralgia  or  is  situated  over  the  vertebral 
spines  or  stomach,  in  the  Joints,  mammae,  skull  or  the  iliac  regions.  Pain  in 
the  skull,  as  if  a  nail  were  being  driven  into  the  bead,  or  a  kettle  were 
simmering  on  top  of  it,  called  by  the  ancient  physicians  clavus  hystericus, 
is  by  many  regarded  as  pathognomonic.  The  whole  cutaneous  surface 
may  be  hypersesthetic,  or  only  parts  of  it.  Sometimes  there  are  ob- 
served hysterical  angina  pectoris  and  hysterical  peritonitis.  All  the 
senses  in  an  hysterical  patient  are  abnormally  acute.  The  genital  organs 
are  often  so  sensitive  that  sexual  intercourse  is  impossible.  On  the  other 
hand,  anassthesia  is  of  frequent  occurrence  in  hysterical  persons  ;  it  may  ap- 
pear in  any  part  of  the  body  and  be  limited  to  a  distinct  portion  of  a  single 
nerve.  The  anassthetic  parts  are  usually  pale  and  their  temperature  sub- 
normal. Anaesthesia  may  be  superficial  or  so  deep  that  pins  can  be  thrust 
into  the  deep  tissues  without  any  expression  of  pain.  The  conjunctiva 
loses  its  sensitiveness  and  may  be  rubbed  or  touched  without  causing  con- 
tractures of  the  lids.  There  may  be  coexistent  loss  of  sensibility  in  the  mus- 
cles, bones,  and  joints.^ 

*  T.  Buzzard  in  Qiiain's  Diction,  of  Med. 

2  Hnghlings- Jackson  advances  the  hypothesis  that  inhihitory  control  of  the  spinal  cord  over  reflex  action 
is  temporarily  suspended,  the  cerebellar  influence  having  full  play. 

3  Jolly. 


HYSTEEIA.  1045 

In  some  instances  the  pharynx  and  epiglottis  may  be  tickled  or  pinched, 
or  irritating  vapors  inhaled  without  producing  the  customary  results. 
Large  faecal  accumulation  in  the  rectum  is  presumably  due  to  similar 
anaesthesia  of  its  mucous  membranes.  There  may  be  hemiopia  in  one  or 
both  eyes,  accompanied  by  loss  of  smell,  taste  and  hearing.  Sensations  as 
if  a  limb  or  part  were  greatly  enlarged  or  attenuated,  as  if  the  feet  were 
being  buoyed  up  or  loaded  with  lead,  or  as  if  pins  and  needles  were  being 
thrust  into  the  waist  are  of  common  occurrence.' 

IV.  Of  the  circulatory  changes,  cardiac  palpitation  is  perhaps  the  most 
common.  Feeble  heart  action,  with  a  small  and  hard,  or  a  full  and  soft 
pulse,  is  frequently  noticed  during  hysterical  fits.  The  abdominal  aorta, 
and  sometimes  other  arteries,  pulsate  so  strongly  as  to  suggest  aneurism.  Ac- 
cording as  there  is  stimulation  or  paralysis  of  the  vaso-motor  nerves  there 
will  be  a  cold,  pale  surface  or  hypersemia,  redness,  and  consequent  profuse 
sweating.  Coldness  of  the  extremities  is  one  of  the  most  common  evidences 
of  vaso-motor  change.  The  dilatation  of  the  vessels  may  become  so  great 
that  hemorrhages  will  occur  in  the  skin,  internal  organs,  genitals,  and 
stomach.  It  is  often  difficult  to  diagnosticate  hysterical  bsematemesis  from 
that  due  to  ulcer.  A  single  observation  is  rarely  sufficient  for  a  diagnosis.* 
The  following  hysterical  phenomena  are  all  undoubtedly  due  to  vaso-motor 
disturbances,  viz.  :  fever  and  chill,  flashes  of  heat  alternating  with  rigors, 
hyperesthesia,  enlargement  and  oedema  of  the  joints,'-'  an  abundant  flow  of 
pale,  clear  urine  deficient  in  salts,  excessive  salivation,  abnormal  dryness 
of  the  mouth,  increased  flow  of  gastric  juice,  an  abundant  secretion  of 
milk,  lasting  for  years,*  and  profuse  uterine  and  vaginal  secretions.* 

Differential  Diagnosis. — Hysteria  may  be  mistaken  for  epilepsy,  multiple 
sclerosis  of  the  hrain  and  spinal  cord,  hypochondria,  neuralgia,  and  urcemic 
coma.  It  is  distinguished  from  ejnlepsy  by  its  slow  onset,  by  incomplete 
coma,  a  normal  pupil,  sobbing  and  crying,  and  absence  of  subsequent 
stupor.  The  tongue  is  not  bitten  in  hysteria.  An  epileptic  seizure  is  short 
and  the  convulsions  are  not  symmetrical. 

Multiple  sclerosis  of  the  train  and  cord  is  often  accompanied  by  parox- 
ysms like  those  of  hysteria  ;  but  between  the  attacks  the  psychical  symptoms 
and  emotional  disturbances  are  absent. 

In  hypochondria  the  patient  is  always  morose ;  there  are  not  those  varia- 
tions in  temper  that  are  so  characteristic  of  hysteria.  Hypochondria  is  rare 
before  the  thirtieth  year,  is  more  common  in  men  than  in  women,  and  is 
geldom  marked  by  convulsions.     The  two  diseases  may  be  conjoined. 

J  Charcot  notices  that  with  hemi-ansesthesia  there  is  usually  ovarian  hyperesthesia  of  the  opposite 
side. 

2  Astley  Cooper  and  Parrot  record  cases  where  hemorrhages  have  occurred  from  the  breast  and  con- 
junctivfe. 

=  Brodie. 

*  Briquet. 

*  Lasegue  has  described,  under  the  name  of  hysteria  peripherique,  a  group  of  cases  of  considerable  in- 
terest, in  which,  although  the  patients  do  not  exhibit  the  general  hysterical  temperament,  the  slightest 
peripheral  irritation  causes  obstinate  muscular  spasms.  Such  are  certain  cases  of  rheumatic  torticollis 
and  of  blepharospasm  from  slight  and  passing  irritation  of  the  conjunctiva.  Lasegue  says  :  "The  tran- 
sition from  the  typical  hysteria  to  the  other  (functional)  diseases  of  the  nervous  system  is  not  abrupt,  but 
by  imperceptible  gradations." 


1046  DISEASES   OF   THE   NERVOUS   SYSTEM. 

The  comatose  state  following  an  hysterical  seizure  is  distinguished  from 
urcemia  by  an  examination  of  the  urine,  by  the  fact  that  dropsy  is  ab- 
sent ;  and  the  coma  is  preceded  by  sobbing,  crying,  and  other  hysterical 
phenomena. 

Neuralgia,  if  of  hysterical  origin,  ceases  when  the  patient's  attention  is 
diverted.  In  genuine  neuralgia  the  pain  follows  the  distribution  of  a  nerve, 
and  there  are  certain  recognizable  painful  spots  ;  in  so-called  hysterical 
neuralgige  the  reverse  is  the  case. 

Organic  paralysis  is  to  be  distinguished  from  hysterical  paralysis  by  the 
plumpness  of  the  limb  or  part  m  the  latter,  and  the  electrical  reaction, 
which  is  normal. 

Prognosis. — The  prognosis  in  hysteria  is  always  favorable,  although  re- 
covery is  rarely  permanent,  but  exacerbations  and  remissions  occur  at  ir- 
regular intervals.  Some  develop  every  phase  of  the  disease  at  different 
epochs.  Its  tendency  is  to  cease  after  the  menopause,  but  it  may  continue 
to  old  age.  Briquet  states  that  when  it  commences  in  youth  it  is  more 
persistent  than  when  it  occurs  later  in  life.  If  associated  with  uterine 
diseases  and  displacements,  the  prognosis  is  better  than  when  it  is  purely 
psychical. '  When  it  is  constitutional,  hereditary,  or  -an  evidence  of  the 
neuropathic  tendency,  even  temporary  recovery  is  rare. 

The  hysterical  contractures,  when  prolonged,  often  cause  permanent  de- 
formities. 

Treatment. — Moral  treatment  is  far  more  efficacious  than  medicines. 
Discipline,  exercise  in  the  open  air,  healthy  occupations,  early  hours,  and, 
if  possible,  a  change  of  residence,  all  exercise  a  marked  influence  on 
hysterical  subjects.  Bromide  of  sodium  or  potassium,  valerian,  asafoetida, 
belladonna,  hyoscyamus,  and  hydrate  of  chloral  are  all  at  times  of  service 
in  controlling  the  more  active  manifestations  of  hysteria.  When  a  cause 
can  be  reached  it  should,  if  possible,  be  immediately  removed  ;  and  uterine 
diseases  and  displacements  must  receive  their  appropriate  treatment.  Iron 
should  be  given  when  anaemia  exists.  Many  authorities  state  that  half 
their  cases  have  been  cured  by  the  use  of  o^Dium,  and  all  agree  that  hys- 
terical patients  tolerate  it  in  large  doses.  The  attacks  may  generally  be 
shortened  by  dashing  cold  water  over  the  patient,  and  sometimes  by  pres- 
sure over  the  ovaries.  Subcutaneous  injections  of  morphine,  or  inhalation 
of  ether  or  chloroform  until  complete  insensibility  is  reached,  are  sometimes 
advisable  when  the  seizure  is  very  violent.^  In  tympanitis  and  colic, 
enemata  of  asafoetida  are  useful.  Hysterical  vomiting,  often  very  ob- 
stinate, is  best  treated  by  the  blandest  possible  diet.  In  paralyses  of 
hysterical  origin  electricity  and  the  internal  use  of  strychnine  are  some- 
times of  service.  Hysterical  pains  are  most  efficiently  relieved  by  hypo- 
dermic injections  of  morphine.  Aphonia  may  be  treated  by  the  elec- 
tric current.     Sea-baths  or  a  course  of  hydrotherapy  are   often   highly 

•  Wunderlich  and  Rullier  describe  cases  of  acute  fatal  hysteria  with  high  temperature,  great  dysphagia, 
and  frequent  epileptiform  convulsions. 

''Reynolds,  quoting  Dr.  Hare,  states  that  forcibly  preventing  the  patient  from  breathing  for  a  certain 
time,  by  holding  the  nose  and  mouth,  is  followed  by  a  long  breath  and  a  relaxation  of  the  spasm. 


HTSTERO- EPILEPSY.  1047 

advantageous  to  hysterical  subjects.  Phosphorus  and  strychnine  are  re- 
garded by  some  as  specifics,  and  may  be  given  in  small  doses.  Children 
who  are  j^eculiar  and  have  a  tendency  to  hysteria,  should  be  subjected  to 
a  firm,  gentle  discipline  during  their  childhood  and  period  of  development. 
The  manner  of  the  physician,  his  conversation  in  the  presence  of  the  pa- 
tient, the  behavior  of  the  friends  and  family  both  during  and  between  the 
paroxysms,  all  have  a  great  influence  upon  the  case. 

HYSTEEO-EPILEPSY. 

This  is  a  very  grave  form  of  hysteria,  attended  by  epileptiform  convul- 
sions and  marked  by  the  occurrence  of  peculiar  anaesthesia,  paralysis,  and 
muscular  contraction.     It  has  no  especial  morbid  anatomy. 

Etiology. — Epilepsy  may  be  the  primary  disease,  and  some  strong  psy- 
chical disease  superinduce  hysteria  ;  or  epilepsy  may  slowly  develop  after 
long-continued  hysteria.  The  etiology  is  the  same  as  that  of  hysteria  ;  but 
puberty,  the  menopause,  and  extreme  fright'  are  among  its  most  frequent 
causes. 

Symptoms. — An  hysterical  aura,  usually  abdominal,  precedes  the  convul- 
sion, which  at  first  is  identical  with  an  epileptic  seizure.  Following  the 
clonic  convulsions  is  a  short  period  of  muscular  relaxation,  during  which 
the  patient  appears  comatose,  but  which  is  soon  followed  by  contortions  of 
the  most  violent  character.  The  motions  may  intentionally  indicate  any 
or  all  of  the  vilest  passions  or  fears,  or  there  may  be  simply  irrational  twist- 
ings.  Opisthotonos  usually  occurs  after  the  attack,  the  patient  usually 
suffering  from  hysterical  excitement,  laughing  or  crying  immoderately,  and 
has  hallucinations  and  delusions  resembling  those  of  delirium  tremens. 
Contractures,  either  paraplegic  or  hemiplegic,  subsequently  occur  in  one 
or  more  limbs,  which  may  be  persistent,  and  yield  only  to  deep  chloroform 
narcosis.  It  is  to  be  remembered  that  these  hysterical  contractures  may  oc- 
cur without  any  other  symptoms  of  hysteria  ever  having  existed,  or  may 
follow  burns.^  After  a  long  duration  they  sometimes  relax  from  a  great 
moral  shock.  During  such  a  fit  the  temperature  may  rise  to  105°  F.'  Ova- 
rian hypersesthesia  almost  invariably  precedes  these  attacks.^  Anaesthesia 
and  analgesia  are  common,  but  usually  affect  only  one  half  of  the  body. 

The  special  senses  may  all  be  affected,  and  color-blindness  is  not  uncom- 
mon. 

DijBferential  Diagnosis. — The  diagnosis  of  hystero-epilepsy  in  a  well-marked 
case  is  easily  made.  The  salient  points  of  hysteria  and  epilepsy  are  com- 
bined, and  the  picture  of  a  patient  in  the  fit  is  one  that  will  not  be  con- 
founded with  any  other  condition. 

Prognosis. — The  prognosis  is  the  same  as  in  hysteria,  and  far  more  favor- 
able than  in  epilepsy. 

»  The  tragedies  of  the  Commune  in  Paris  during  the  Franco-Prussian  war  are  said  to  have  produced  many 
severe  attacks  in  hysterical  females. 
^-  Progres  Medical,  Feb.  and  March,  188.3. 
'^  Charcot. 
*  Charcot  states  that  ovarialgia  is  an  important  part  of  the  seizure. 


1048  DISEASES    OF   THE    NERYOUS    SYSTEM. 

Treatment. — The  treatment  will  require  a  combination  of  the  remedies 
proposed  for  hysteria  and  epilepsy  in  the  proportion  that  each  enters  as  an 
element  of  the  disease.  Metallo-therapeutics  have  been  extensively  em- 
ployed in  the  treatment  of  this  affection.  A  fevi^  discs  of  metal  are  bound 
at  intervals  around  an  anaesthetic  limb  ;  in  ten  to  twenty  minutes  sensation 
returns  to  the  skin  around  the  discs,  and  then  to  the  whole  limb,  but,  un- 
fortunately, m  the  mean  time  corresponding  parts  on  the  other  limb  grad- 
ually lose  their  sensibility,  and  the  results  are  not  permanent.  The  slight- 
est electrical  currents  produce  the  same  results.  Contractures  of  years' 
duration  often  can  be  cured  or  transferred  in  like  manner.  Metals,  mag- 
nets, bits  of  wood — all  have  produced  the  same  effect.  Different  metals 
act  on  different  subjects.  Gold,  silver,  iron,  tin  and  copper  have  all  been 
used.  Long-continued  blistering  and  Faradization  have  removed  contrac- 
tures of  long  standing. 

CATALEPSY. 

Catalepsy  is  a  functional  disease  of  the  nervous  system,  closely  allied  to 
hysteria  and  epilepsy.  It  is  characterized  by  loss  of  consciousness,  sensa- 
tion and  volition,  accompanied  by  a  peculiar  muscular  rigidity  in  which 
the  limbs  remain  for  some  time  in  whatever  position  they  are  placed. 
There  are  no  appreciable  pathological  changes,  but  the  muscular  rigidity 
is  generally  considered  to  be  of  centric  origin. 

Etiology. — Catalepsy  may  occur  at  any  age,  but  is  rarely  met  with  except 
in  females  about  the  age  of  puberty,  and  is  usually  associated  with  hys- 
terical phenomena.  It  may  precede  melancholia  and  epilepsy.  Trau- 
matism, strong  emotions,  fright,  shock,  and,  in  many  instances,  religious 
excitement  may  induce  an  attack.  Hereditary  influence  is  frequently 
marked,  and  it  occurs  in  families  where  insanity,  mania,  epilepsy,  etc.,  have 
occurred. ' 

Symptoms. — Catalepsy  occurs  in  paroxysms  which  are  either  regular  or 
irregular.  Headache,  vertigo,  hiccough,  etc.,  may  precede  the  attack. 
Consciousness  is  suddenly  lost,  and  the  limbs — remaining  in  the  position 
occupied  at  the  onset — are  as  rigid  as  if  petrified,  soon  relax  a  little,  how- 
ever, and  can  be  moved,  but  will  remain  in  whatever  position  they  are 
placed.  They  resist  passive  movement  as  if  made  of  wax,  hence  the  name 
flexihilitas  cerea.  The  rigidity  slowly  yields  to  the  force  of  gravity.  Sen- 
sibility and  reflex  movement  may  be  totally  or  partially  lost ;  rarely  is 
there  paroxysmal  hypersesthesia.  The  respiration  and  heart  movements 
are  weak  ;  the  face  is  expressionless,  and  often  has  a  death-like  appearance. 
The  skin  is  cold,  and  the  temperature  is  commonly  lowered  perhaps  2°  or 
3°  below  normal.  Substances  placed  in  the  back  of  the  mouth  are  slowly 
swallowed.  In  a  few  cases  there  is  only  partial  loss  of  consciousness,  the 
patient  being  able  to  appreciate  strong  sensorial  or  emotional  impressions. 
When  the  attack  is  of  short  duration  it  vanishes  as  quickly  as  it  appeared  ; 
and  an  impression  upon  the  patient  remains  like  that  following  a  confused 
dream.     When  the  attack  lasts  for  many  hours  or  days  several  paroxysms 

1  Eulenburg  inclines  to  the  view  that  malarial  infection  may  cause  it. 


NEURASTHENIA,  1049 

go  to  make  up  the  whole  attack.  Between  the  attacks  there  are  no  symp- 
toms as  a  rule. '  The  attacks  may  occur  at  regular  intervals  ;  tlie  slightest 
mental  disturbance  or  excitement  may  bring  on  a  paroxysm. 

Differential  Diagnosis. — True  catalepsy  cannot  be  mistaken  ;  but  it  may 
be,  and  often  has  been,  successfully  simulated. 

Prognosis. — The  prognosis  is  favorable,  except  in  those  cases  where  there 
is  a  marked  nervous  tendency  in  the  family.  The  prognosis  is  best  where 
there  are  no  symptoms  between  the  attacks. 

Treatment. — Treatment  should  be  directed  more  especially  to  the  accom- 
panying hysterical  diathesis,  but  we  may  endeavor  to  rouse  the  patient  by 
the  use  of  ammonia,  snuflp,  or  the  Faradic  current.  An  emetic  will  gener- 
ally cut  short  an  attack. °  The  wet  pack  and  the  cold  douche  have  been 
used.  Between  the  attacks  iron,  quinine  and  antispasmodics — valerian 
especially — are  indicated. 

iraUEASTHElSnA. 

Neurasthenia  spinalis  is  a  functional  weakness  of  the  spinal  cord;  or,  as 
Eosenthal  calls  it,  a  depressed  form  of  spinal  irritation.'  It  is  commonly 
known  as  nervous  debility.  Eolando,  Luys  and  others  have  advanced  views 
concerning  the  cerebellum  that  may  lead  to  this  organ  being  regarded  as 
the  seat  of  the  disorder.  Some  authors  claim  that  it  is  an  augemic  condition 
of  the  spinal  cord,  but  its  morbid  anatomy  is  not  as  yet  determined. 

Etiology. — Men  are  far  more  liable  to  this  condition  than  women.  It 
often  develops  at  puberty,  but  is  common  in  adult  and  middle  life.  It  is 
most  frequent  in  those  of  a  neuropathic  tendency.  Sexual  excesses,  mas- 
turbation and  onanism  are  said  to  induce  it.  Excessive  mental  labor,  late 
hours,  long-continued  emotional  disturbances  of  any  kind,  insomnia,  insuf- 
ficient or  improper  food,  and  excessive  use  of  tobacco  or  alcohol  may  excite 
it  in  those  who  are  predisposed  to  neuroses.  Rosenthal  claims  that  the  pro- 
longed action  of  these  causes  in  the  young  produces  irritability  of  the  med- 
ullary and  vaso-motor  centres,  and  thus  the  vascular  equilibrium  of  the  cord 
is  lost. 

Symptoms. — These  patients  are  weak,  easily  fatigued  and  prostrated  by 
slight  muscular  exertion.  They  are  languid  and  despondent.  There  is 
aching  in  the  limbs,  the  sleep  is  broken,  or  there  is  actual  insomnia,  and 
they  complain  that  they  are  always  tired  and  the  subjects  of  nervous  debil- 
ity. They  suffer  constantly  from  dorsal  and.  lumbar  pains  and  nocturnal 
emissions,  and  the  passage  of  a  urethral  sound  produces  excessive  pain  and 
sometimes  convulsions.  The  sexual  powers  are  enfeebled.  During  excite- 
ment or  after  the  use  of  alcoholic  stimulants,  neurasthenic  patients  are  able 
to  perform  a  large  amount  of  mental  labor,  but  afterwards  they  are  greatly 
prostrated.  The  emotions  are  easily  excited,  and.  they  often  imagine  that 
they  are  the  subjects  of  some  grave  organic  disease.     There  is  a  tendency 

1  Eulenburg  states  that  cataleptic  children  are  often  remarkably  bright. — Ziemsseti's  Encyc. 
'  Gowers  advocates  the  subcutaneous  injection  of  apomorphia — one-twentieth  to  one-twelfth  grain. 
'  Erb  claims  that  it  is  not  a  manifestation  of  hypochondria,  and  that,  although  often  combined  with  It, 
it  is  to  be  regarded  as  distinctly  of  spinal  origin. 


1050  DISEASES    OF   THE    NERVOUS    SYSTEM. 

to  melancholia  and  hypochondriasis.  Neurasthenia  is  not  at  first  accom, 
panied  by  anaemia,  but  later  the  insomnia  and  anorexia  induce  it.  The 
tongue  is  coated.  Flatulence,  dyspepsia,  and  dilatation  of  the  stomach 
are  usually  ]3resent. 

Often  the  patients  have  a  healthful  appearance,  which  leads  one  to  suspect 
that  they  are  feigning  disease. 

Differential  Diagnosis.  — Neurasthenia  may  be  mistaken  for  incipient  ataxia, 
incipient  myelitis,  or  commencing  vertebral  caries. 

In  ataxia  the  lancinating  pains,  disorders  of  sensation,  the  iron  band  sen- 
sation, the  ocular  symptoms  and  the  increased  galvanic  excitability  will 
enable  one  to  reach  a  diagnosis.  The  paralysis  which  occurs  in  myelitis 
distinguishes  it  from  neurasthenia. 

In  spinal  caries  the  pain  on  motion  and  the  angular  curvature,  in  con- 
nection with  the  traumatic  history  of  the  case,  will  establish  the  diagnosis. 

Prognosis. — The  prognosis  in  neurasthenia  is  always  good.  It  may  con- 
tinue for  months,  or  relapses  occur  ;  but  complete  recovery  may  always 
finally  be  reached  under  proper  treatment. 

Treatment. — The  most  important  indication  in  this  condition  is  to  secure 
absolute  rest.  Change  of  scene,  nutritious  diet,  outdoor  life,  and  especially 
sound  sleep  at  night  tend  to  produce  a  cure.  Sea  bathing  is  highly  rec- 
ommended, and  a  light  wine  or  beer  with  meals  is  frequently  of  service.  The 
functions  of  the  skin  should  be  carefully  attended  to.  Iron,  strychnine  and 
some  form  of  the  hypophosphites  are  indicated. 


CHOREA. 

{St.  Vitus's  Dance.) 

Chorea  is  a  disease  of  the  nervous  system  marked  by  clonic  muscular  con- 
tractions without  order  or  rhythm,  which  tend  to  subside  spontaneously 
after  a  few  weeks'  duration. 

Morbid  Anatomy. — Chorea  has  usually  been  regarded  as  a  purely  func- 
tional disease,  but  recent  investigations,  although  leaving  the  pathology 
still  somewhat  obscure,  seem  to  indicate  that  active  hyperaemia  of  the 
brain  and  cord  is  always  present,  if  not  the  exciting  morbid  condition,  and 
is  due  to  vaso-motor  disturbance,  which  may  be  associated  with  the  rheu- 
matic diathesis  or  result  from  various  mental  and  reflex  irritations. 

The  occasional  occurrence  in  chorea  of  capillary  emboli  and  thrombi, 
with  consequent  minute  points  of  softening  in  the  gray  matter  of  the 
brain,  corpora  striata,  optic  thalami  and  cord,  together  with  the  fact  that 
in  nearly  all  fatal  cases  endocarditis,  with  valvular  vegetations,  is  present, 
has  given  rise  to  the  supposition  that  these  conditions  represent  the 
pathology.  The  commonly  unilateral  nature  of  the  disease,  its  cessation 
during  sleep,  the  absence  of  large  emboli  with  consequent  paralysis,  and 
finally  the  fact  that  it  is  only  in  a  small  proportion  of  cases  that  the 
capillaries  are  found  obstructed,  are  serious  and  fatal  objections  to  this 
theory. 


C'HOKEA.  1051 

Whatever  the  morbid  condition,  it  probably  affects  more  especially  the 
corpus  striatum,  thalamus,  or  a  single  hemisphere  primarily,  but  in  severe 
cases,  when  the  muscles  of  deglutition  and  plionation  are  affected,  extends 
to  the  medulla.  An  ataxic  gait  occasionally  indicates  disturbance  of  the 
cord. 

Etiology. — Chorea  is  most  frequently  met  with  between  the  ages  of  six 
and  sixteen,  i.e.,  from  second  dentition  until  puberty,  in  children  whose 
parents  have  suffered  from  hysteria,  epilepsy,  and  other  forms  of  func- 
tional nervous  disease  ;  from  two-thirds  to  three-fourths  of  all  cases  occur 
in  girls.  Feebleness  of  constitution,  and  the  injurious  system  of  forcing 
the  education  of  children,  as  well  as  the  conditions  which  tend  to  the 
premature  development  of  the  sexual  instincts,  predispose  to  chorea. 
Anaemia,  chlorosis,  onanism,  and  anomalies  of  menstruation  are  also  pre- 
disposing causes. 

Acute  articular  rheumatism  and  its  cardiac  complications  bear  such  an 
intimate  relationship  to  chorea  that  many  authorities  regard  them  as  one 
and  the  same  affection  under  different  forms.  The  rheumatic  diathesis 
and  the  resulting  cardiac  disease  must  certainly  be  accepted  as  among  the 
most  important  causes  of  chorea.  The  more  directly  exciting  causes  are 
fright,  shock,  and  extreme  mental  labor  or  any  form  of  severe  nervous 
disturbance. 

Symptoms. — The  onset  is  seldom  well  marked,  although  cases  are  record- 
ed where,  after  a  fall  or  shock,  not  more  than  four  hours  have  elapsed  before 
distinct  choreiform  movements  occurred.  It  may  be  said  that  in  these 
cases  recovery  is  also  rapid.  As  a  rule,  the  child's  disposition  becomes 
irritable  or  moody,  and  although  choreic  subjects  are  very  excitable,  there 
is  decided  mental  weakening,  indicated  by  loss  of  memory  and  interest  in 
things  that  have  before  interested  them.  The  sleep  is  disturbed  and  hal- 
lucinations are  common,  and  actual  mania  may  be  a  precursor  of  chorea. 

The  first  direct  indications  of  the  disease  are  a  restlessness  of  movement 
and  clumsy  handling  of  the  limbs.  There  will  usually  for  awhile  be  inter- 
vals when  these  children  act  naturally  for  a  short  time,  but,  if  observed  care- 
fully, and  especially  when  they  are  conscious  of  being  watched,  they  are 
seen  to  drag  a  foot,  fidget  with  their  fingers,  twitch  the  shoulders,  or  jerk 
the  head  in  a  peculiar  manner.  As  they  gradually  lose  control  of  their 
movements  they  stumble  in  walking,  spill  their  food  or  drink,  and  fre- 
quently drop  articles  they  may  be  holding.  The  choreic  movements  are 
usually  unilateral,  at  first  confined  to  one  hand,  leg,  or  side  of  the  face, 
and  in  a  small  per  cent,  of  cases  the  manifestations  remain  limited  to  one 
side,  but  more  commonly  extend  to  the  other  side  within  a  few  days.^ 

In  the  fully  developed  disease  the  symptoms  vary  in  degree  rather  than 
kind.  In  the  mildest  cases  a  child  simply  seems  awkward,  breaking  dishes, 
stumbling  about  the  room,  hurting  himself  with  knife  and  fork,  or,  in  the 
case  of  older  children,  never  being  able  to  correctly  perform  tasks  where 

>  Broadbent  considers  the  parallelism  between  hemichorea  and  hemiplegia  so  perfect  as  to  suggest  at 
once  that  the  two  affections  represent  different  conditions  of  the  same  nerve-centres,  and  that  it  is 
made  more  complete  by  the  very  discrepancies  as  they  may  at  first  sight  appear. 


1052  DISEASES   OF   THE   NEEVOUS   SYSTEM. 

slight  dexterity  is  required.  Irregular  action  of  the  muscles  of  speech 
may  occur,  and  words  may  be  uttered  against  the  will  of  the  patient. 
Spontaneous  jDain  is  often  complained  of  in  the  affected  side. 

In  the  worst  form  of  the  disease  every  feature  and  limb  may  be  hideously 
contorted,  the  teeth  ground  together  or  snapped  off,  and  bones  may  be 
broken.  A  patient  will  turn  somersaults  without  rest,  rush  around  in  a 
circle,  colliding  with  nearly  everything  in  the  room ;  or,  if  in  bed,  may  be 
suddenly  contorted  and  thrown  therefrom  with  violence  enough  to  produce 
a  fracture  or  dislocation.  Between  these  two  extremes  are  cases  of  every 
degree,  but  in  all  the  convulsions  are  made  up  of  irregular,  sudden,  im- 
pulsive movements,  which  are  entirely  involuntary  and  aggravated  by  every 
attempt  at  voluntary  movements.  After  the  muscles  involved  have  been 
in  incessant  action  and  violent  contraction  for  hours,  muscular  exhaustion 
does  not  occur.  In  most  instances,  however,  the  muscles  enjoy  complete 
repose  during  sleep.  When  this  is  not  the  case  rapid  and  intense  anaemia 
occurs.  As  in  these  cases  movement  is  almost  continuous,  and  the  patient 
can  neither  eat  nor  be  comfortably  fed,  death  from  exhaustion  may  result. 

Chorea  of  the  laryngeal  muscles  is  marked  by  a  monotonous  voice  having 
a  deep  pitch,  and  deglutition  is  often  greatly  interfered  with.  The  pupils 
are  commonly  dilated  and  the  special  senses  may  be  slightly  blunted,  but 
the  cutaneous  sensibility  is  rarely  affected.  The  bowels  are  constipated  as 
a  rule,  although  sometimes  the  fseces  are  involuntarily  discharged.'  After 
chorea  has  lasted  for  a  long  time  the  heart's  action  is  disturbed  ;  ansemia  is 
marked,  and  the  mental  condition  of  the  child  approaches  that  of  the  idiot. 
In  girls  who  are  old  enough  the  menstrual  functions  will  usually  be  de- 
ranged. The  skin  is  harsh  and  dry,  and  in  this  class  of  patients  hysteria 
often  develops  as  a  sequel. 

Chorea  is  almost  invariably  accompanied  by  some  paresis  and  often  by 
complete  paralysis  during  or  preceding  the  development  of  the  con- 
vulsions. 

Differential  Diagnosis. — Disseminated  sclerosis  of  the  nerve  centres  is 
accompanied  by  tremor  and  jactitation  that  may  be  mistaken  for  chorea, 
especially  as  it  is  a  disease  occurring  in  children.  But  ankle-clonus,  paresis 
of  both  lower  extremities,  and  the  occurrence  of  tremor  on  voluntary  ex- 
citation of  the  muscles,  will  decide  the  case.  Hysteria  and  epilepsy  are 
readily  distinguished  from  it,  as  is  also  the  tremor  of  old  age. 

Prognosis. — Chorea  is  a  chronic  disease  of  varying  duration,  but  in  most 
cases  lasting  for  two  or  three  months.  Eelapses  frequently  occur  dur- 
ing puberty;  but  may  occur  after  intervals  of  twenty  or  thirty  years. 
Complete  recovery  is  the  rule  ;  the  patient  fully  recovers  his  intelligence 
and  muscular  strength.  Among  children  the  mortality  is  about  five  per 
cent.,  and  death  is  usually  preceded  by  delirium,  and  is  due  usually  to 
asthenia  or  some  complication.  Hemiplegia,  aphasia,  hemiansesthesia, 
anaemia,  heart  disease,  rheumatism,  and  erysipelas  or  abscesses  originating 
in  wounds  which  the  sufferer  inflicts  on  himself,  may  be  reckoned  among 
the  complications.     Abortion  or  premature   delivery  may  occur  when  a 

1  Bence-Jones  states  that  the  amount  of  urea  excreted  is  increased. 


SUNSTROKE.  1053 

mother  is  choreic.      Very  rarely   does  jiermanent  mental   derangement 
follow. 

Treatment. — Should  an  exciting  cause  be  discovered  (constipation  or  in- 
testinal worms),  it  must  be  immediately  removed.  In  all  cases  mental  and 
bodily  rest,  a  generous  but  bland  diet,  and  pleasant,  and,  if  possible,  rural 
surroundings  should  be  ordered.  Children  with  chorea  should  not  go  to 
school.  Many  authorities  advocate  a  generous  wine  in  connection  witli 
iron.  Sleep  should  be  secured  by  the  use  of  hydrate  of  chloral  if  necessary  ; 
Harley  advocates  conium.  The  most  useful  drugs  are  arsenic,  zinc,  the 
bromides,  and  hydrate  of  chloral.  Arsenic  has  given  me  better  results  than 
any  other  drug  ;  it  must  be  given  in  proportionately  increasing  doses  until 
its  specific  physiological  effect  is  produced.  Copper,  the  silver  salts,  and 
strychnia  are  much  used  by  the  French.'  Weir  Mitchell  has  successfully 
used  salicylate  of  soda,  probably  in  rheumatic  cases.  In  extreme  cases 
chloroform  and  other  anassthetics  may  be  needed.  The  hypodermic  injec- 
tion of  curare,  friction-electricity,  and  galvanism  are  recommended.  Baths, 
wet  packs,  or  a  thorough  rubbing  often  act  beneficially,  and  the  ether 
spray  along  the  spine  seems  to  induce  sleep  and  diminish  violence  of  the 
choreic  movements  * 

SUNSTROKE. 

{Insolation.) 

Insolation  is  that  complex  of  symptoms  occurring  in  persons  exposed  to 
extreme  heat  under  unfavorable  circumstances. 

Morbid  Anatomy. — The  heart  is  usually  firmly  contracted,  but  it  may  be 
flaccid.  The  left  heart  is  empty,  while  the  right  side  and  the  venous  tracts 
are  filled  with  dark,  often  fluid  blood.  The  blood  is  seldom  coagulated  ; 
its  corpuscles  are  crenated  and  do  not  tend  to  form  rouleaux,  and  contain 
less  oxygen  than  normal.  The  lungs  are  intensely  congested,  oedematous, 
and  sometimes  exhibit  spots  of  hemorrhage.  The  spleen  is  swollen 
and  soft,  and,  with  the  kidney  and  liver,  exhibits  cloudy  swelling  or  paren- 
chymatous degeneration.  The  meninges  are  intensely  hypergemic,  and  there 
may  be  evidences  of  incipient  meningitis.  The  ventricles  of  the  brain  con- 
tain more  or  less  serum,  and  the  brain  substance  itself  is  congested  or  hem- 
orrhage has  occurred  into  it.  The  cord  is  sometimes  abnormally  soft.  In 
severe  cases  the  body  is  covered  with  ecchymoses,  and  sub-serous  hemor- 
rhages are  common.  In  the  neck  the  sympathetic  ganglia,  the  vagi,  and 
the  connective-tissue  are  surrounded  by,  or  infiltrated  with  blood.  Eigor 
mortis  comes  on  very  rapidly.^ 

Insolation  generally  results  from  exposure  to  heat,  in  persons  who  are 
exhausted  by  either  mental  or  physical  labor. 

'  Gaz.  Medical,  Paris,  Oct.,  1846.    Jour,  de  VAnat.  et  de  Phys.,  1874 ;  also  Trousseau. 

''In  the  Children's  Hospital  at  Paris  much  reliance  is  placed  on  gymnastic  exercise,  performed  with 
pleasant  surroundings  and  music. 

3  Very  recently  Arndt  states  that  in  his  autopsies  there  was  anasmia  of  the  brain  and  its  membranes  ; 
and  that  observers  must  have  been  misled  by  the  blood  escaping  from  large  congested  vessels,  and  running 
over  an  anaemic  brain.  By  him  all  the  viscera  are  described  as  pale  and  oedematous.  Virchow's  Archiv., 
vol.64,  pp.  15-39.    See  also  Koster  in  Berlin.  Klin.  Wochen.,  No.  34,  1875.    Also  for  July  17th,  1876. 


1054  DISEASES  OF  THE  KERVOUS   SYSTEM. 

Etiology. — Workmen,  soldiers  on  the  march,  stokers  and  cab-drivers,  or 
brain-workers  and  those  who  are  suffering  anxiety  or  mental  distress  are 
more  liable  to  be  overcome  by  the  heat.  Hot,  wet,  muggy  days — our  Au- 
gust dog-days — are  the  most  favorable  for  its  occurrence.  Acclimatization 
has  very  much  to  do  with  its  development.  Nearly  all  new  arrivals  in  India 
at  first  suffer  more  or  less  severely  from  the  heat.  Nevertheless,  when  a 
certain  temperature  of  the  air  is  reached  all  alike  succumb.'  Dry,  hot 
winds  are  not  prejudicial.  In  Dakota  men  can  work  all  day  exposed  to  the 
sun  when  the  temperature  of  the  air  is  at  least  140'^  to  160"  F.,  while  in 
New  York  on  a  cloudy,  wet  day  in  August,  with  the  temperature  at  only 
93°  F.,  large  numbers  of  men  and  animals  are  prostrated.  The  vigorous, 
thin,  healthy  individual  who  leads  a  temperate  and  regular  life  seldom 
suffers  from  the  heat;  while  those  who  drink  freely  of  alcoholic  beverages 
and  dissipate  during  the  summer  months  are  those  that  most  commonly 
suffer.     Large  immbers  are  affected  just  after  eating  a  hearty  meal.^ 

Symptoms. — The  majority  of  cases  occur  in  the  middle  of  the  day.  In 
mild  cases  the  patient  suddenly  becomes  exhausted,  and  probably  faints  or 
becomes  semi-comatose.  He  is  utterly  prostrated  ;  the  skin  is  pale,  cold,  and 
moist,  the  pulse  is  quick  and  feeble,  various  colored  spots  appear  before  the 
eyes,  and  all  kinds  of  symptoms  are  referred  to  the  head — floating,  swim- 
ming, vertigo,  fulness,  neuralgic  pains,  etc.  These  cases  may  recover,  or 
collapse  may  terminate  fatally  from  heart  failure. 

In  the  foudroyante  form  a  man  may  be  struck  down  suddenly,  or  there 
may  be  prodromata,  which  are  generally  depression  of  spirits,  muscular 
weakness,  dyspnoea,  epigastric  oppression,  and  perhaps  nausea  and  vomit- 
ing. Unconsciousness  suddenly  follows  ;  the  skin  is  cold,  the  pulse  is  fee- 
ble, respiration  and  circulation  are  markedly  interfered  with,  and  death 
may  result  from  heart-failure  due  to  injury  of  the  nerve  centres  from  sud- 
den elevation  of  temperature.  Reaction  may  set  in,  but  it  is,  at  best,  te- 
dious and  imperfect.     This  form  is  a  true  coup  cle  soleil. 

In  another  form  called  tliermic  fever  the  temperature  rises  to  108°  oi 
110°  F.,  or  even  higher.  This  is  due  to  the  influence  of  heat  on  the 
nerve  centres  and  subsequent  action  upon  the  vaso-motor  system.  It  often 
occurs  at  night  and  in  those  who  are  dissipated  or  worn  out,  or  are  in  the 
midst  of  anti-hygienic  surroundings.  There  is  great  restlessness,  thirst, 
and  dyspnoea.  The  skin  is  burning  hot,  and  either  dry  or  moist.  The 
upper  part  of  the  body  is  congested  and  livid  ;  the  pulse  may  be  full  and 
labored  or  quick  and  jerking,  and  the  carotids  pulsate  forcibly.  The 
pupils  are  at  first  contracted  but  later  widely  dilated,  and  the  frequent 
micturition  of  the  early  stages  gives  place  to  urinary  suppression.  De- 
lirium and  epileptiform  convulsions  are  common.  Toward  the  end  the 
pulse  becomes  extremely  rapid  and  feeble,  the  patient  passes  into  a  com- 
plete coma,  the  breathing  is  sighing  or  stertorous,  sometimes  peculiarly 
moaning,  and  the  urine  and  faeces  are  passed  involuntarily.     Some  of  these 


>  The  East  Indian  loomarna,  or  hot  wind  stroke. 

^  J.  Fayrer  states  that  the  most  frequent  cases  are  those  that  come  on  in  houses,  ships,  tents,  laundries, 
cook-rooms,  etc.,  during  the  night,  or  in  the  day,  away  from  the  direct  solar  rays. 


SPINAL  lERITATIOK.  1055 

cases  are  marked  by  persistent  vomiting  and  purging ;  sucla  cases  rarely 
recover. 

Differential  Diagnosis. — Severe  cases  attended  by  hyperpyrexia  cannot  be 
confounded  with  any  other  disease.  Moderately  severe  cases,  however, 
may  be  mistaken  for  acute  meningitis.  In  the  latter  the  projectile  vomit- 
ing, the  boat-belly,  the  pale  face,  the  tdche  cereirale,  and  the  tense,  hard, 
wiry  pulse  are  in  striking  contrast  to  the  symptoms  of  the  former.  Tlie 
history  of  the  case  is  always  important.  Under  the  head  of  acute  alco- 
holismus,  are  given  the  symptoms  of  alcoholic  coma,  which  may  be  con- 
founded with  sunstroke. 

Prognosis. — The  prognosis,  except  in  mild  cases,  is  very  bad  ;  nearly  one- 
half  die.  Many  who  recover  are  invalids  for  life.  Among  the  sequelaD 
are  a  sub-acute  or  chronic  meningitis,  epilepsy,  insanity  (in  every  degree), 
partial  paraplegia  or  hemiplegia,  loss  of  memory,  blindness,  extreme  in- 
tolerance of  heat,  almost  constant  headache  and,  in  many  cases,  great  irri- 
tability of  temper. 

Treatment. — In  all  cases  the  patient  must  have  absolute  rest  and  plenty 
of  cool,  fresh  air.  The  more  these  i^atients  are  carried  about  the  worse 
their  chances.  All  tight  or  needless  clothing  should  be  at  once  removed. 
Stimulants  are  often  necessary  ;  if  they  excite  vomiting  they  should  be 
given  hypodermically  or  as  enemata.  Ether,  mnsk,  carbonate  of  ammonia, 
turpentine,  etc.,  are  recommended. 

In  most  cases  the  cold  water  treatment  is  the  best.  The  patient  should 
be  taken  to  the  nearest  pumj:),  stream,  or  water-tank  and  immersed  for  a 
considerable  time,  or  a  stream  of  cold  water  Should  be  poured  over  the 
head,  neck  and  back.  Between  the  baths  dry  cnps  may  be  applied,  and 
during  the  baths  stimulants  may  be  given  if  the  pulse  demands  them.  A 
patient  should  always  be  removed  from  the  bath  before  the  temperature 
falls  to  normal.  Purgative  enemata  and  cardiac  stimulation,  with  the 
cold  water  treatment,  are  all  that  is  required  in  those  moderately  severe 
cases  where  the  temperature  does  not  rise  above  105°  F. 

In  thermic  fever,  venesection  is  contra-indicated.  Ice  water  should  be 
applied  to  the  surface,  the  bowels  should  be  moved  by  a  brisk  saline,  and 
morphine  and  quinine  given  hypodermically.  Blisters  about  the  nuchal 
region  are  often  beneficial.  The  severe  cerebral  symptoms  in  this  form 
are  often  relieved  by  the  inhalation  of  ether  or  chloroform.  These  patients 
need  careful  watching  during  convalescence,  and  should  remove  to  a  cool 
climate,  and  engage  in  no  business  that  demands  active  brain  work.  It  is 
in  this  last-named  variety  that  rapid  lowering  of  the  temperature  by  the 
application  of  cold  to  the  surface  is  of  the  greatest  importance. 

sphntal  iekitation. 

This  is  always  functional.  Strictly  speaking,  it  has  no  morbid  anatomy, 
but  in  most  cases  is  associated  with  congestion  or  ansemia. 

Etiology. — It  occurs  chiefly  in  women  between  the  ages  of  fifteen  and 
twenty-five.     Spinal  shock,  or  concussion  from  any  cause,  and  all  those 


1056  DISEASES   OF  THE  NEEVOUS  SYSTEM. 

practices  and  habits  which  cause  nervous  strain  and  result  in  nervous  ex- 
haustion, may  also  produce  spinal  irritation.  Chronic  alcoholism  and  the 
opium  habit  may  also  induce  it.  All  severe  diseases  where  there  is  a  pro- 
longed drain  '  on  the  system  will  be  followed  by  spinal  irritation.  A  neu- 
ropathic tendency  or  hysteria  often  accompanies  or  causes  spinal  irrita- 
tion. 

Symptoms. — The  one  constant  and  special  symptom  of  spinal  irritation  is 
tenderness,  which  may  be  excited  either  by  pressure  or  motion.  It  may 
extend  along  the  entire  spine,  or  be  localized  over  a  single  vertebra.  This 
tenderness,  which  varies  greatly  in  degree,  becomes  marked  on  the  ap- 
plication of  heat,  cold,  electricity,  and  other  irritants.  The  spinous  proc- 
ess is  the  place  where  pressure  causes  greatest  pain,  and  if  severe  it 
may  excite  convulsions  and  paraplegic  or  cataleptic  symptoms.  Tactile 
hypersesthesia  is  very  marked,  but  anesthesia  is  rare,  and  myalgia  may  co- 
exist with  pains  in  internal  organs.  In  about  half  the  cases  it  is  spon- 
taneous ;  its  character  is  very  variable,  but  its  seat  is  generally  at  the 
point  of  exit  of  the  nerves  from  the  spinal  column. 

Motor  disturbances  are  common.  Weariness,  heaviness,  and  pseudo- 
paraplegia  of  the  lower  limbs  follow  the  slightest  exertion.  Contraction 
occurs  in  some  muscles,  especially  those  of  the  forearm,  and  twitchings, 
spasms,  and  choreic  movements  may  be  present.  Cardiac  palpitation  is 
very  common  ;  and  nausea  and  vomiting,  nervous  cough,  embarrassed 
phonation,  deglutition,  and  breathing,  or  attacks  of  fainting  are  not  un- 
common. 

Patients  with  spinal  irritation  are  depressed,  melancholy,  and  irritable, 
and  subject  to  insomnia,  headache,  dizziness,  and  disturbances  of  the 
special  senses.  Yaso-motor  changes  are  marked.  The  extremities  are  cold, 
sometimes  blue,  and  the  face  alternately  pales  and  flushes. 

When  the  point  of  tenderness  is  in  the  cervical  region  the  pains  are  re- 
ferred to  the  head,  pharynx,  and  chest,  and  are  associated  with  psychical 
disturbances.  When  it  is  lower  there  are  respiratory  and  cardiac  symptoms, 
and  if  in  the  dorsal  region  it  is  accompanied  by  pain  in  the  stomach,  with 
dyspepsia,  nausea,  and  vomiting.  This  last  is  the  most  frequent  seat  of 
the  disease.  Lumbar  spinal  irritation  is  less  common  and  is  indicated  by 
neuralgic  pains  and  weakness  in  the  lower  limbs,  myalgia  in  the  abdomi- 
nal and  lumbar  regions,  spasm  of  the  vesical  and  anal  sphincters,  uterine 
and  ovarian  pains,  and  disorders  of  menstruation. 

In  many  cases  there  is  dysuria  and  vesical  spasm,  increased  desire  to 
urinate,  and  the  discharge  of  a  large  amount  of  pale,  limpid  urine  may 
occur.  Sometimes  the  liver,  kidneys,  or  bowels  are  the  seat  of  functional 
derangements.  The  disease  may  progress  slowly  or  it  may  be  of  short  du- 
ration, and  rapidly  become  severe  or  as  rapidly  improve. 

The  symptoms  are  always  variable  and  inconstant,  and  the  pains  often 
shift  from  one  part  to  another.  No  true  paralysis  of  limbs  or  of  the  sphinc- 
ters ever  occurs.  Sometimes  spinal  irritation  will  suddenly  pass  into  neu- 
rasthenia. 

»  Hammoud  calls  spinal  irritation  anoBmia  of  the  posterior  columns  of  the  cord. 


TETAKUS.  1057 

Differential  Diagnosis. — Spinal  irritation  may  be  mistaken  for  spinal  con- 
gestion,  meningitis,  myelitis,  tumors,  and  tetany. 

In  spinal  congestion  there  is  no  tenderness.  Paralytic  symptoms  are 
frequently  present,  and  gastric  and  cardiac  derangements  are  never  prom- 
inent. In  spinal  congestion  the  symptoms  are  aggravated  by  the  supine 
position,  in  spinal  irritation  the  reverse  is  the  case.  It  is  claimed  that  the 
subcutaneous  injection  of  one-thirtieth  grain  of  strychnine  will  aggravate 
the  symptoms  in  spinal  congestion,  while  in  spinal  irritation  its  adminis- 
tration affords  relief.  Spinal  irritation  is  of  much  longer  duration  than 
congestion. 

Spinal  meningitis  is  accompanied  by  pyrexia,  and  the  pain  in  the  spine 
is  increased  by  motion,  so  that  the  patient  assumes,  and  remains  in  a  fixed 
position.  The  pain  is  violent  and  diffused  in  meningitis,  and  muscular 
spasms  occur  in  the  back  and  neck,  which  are  never  present  in  spinal  irri- 
tation. 

The  presence  of  the  iron-band  sensation  about  the  waist,  paralyses,  vesi- 
cal irritation,  and  relaxation  of  the  sphincters,  and  anaesthesia,  especially 
in  the  early  part  of  the  disease,  are  almost  diagnostic  of  myelitis,  and  are 
never  met  with  in  spinal  irritation. 

Spinal  irritation  is  differentiated  from  spinal  tumors  by  the  fact  that  in 
the  latter  the  symptoms  are  localized,  permanent,  and  unaccompanied  by 
visceral  derangements,  which  in  irritation  assume  such  a  variety  of  forms. 

The  rare  disease  called  tetany  by  Trousseau  is  differentiated  from  spinal 
irritation  by  the  muscular  contractions,  which  are  accompanied  by  trem- 
bling, ansesthesia,  and  a  feeling  of  intense  fatigue. 

Prognosis. — The  prognosis  is  favorable,  although  after  apparent  recovery 
the  disease  is  apt  to  return.  Very  frequently  it  resists  treatment,  especially 
if  gout,  rheumatism,  scrofula  or  syphilis  exist. 

Treatment. — The  remedies  which  are  employed  in  the  treatment  of  anae- 
mia are  always  indicated  in  spinal  irritation.  Alcoholic  stimulants  are 
usually  of  service  and  in  many  cases  must  be  given  freely,  combined  with 
a  meat  diet  and  exposure  to  sunlight  and  fresh  air.  Injections  of  morphia 
or  atropia  combined  with  strychnine  should  be  given  over  the  site  of  ten- 
derness, the  dose  at  first  being  small  and  gradually  increased  to  the  point 
of  relieving  pain.  Aconite  and  veratria  may  be  applied  locally  in  the  form 
of  an  ointment.  The  galvanic  current  and  the  Faradic  current  in  some 
cases  will  give  immediate  relief.  The  daily  application  of  the  ice-poultice 
or  the  actual  cautery  is  highly  recommended.  Absolute  rest  in  the  coun- 
try with  a  highly  nutritious  diet  often  does  more  for  this  class  of  patients 
than  any  other  treatment. 

TETAIfUS. 

Tetanus  or  loch-jaw  is  a  tonic  spasm  with  paroxysmal  exacerbations  of 
the  voluntary  muscles  ;  those  of  the  lower  jaw,  neck,  and  pharynx  are  usu- 
ally first  affected.     Acute  and  chronic  varieties  are  recognized  ;  the  latter 
ia  called  tetanus  mitis. 
67 


1058  DISEASES    OF   THE   NERVOUS   SYSTEM. 

Morbid  Anatomy. — There  are  bo  constant  lesions  in  tetanus,  and  those 
which  are  commonly  present  are  quite  as  possibly  secondary  as  primary. 

In  traumatic  tetanus  the  nerves  supplying  the  affected  parts  are  some- 
times inflamed,  but  even  this  condition  is  not  invariably  present.  In  the 
cord  there  is  often  more  or  less  hypersemia,  with  slight  effusion,  and  per- 
haps extravasation.  This  is  frequently  attended  by  some  cedematous  soften- 
ing and  interstitial  exudation  of  finely  granular  or  structureless  matter, 
especially  in  the  gray  substance,  in  the  fissures,  and  on  the  surface  of  the 
cord.  Notwithstanding  the  frequent  occurrence  of  such  lesions  the  pecu- 
liar etiological  relation  which  injuries  bear  to  the  disease  renders  it  probable 
that  the  primary  disturbances  are  purely  functional  and  reflex  in  their 
nature,  or  due  to  some  peculiar  blood-poison.'  Tetanus  is  usually  traumat- 
ic and  may  follow  the  most  trivial  injury,  as  a  splinter  in  the  finger,  but 
is  more  apt  to  develop  after  compound  or  complex  fractures,  lacerated, 
crusbed,  and  punctured  wounds,  and  wounds  comjDlicated  by  the  presence 
of  foreign  bodies.  It  may  occur  after  abortion  or  normal  delivery,  and 
trismus  nascentium  is  ascribed  to  the  wound  at  the  navel. 

Climatic  conditions  have  a  distinctly  exciting  influence  in  the  production 
of  tetanus.  It  is  much  more  common  in  hot  than  in  temperate  climates, 
and  rapid  changes  of  temperature,  cold  and  wet,  are  especially  favorable  to 
its  development.  It  is  said  that  fright,  anxiety,  or  depression  markedly 
predisposes  to  its  occurrence,  as  in  armies  it  prevails  most  extensively  among 
the  defeated. 

Clinically,  tetanus  can  be  excited  by  strychnine,  ergotin,  brucine,  picro- 
toxin,  and  caffein.  Occasionally  tetanus  arises  from  unknown  influences, 
when  no  wound  or  abrasion  is  present  and  when  the  only  possible  assignable 
cause  is  exposure  to  wet  and  cold. 

Tetanus  may  occur  at  any  age  and  in  either  sex,  but  is  most  frequent  in 
adult  males. 

Symptoms. — Tetanus  generally  comes  on  in  from  six  to  twelve  days  after 
the  injury,  but  may  be  delayed  three  or  four  weeks  or  appear  within  a  few 
hours.  In  the  largest  number  of  cases  it  begins  with  stiffness  of  the  mus- 
cles of  the  neck  and  jaw.  This  quickly  extends  to  the  muscles  of  mastica- 
tion and  facial  expression  ;  the  patient's  jaw  becomes  locked  and  the  head 
fixed,  and  the  face  wears  a  peculiar  frown.  The  tonic  stiffness  is  aggra- 
vated by  every  attempt  to  use  the  muscles.  Deglutition  is  difficult,  and 
later  becomes  almost  impossible.  By  degrees  the  other  muscles  are  in- 
volved, the  trunk  is  stiff  and  more  or  less  curved,  the  abdomen  tense  and 
hard,  and  the  limbs  extended  and  rigid.  When  the  diaphragm  is  moved, 
a  sharp,  sudden  pain  shoots  through  the  body  from  the  ensiform  cartilage, 
which  is  considered  diagnostic.  It  is  accomjDanied  by  intense  dyspnoea. 
This  general  rigidity  of  the  muscles  is  continuous  and  progressive,  but  is 
marked  by  paroxysmal  attacks  in  which  all  the  symptoms  are  immensely 
exaggerated.  They  are  excited  by  any  muscular  action,  by  jars  and  other 
slight  causes,  or  may  occur  spontaneously.  During  a  spasm  all  the  muscles 
become  powerfully  contracted.     The  limbs  are  extended,  the  back  arched, 

1  Sir  T.  Watson. 


FACIAL   PARALYSIS.  1059 

and  the  face  assumes  the  risus  sardonicus.  The  head  is  retracted,  and 
the  patient  may  rest  only  on  his  head  and  heels.  The  respiratory  muscles 
suffer  also,  and  respiration  may  be  entirely  arrested,  and  the  face  become 
cyanotic.  As  the  paroxysm  passes  away  it  is  only  a  remission  ;  the  muscles 
are  still  hard  and  stiff,  the  jaw  closed,  and  the  respiration  rapid  and  shal- 
low. The  intense  cramping  pain  of  the  paroxysm  gives  place  to  a  heavy 
ache  and  soreness. 

Notwithstanding  the  severity  of  the  disease,  consciousness  and  intelli- 
gence are  rarely  impaired,  and  the  temperature  and  pulse-rate  are  only 
elevated  on  account  of  the  muscular  action.  Just  before  death,  however, 
in  many  instances,  there  is  a  rapid  and  enormous  rise  in  the  temperature, 
which  may  reach  112'^  or  114°  F.  The  urine  is  scanty,  the  bowels  are  con- 
stipated, and  the  body  is  bathed  in  a  profuse  sweat.  Reflex  irritability  is 
increased  to  a  high  degree  throughout. 

Differential  Diagnosis. — The  absence  of  headache,  delirium,  and  coma, 
and  a  normal  temperature  in  the  intervals  between  tlie  attacks,  will  suffice 
to  distinguish  tetanus  from  any  cerebral  or  cerehro-^pinal  inflammation. 

Hysteria,  hystero-epilepsy,  and  sometimes  ejjilepsy  may  simulate  it,  but 
the  development  of  the  disease  quickly  affords  a  diagnosis. 

Strychnia  poisoning  is  to  be  differentiated  by  the  history  of  the  case  and 
the  examination  of  voided  matter.  In  strychnia  poisoning,  consciousness 
is  lost,  and  the  muscles  of  the  jaw,  head,  and  neck  are  last  and  least 
affected. 

Prognosis. — Tetanus  usually  terminates  fatally  before  the  tenth  day  ;  but 
if  the  twelfth  day  be  passed  and  the  temperature  does  not  pass  102°  F., 
and  the  respiratory  muscles  are  not  involved  ;  or  if  the  disease  has  occurred 
at  a  remote  period  from  the  reception  of  the  wound,  the  outlook  is  quite 
hopeful.  When  the  patient  is  young,  when  strabismus  occurs,  or  the 
wound  is  very  recent,  and  when  rigidity  appears  early  the  case  is  nearly 
always  fatal. 

Treatment. — So  far  as  is  known,  no  treatment  has  any  controlling  effect 
upon  tetanus.  Innumerable  remedies  have  been  tried,  with  equally  bad 
results.  A  highly  nutritious  diet,  with  alcoholic  stimulants,  is,  perhaps, 
the  best  treatment.  Alimentation  must  be  carried  on  by  a  stomach-tube 
or  by  the  rectum.  Recently,  curare,  nitrite  of  amyl,  and  hydrate  of  chloral 
(in  forty-grain  doses)  seem  to  be  the  favorite  drugs.  Locally,  ice  and  cold 
effusions  to  the  spine  prove  beneficial,  although  hot  applications  are  more 
grateful  to  the  patient. 

The  utmost  care  should  be  taken  to  avoid  all  irritation  and  to  Keep  the 
patient  in  the  most  absolute  quiet. 

FACIAL    PARALYSIS. 

{Bell's  Paralysis.) 

Bell's  paralysis  is  a  paralysis  of  the  muscles  of  the  face  due  to  any  lesion 
implicating  the  nucleus  or  fibres  of  the  seventh  pair  of  nerves. 

Etiology. — It  may  be  caused  within  the  skull  by  blood  extravasations. 


1060  DISEASES    OF   THE    NERVOUS    SYSTEM. 

tumors,  and  inflammatory  products,  which  give  rise  to  pressure.  Fracture 
and  morbid  growths  may  cause  pressure  on  the  nerve,  in  its  passage 
through  the  cranial  bones,  sufficient  to  produce  the  paralysis.  It  may 
occur  in  connection  with  disease  of  the  internal  or  middle  ear  and  from 
local  neuritis.  Outside  the  skull,  blows,  wounds,  swellings  of  the  parotid 
gland  or  other  tumors  may  cause  it.  It  is  most  frequently  the  result  of  a 
draught  of  cold  air  on  the  side  of  the  face,  especially  while  sleeping. 

Symptoms. — Its  onset  is  usually  gradual  ;  but  when  fully  developed  its 
symptoms  are  striking  and  characteristic.  All  the  muscles  supjolied  by  the 
seventh  nerve  on  one  side  of  the  face  are  paralyzed.  The  forehead  is  smooth 
and  motionless  on  the  paralyzed  side,  the  corner  of  the  mouth  is  drawn  to 
the  opposite  side,  and  the  paralyzed  side  closes  less  perfectly  than  the  other. 
The  patient  cannot  close  the  eye  on  the  affected  side.  As  soon  as  the  face 
is  moved  the  paralysis  is  unmistakable.  Whistling  and  drinking  are  im- 
possible. Certain  letters,  as  P  and  B,  cannot  be  jDronounced;  food  collects 
between  the  cheek  and  teeth  on  the  palsied  side.  The  tears  run  down  over 
the  cheek,  and,  if  the  chorda  tympani  is  involved,  the  sense  of  taste  is  per- 
verted or  destroyed  on  one-half  of  the  anterior  portion  of  the  tongue.  At 
the  same  time  the  salivary  secretion  is  diminished.  The  uvula  is  usually 
deflected;  the  alaof  the  nose  becomes  flaccid,  and  the  nostril  on  the  affect- 
ed side  is  narrowed  and  loses  its  rotundity.  Imperfect  closure  of  the  eye 
exposes  the  organ  to  all  sorts  of  injuries,  hence  disease  of  the  cornea  and 
conjunctiva  is  very  common.  During  the  first  two  or  three  days  the  mus- 
cles show  increased  irritability  to  the  electrical  current ;  but  they  gradually 
lose  their  Faradic,  while  they  retain  their  galvanic  irritability. 

DiiFerential  Diagnosis. — When  otorrhoea,  disturbances  of  hearing,  obliquity 
of  the  uvula,  diminished  salivary  secretion,  and  loss  of  taste  occur,  the  origin 
of  the  paralysis  is  within  the  aquseductus  Fallopii.  When  the  taste  is  nor- 
mal and  the  uvula  straight  the  cause  is  usually  peripheral,  e.  g.,  cold.  In 
these  cases  also  electro-muscular  contractility  is  rapidly  lost.  The  origin 
may  be  supposed  to  be  central  when  other  nerves  are  involved.  Bell's  palsy 
is  usually  associated  with  paralysis  of  the  sixth  nerve. 

Prognosis. — In  organic  disease  of  the  brain  or  with  lesions  of  bone  the 
prognosis  is  unfavorable.  When  arising  from  cold,  slight  injuries,  or  syph- 
ilis the  prognosis  is  favorable.  Complete  recovery  is  usually  reached  in  two 
or  three  months.  There  is  no  rule  by  which  one  can  estimate  its  duration. 
The  more  the  electro-muscular  contractility  is  diminished  the  less  the 
chances  of  complete  recovery. 

Treatment. — When  due  to  cold,  apply  a  few  leeches  to  the  mastoid  proc- 
ess, followed  by  hot  fomentations  ;  subsequently  blisters  behind  the  ear  and 
other  counter-irritants  may  be  resorted  to,  and  the  alternate  Faradic  and 
voltaic  currents  are  to  be  relied  upon.  Massage  and  shampooing  may  be 
tried.  Cowers  recommends  inunctions  of  oleate  of  morphia.  When  due 
to  syphilis,  anti-syphilitics  are  indicated.  Niemeyer  recommends  mercu- 
rial ointment. 


PAKALYSIS   AGITAK8.  lOGl 


PAEALTSI8    AGITANS. 


Shaking  palsy,  or  the  trembles,  is  a  disease  of  advanced  life  characterized 
by  motor  weakness  and  tremors  of  the  voluntary  muscles,  especially  of  the 
limbs,  occurring  independently  of  muscular  exertion,  which  are  finally  fol- 
lowed by  paralytic  symptoms. 

Morbid  Anatomy. — As  yet  no  constant  changes  have  been  discovered. 
Some  authorities  consider  it  of  spinal,  others  of  cerebral  origin.  Among 
the  former  are  Charcot,  Lebert,  Marshall  Hall,  and  Rosenthal.  Among 
the  latter  are  Oppolzer  and  Skoda.  Senile  changes  in  the  brain  and  cord 
are  found  in  a  certain  number  of  cases.  There  may  be  sclerotic  jiatches  in 
the  pons,  the  medulla  oblongata,  the  optic  thalamus,  and  hippocampus 
major,  and  Charcot  has  found  increase  of  the  ei3ithelium  of  the  central 
canal  in  the  cord  with  pigmentation  of  the  cells  in  the  j)osterior  columns 
of  Clark.  Diseased  arteries  and  slight  sanguineous  exudations  have  also 
been  noticed. 

Etiology. — Earely  occurring  before  forty,  the  liability  to  it  is  increased 
every  year  thereafter.  It  is  more  common  in  men  than  women,  and  occurs 
chiefly  in  the  lower  classes.  Violent  emotions,  as  grief,  fear,  anger  or  dis- 
tress of  mind,  degeneration  of  the  heart  and  vessels,  and  great  bodily 
fatigue  and  exposure,  are  among  its  exciting  causes.  There  are  no  indica- 
tions that  the  disease  is  hereditary. 

Symptoms. — In  nearly  all  cases  paralysis  agitans  is  insidious  in  its'  ap- 
proach, and  begins  in  one  foot,  hand,  or  possibly  a  single  finger  or  the 
thumb,  as  a  slight  oscillating  motion,  which  is  quite  rhythmical  and  charac- 
teristic. For  a  time  this  trembling  may  be  intermittent,  but  appears  with- 
out any  apparent  cause  and  unexpectedly.  In  this  early  stage  it  can  possi- 
bly be  arrested  by  an  effort  of  the  will,  a  condition  in  marked  contrast 
with  the  very  decided  increase  in  the  tremor  which  late  in  the  disease 
follows  every  effort  to  control  the  muscles.  As  the  disease  advances  simi- 
lar oscillating  movements  affect  the  muscles  of  the  forearm,  arms  and 
shoulder,  and  the  entire  limb  is  in  a  continuous  tremble.  The  remaining 
limb  of  the  affected  side  usually  becomes  involved  before  the  disease  crosses 
the  median  line.  Pain,  weariness  and  stiffness  in  the  affected  muscles  pre- 
cede, in  some  cases,  the  development  of  the  characteristic  tremors ;  or  the 
disease  may  attain  its  full  development  through  a  series  of  increasingly  fre- 
quent sudden  attacks  of  tremor  lasting  only  a  few  days  each. 

At  the  height  of  the  disease  nearly  all  the  limbs  are  involved  in  an  inces- 
sant motion  which  is  liable  to  severe  exacerbation  upon  muscular  exertion 
or  during  mental  disturbance,  and  which  ceases  only  during  sleep  or  anses- 
thesia. 

Later  on,  rigidity,  painful  cramps,  and  contractions  affect  not  only  the 
muscles  of  the  limbs  but  also  those  of  the  trunk,  neck  and  face,  giving  the 
patient  quite  a  characteristic  appearance.  The  countenance  assumes  a 
fixed,  staring  look  of  distress,  the  head  is  drawn  forward  and  the  trunk 
flexed  ;  the  lower  limbs  and  arms,  which  are  drawn  away  from  the  side. 


1062  TSEASES    OF   THE    NEEVOUS   SYSTEM. 

are  rigid,  and  all  the  joints  are  flexed,  often  causing  marked  deformity  of 
the  hands.  Altliough  the  rigidity  of  the  limbs  does  not  prevent  walking, 
the  patient's  gait  is  characteristic.  As  he  rises,  or  when  he  stands,  there 
is  great  unsteadiness  and  difl&cnlty  in  maintaining  equilibrium,  which,  as 
he  starts  to  walk,  causes  him  to  run  forward  to  avoid  falling.  This  dis- 
turbance of  equilibrium  is  not  associa.ted  with  vertigo. 

The  muscles  of  respiration  and  deglutition  are  not  involved,  but  the  voice 
is  often  tremulous  and  speech  is  slow,  hesitating  and  laborious,  so  that 
words  are  distinctly  broken  up  into  syllables.  Although  muscular  move- 
ments are  attended  with  extreme  fatigue,  the  force  of  the  contractions  is 
but  slightly  diminished  until  late  in  the  disease,  when,  from  increase  in  the 
rigidity,  the  patient  takes  to  his  bed,  and  the  muscles  suffer  in  their  nutri- 
tion or  become  distinctly  fatty. 

As  the  end  approaches,  the  memory  and  intelligence  fail  in  connection 
with  the  generally  defective  nutrition.  Although  the  disease  may  last  for 
twenty  or  thirty  years,  death  most  commonly  results  from  some  intercur- 
rent disease. 

DiiFerential  Diagnosis. — In  disseminated  sclerosis  tremors  occur  only 
when  the  muscles  are  in  use  ;  the  disease  begins  in  the  lower  limbs,  affects 
younger  persons,  and  paralysis  occurs  early.  The  patient  has  no  tendency 
to  run  forward,  and  does  not  present  the  peculiar  physiognomy  of  shaking 
palsy.  Senile,  alcoholic,  lead  and  mercurial  trembling  are  readily  diagnos- 
ticated by  the  previous  history  and  concomitant  symptoms. 

Prognosis. — Paralysis  agitans  is  a  very  chronic  disease,  and  the  outlook  is 
never  favorable.  It  may  last  twenty-five  years.  After  a  few  years  the 
muscles  waste,  the  patient  is  confined  to  his  bed,  there  is  physical  and 
mental  exhaustion,  bed-sores  form,  and  death  results  from  asthenia  or 
complications.  The  more  common  complications  are  acute  lobar  pneu- 
monia and  pleurisy.  Paralysis  agitans  has  been  recovered  from  in  the 
early  stages,  but  Eulenberg  says  that  there  is  reason  to  doubt  the  diagno- 
sis in  such  cases.  ^ 

Treatment. — No  definite  results  have  been  attained  by  the  use  of  any 
remedy.  All  the  nerve  stimulants,  tonics,  and  sedatives  have  been  em- 
ployed, of  which  Charcot  considers  hyoscyamus  the  only  useful  one,  and 
the  effects  of  this  are  temporary.  The  constant  current  has  seemed  to 
have  some  value  as  a  distinctly  curative  agent.  Beyond  this,  general  tonic 
treatment  is  the  most  that  can  be  attempted,  and  this  should  never  be 
omitted. 

LOCALIZED    SPASM   AOT3   PAEALYSIS. 

{Scrivener's  Palsy,  etc.) 

Writer's  cramp  is  one  of  the  more  common  varieties  of  anomalous  mus- 
cular movements,  or  of  those  diseases  which  Duchenne  calls  "  functional 

1  Handfield  Jones  thinks  that  there  are  two  forms  :  one,  entirely  incurable,  occuring  in  old  persons  and 
depending  upon  organic  changes  in  the  central  nervous  system  ;  the  other,  in  younger  persons,  curable 
and  probably  not  dependent  upon  organic  changes. 


LOCALIZED   SPASM   AND   PARALYSIS.  1063 

impotences."  Of  essentially  the  same  nature  are  piano-players'  cramp  and 
the  inability  of  tailors,  dairymen,  bricklayers,  or  telegraphers  to  execute 
movements  to  which  they  have  long  been  accustomed. 

Morbid  Anatomy. — It  has  been  thought  that  degenerative  changes  occur 
in  the  spinal  cord,  but  according  to  Dr.  Eeynolds  these  diseases  are  due  to 
a  perverted  nutrition  of  these  parts. 

Duchenne  believes  that  the  primary  change  is  in  the  nei-ve  centres,  and 
gives  as  a  strong  argument  in  favor  of  this  view  the  fact  that  the  malady  very 
quickly  affects  the  left  hand,  when  this  is  used  to  supply  the  right  in  one 
who  has  writer's  cramp.  Dr.  Poore,  however,  suggests  that  the  lesion  in 
typical  cases  is  at  the  periphery,  either  in  the  muscles  themselves,  or  in  their 
terminal  motor  nerves.  He  attributes  the  disease  to  over-use  and  over- 
fatigue, not  to  central  changes ;  and  states  that  muscles  which  are 
trained  to  worlc  in  order  together  no  longer  do  so  when  even  one  of  them 
fails. 

Etiology. — Writer's  cramp,  like  other  similar  conditions,  as  from  violin  or 
piano-playing,  telegraphing,  mili^ing,  etc.,  is  for  the  most  part  induced 
by  long-continued  use  of  the  affected  muscles. 

Symptoms. — It  will  be  sufficient  to  describe  writer's  cramp  as  a  type  of 
all  this  class  of  spasms,  since  they  differ  only  in  the  muscles  involved.  It 
generally  commences  with  a  sense  of  weight  or  stiffness  in  the  affected 
muscles,  together  with  discomfort  and  indefinite  pain,  which  is  perhaps 
relieved  by  strong  contractions  or  stretching  the  muscles.  This  uneasi- 
ness slowly  increases,  and  there  is  added  a  tendency  to  spasmodic  movements 
which  renders  the  handwriting  irregular  and  covered  with  unnecessary 
lines. 

The  pain  and  spasm  at  first  follow  only  prolonged  use  of  the  pen,  but 
soon  are  induced  very  readily,  until  at  length  all  attempts  at  writing  are 
abandoned.  In  the  earlier  stages  the  patient  is  able  to  control  the  spasms 
somewhat  and  to  relieve  them  by  holding  his  pen  in  an  unusual  way  or 
by  some  other  device.  For  a  time  also  after  more  delicate  manipulations 
are  impossible,  he  can  still  perform  coarser  operations,  but  the  disease  al- 
most invariably  extends  so  long  as  the  muscles  are  kept  in  use,  and  may 
result  in  severe  spasm  whenever  any  attempt  is  made  to  use  the  hand  in 
writing.  Occasionally  it  assumes  a  paralytic  form  and  the  patient  is  un- 
able to  hold  a  pen  at  all,  or  pain  may  be  a  prominent  symptom,  radiating 
up  the  arm  as  a  severe  neuralgia. 

The  disease  may  affect  any  or  all  the  muscles  of  the  hand  or  arm,  and  it 
rarely  extends  to  the  shoulder  and  trunk.  More  commonly  the  extensors 
and  flexors  of  the  thumb  or  index  finger  are  affected,  but  though  there  is 
generally  a  distinct  loss  of  power  the  muscles  act  perfectly  in  any  motions 
save  those  which  induced  the  disease. 

In  the  other  forms  of  local  spasm  the  general  history  will  be  the  same, 
and  the  deformities  and  disturbances  will  depend  entirely  upon  the  action 
of  the  muscles  implicated.  It  is  more  likely  to  occur  in  those  who  merely 
copy  than  those  who  write  an  equal  amount,  but  think  at  the  same  time — 
as  authors  and  journalists. 


1064  DISEASES   OF  THE   NERVOUS  STrriTEM. 

Differential  Diagnosis. — The  history  of  the  case  is  all-important,  and  will 
generally  be  sufficient  for  a  diagnosis. 

Lead  palsy,  with  which  scrivener's  palsy  maybe  confounded,  is  generally 
preceded  by  several  attacks  of  lead  colic  ;  there  is  the  peculiar  blue  line  at 
the  margin  of  the  teeth,  the  skin  assumes  an  earthy  hue,  and  the  "  drop- 
wrist"  exists,  conditions  which  do  not  occur  in  writer's  cramp. 

Paralysis  agitans,  disseminated  sclerosis,  and  the  trembling  due  to  old 
age  or  to  chronic  alcoJiolisinus  will  be  readily  differentiated  by  the  bistory. 

Prognosis. — The  prognosis  is  favorable.  The  shorter  the  duration  of  the 
condition,  and  the  greater  the  opportunity  the  patient  has  to  give  the  part 
rest,  the  better  the  outlook.  Writer's  cramp  is  much  more  easily  relieved 
in  the  weak  and  nervous  than  in  the  strong  and  robust. 

Treatment. — Absolute  rest  is  essential,  and  will  sometimes  alone  be  suffi- 
cient for  a  cure.  The  mild  galvanic  current,  blistering  along  the  nerve- 
trunks,  should  they  be  tender,  and  rhythmical  exercise  of  the  affected  mus- 
cles short  of  fatigue,  is  otten  of  marked  service.  Morphine  hypodermically 
may  relieve,  but  does  not  effect  a  cure.  The  mind  and  body  must  have  rest 
as  well  as  the  muscles.  Hypodermic  injections  of  atropia,  strychnia,  and 
Fowler's  solution  have  been  used  with  success.  Massage  to  the  part  is  rec- 
ommended by  Beard.  In  my  experience  the  only  course  which  has  been 
followed  by  markedly  beneficial  results  has  been  absolute  rest  of  the  affected 
muscles,  with  sea  bathing  and  the  internal  use  of  iron. 

CHEOlSriC  LEAD  poiso]snKa. 

(Lead  Palsy.) 

This  is  a  morbid  condition  produced  by  the  introduction  of  tbe  salts  of 
lead  into  the  system,  either  through  the  mucous  surfaces  or  the  skin. 

Morbid  Anatomy. — After  the  salts  of  lead  have  been  received  into  the 
system,  they  become  deposited  in  various  tissues  or  are  discharged  by  the 
emunctories.  They  have  been  found  in  all  the  tissues  of  the  body.  They 
are  eliminated  mainly  by  the  kidneys.  In  the  paralysis  caused  by  lead 
poisoning  the  muscles  and  nerves  are  early  affected  ;  later  the  nerve- 
centres  become  implicated.  It  is  probable  that  the  lead  deposited  in  the 
affected  tissues  impairs  their  function  and  leads  to  their  degeneration  when 
the  paralysis  has  existed  for  a  long  time. 

Etiology. — The  sources  of  lead  poisoning  are  numerous  :  painters  and 
workers  in  lead  are  those  most  frequently  affected.  Drinking-water,  wines, 
and  ales  frequently  become  impregnated  with  it,  and  then  become  a  source 
of  infection.  The  application  of  lead  powder  as  a  cosmetic  to  the  face  and 
neck  has  caused  lead-poisoning.  Some  persons  are  much  more  susceptible 
to  its  poisonous  influences  than  others  ;  I  have  known  a  few  doses  of  lead 
taken  as  a  medicine  to  give  rise  to  pronounced  symptoms  of  lead  poisoning. 

Symptoms. — The  general  health  of  those  who  are  the  subjects  of  chronic 
lead  poisoning  is  always  more  or  less  impaired.  Their  skin  becomes  sallow, 
dry  and  harsh,  they  suffer  from  dyspeptic  symptoms,  loss  of  appetite,  and 


CHRO]SriC    LEAD    POISO]SriN"G.  1065 

constipation.  A  blue  line  forms  along  the  edge  of  the  gums  immediately 
adjoining  the  teeth,  which  is  regarded  by  some  as  diagnostic  of  lead  poison- 
ing— it  is  often  present  in  those  working  in  lead  who  are  free  from  other 
symptoms. 

The  most  important  and  characteristic  symptoms  are  intestinal  colic, 
and  affections  of  the  nervous  system.  Lead  colic  has  been  considered  in 
the  list  of  Intestinal  Diseases.  The  most  frequent  of  the  nervous  affections 
is  drop- wrist  from  paralysis  of  the  extensors  of  the  fore-arm.  It  generally 
comes  on  gradually  after  one  or  two  attacks  of  colic.  Sometimes  its  ad- 
vent is  sudden.  In  painters  the  right  hand  is  first  affected,  but  after  a 
time  both  hands  are  involved.  The  signs  of  lead  palsy  are  loss  of  power 
over  the  extensor  muscles  of  the  fore-arm  ;  first  the  patient  is  unable  to  ab- 
duct the  thumb,  then  to  extend  the  finger,  then  to  extend  the  hand  on  the 
fore-arm,  and  the  hand  drops  when  the  arm  is  held  in  a  prone  position. 
The  paralysis  is  generally  limited  to  the  muscles  supplied  by  the  radial 
nerve. 

The  paralyzed  muscles  waste  rapidly  and  lose  to  a  greater  or  less  degree 
their  electro-contractility ;  there  is  no  loss  of  sensation  in  the  paralyzed 
limb,  and  not  infrequently  it  is  the  seat  of  severe  joains  and  tenderness. 
In  some  instances  other  muscles  besides  those  of  the  fore-arm  are  affected, 
as  the  deltoid  and  triceps,  and  the  palsy  may  involve  the  muscles  of  the 
lower  extremity,  especially  the  extensors  of  the  foot  and  leg.  In  rare  in- 
stances all  the  voluntary  muscles  are  involved.  G-outy  subjects  are  pe- 
culiarly susceptible  to  lead  poisoning,  and  in  such  cases  the  cirrhotic  kidney 
almost  always  exists,  giving  rise  to  albuminuria  and  the  other  phenomena 
of  the  cirrhotic  form  of  Bright's  disease. 

This  condition  is  often  accompanied  by  amaurosis  and  other  grave  ner- 
vous symptoms. 

Differential  Diagnosis. — The  diagnosis  of  lead  colic  has  been  considered 
under  the  head  of  Intestinal  Colic.  Lead  palsy  may  be  distinguished  from 
other  forms  of  palsy,  by  the  history  of  the  case,  by  the  absence  of  cerebro- 
spinal disturbance,  and  by  the  blue  line  on  the  gums.  When  the  muscles 
of  a  paralyzed  limb  respond  to  the  influence  of  the  electric  current  lead 
poisoning  may  be  excluded. 

Prognosis. — Chronic  lead  poisoning  is  rarely  a  direct  cause  of  death, 
although  it  may  exist  for  years,  the  longer  its  duration  the  less  pvosjDCct 
there  is  of  complete  recovery.  Extreme  wasting  of  the  paralyzed  muscles 
with  loss  of  electric  contractility  renders  the  prognosis  unfavorable.  In 
some  instances  the  muscular  power  may  be  regained  when  the  excitability 
does  not  return. 

In  most  cases  the  general  health  is  not  seriously  impaired,  and  the  re- 
covery from  the  paralysis,  if  not  complete,  is  partial.  The  fatal  cases  are 
those  which  have  been  a  long  time  exposed  to  the  jjoisonous  influence  of 
lead,  and  who  have  been  intemperate. 

Treatment. — The  first  thing  to  be  accomplished  is  to  remove  the  patient 
from  all  sources  of  lead  poisoning.  Extreme  personal  cleanliness  is  im- 
portant for  those  who  cannot  avoid  such  exposure.     The  habitual  use  of 


1066  DISEASES    OF   THE   NERVOUS   SYSTEM. 

lemonade  made  with  sulphuric  acid  is  regarded,  to  some  extent,  as  pro- 
tective ;  it  acts  by  converting  the  carbonate  and  other  salts  of  lead  in  the 
stomach  into  the  insohible  sulphate.  Various  methods  have  been  proposed 
for  removing  the  lead  from  the  system,  the  most  effective  of  which  is  baths 
containing  some  soluble  sulphide.' 

Iodide  of  potassium  is  recommended  on  the  ground  that  the  iodide 
makes,  with  the  insoluble  salts  of  lead  deposited  in  the  tissue,  a  new  soluble 
salt,  which  can  be  eliminated  by  the  kidneys.  Its  administration  should 
begin  with  fifteen  grains  a  day,  and  be  gradually  increased  to  thirty  grains 
a  day ;  it  may,  in  anaemic  subjects,  be  combined  with  chloride  of  iron.  The 
bowels  should  always  be  kept  freely  open. 

The  only  effectual  remedy  for  restoring  the  paralyzed  muscle  is  electric- 
ity in  the  form  of  Faradization.  Its  application  should  not  be  continued 
more  than  ten  or  fifteen  minutes  three  times  a  day  for  two  or  three  months. 
Severe  shocks  should  be  carefully  avoided,  although  a  current  of  high 
tension  causes  no  movement  in  the  paralyzed  muscles.  It  is  important  that 
each  paralyzed  muscle  should  be  treated  separately. 

CHEONIO    MEECIJEIALISM. 

{Mercurial  Tremor.) 

Chronic  mercurial  poisoning  may  result  from  the  long-continued  intro- 
duction of  mercury  into  the  system,  either  through  the  stomach,  respiratory 
organs,  or  skin. 

Morbid  Anatomy. — ISTo  characteristic  lesions  have  been  discovered  in  those 
who  have  died  of  chronic  mercurialism,  except  the  deposit  of  mercury  in 
the  tissues,  especially  the  brain,  liver  and  kidneys. 

Etiology. — Workers  in  mercury,  as  gilders,  looking-glass  manufacturers, 
and  those  engaged  in  quicksilver  mining,  are  those  who  chiefly  suffer  from 
chronic  mercurialism,  although  it  may  result  from  its  long-continued 
medicinal  use.  Those  who  are  exposed  to  its  fumes  are  especially  liable 
to  its  poisonous  effects. 

Symptoms. — The  manifestations  of  chronic  mercurialization  are  mainly 
confined  to  the  nervous  and  muscular  system,  and  may  be  designated  as 
mercurial  tremors.  Its  first  indication  is  a  tremulousness  of  the  hands 
and  arms,  accompanied  by  numbness  and  tingling,  with  pain  in  the 
joints.  These  symptoms  may  continue  for  years  without  interfering 
materially  with  the  general  health  of  the  individual ;  but  sooner  or  later 
the  entire  muscular  system  becomes  invaded,  and  speech,  deglutition,  and 
respiration  are  more  or  less  interfered  with.  Choreic  movements  occur, 
the  patient  is  unable  to  walk  or  stand  without  assistance,  and  the  face  \h 
contorted  by  muscular  spasms  ;  while  the  patient  is  in  the  recumbent  pos- 
ture and  makes  no  muscular  efforts,  the  muscular  spasms  cease,  but  as 
soon  as  he  attempts  to  stand  or  move,  the  choreic  movements  commence. 

In  an  advanced  stage  of  the  disease  the  convulsive  movements  do  not 

1  Dr.  Pereira  recommends  baths  medicated  by  dissolving  sulphide  of  potassium  in  the  proportion  of 
two  ounces  in  fifteen  gallons  of  water. 


VEETIGO.  10G7 

entirely  cease  wlien  the  joatient  is  in  the  recumbent  posture.  After  the 
tremors  have  continued  for  a  long  time  and  have  been  severe,  the  patient 
loses  appetite,  becomes  sallow  and  emaciated,  and  cerebral  symptoms  de- 
velop, the  most  constant  of  which  are  headache,  vertigo,  delirium,  and 
epileptic  convulsions. 

LifFerential  Diagnosis. — Mercurial  tremor  may  be  confounded  with  mul- 
tiple sclerosis,  paralysis  agitans,  and  chorea.  But  a  history  of  exposure 
to  mercurial  poisoning,  and  the  fact  that  the  nervous  symptoms  were  pre- 
ceded by  ptyalism,  ulcerated  gums,  mercurial  fetor  of  the  breath,  nausea, 
colicky  pains  and  diarrhcBa,  are  generally  sufficient  to  establish  a  diagnosis. 
It  is  also  to  be  remembered  that  in  paralysis  agitans  the  muscles  of  the 
head  and  neck  are  not  involved  in  the  convulsive  movements,  and  that  the 
position  of  the  patient  does  not  influence  the  spasms. 

Prognosis. — Mercurial  tremor  does  not  often  directly  cause  death,  but  if 
exposures  to  the  causes  of  mercurial  poisoning  are  continued,  death  may 
result  from  exhaustion,  intestinal  or  cerebral  complications,  or  from  in- 
tercurrent disease. 

Treatment. — As  soon  as  any  of  the  symptoms  of  mercurial  poisoning  are 
present,  the  individuals  must  immediately  be  removed  from  all  chance  of 
exposure  to  the  poison.  If  this  cannot  be  effected,  and  they  are  compelled 
to  continue  occupations  where  they  are  exposed  to  the  fumes  of  mercury, 
they  must  wear  a  protection  over  their  face,  and  exercise  the  greatest  per- 
sonal cleanliness. 

Drugs  are  of  little  service,  the  treatment  is  altogether  prophylactic. 

VERTIGO. 

Vertigo  has  been  well  defined  as  the  consciousness  of  disordered  equili- 
bration. It  may  vary  from  an  uncomfortable  sensation  to  one  in  which  the 
patient  is  unable  to  maintain  his  equilibrium.  It  may  be  momentary  or  of 
long  duration. 

Morbid  Anatomy. — Lesions  are  only  found  in  labyrinthine  or  apoplecti- 
form vertigo,  called  Meniere's  disease  ;  all  other  varieties  are  purely  func- 
tional. In  aural  vertigo  there  may  be  found  hemorrhage,  congestion,  or 
inflammation  of  the  labyrinth  ;  or  there  may  be  evidences  of  otitis  media, 
obstruction  of  the  Eustachian  tube,  or  the  presence  of  foreign  bodies  which 
press  upon  the  tympanic  membrane. 

Etiology. — Vertigo  has  been  divided  into  ocular,  aural,  stomachic,  ner- 
vous, epileptic,  and  gouty. 

I.  Paralysis  of  a  single  muscle  may  cause  ocular  vertigo. 

II.  Meniere's  disease  may  be  caused  by  disease  of  the  semicircular 
canals  and  cochlea,  tympanic  catarrh,  or  spasm  of  the  tensor  tympani, 
paralysis  of  the  stapedius,  or  by  syringing  the  ears,  esi^ecially  when  the 
tympanic  membrane  is  perforated.  Wax  and  foreign  bodies  in  the  meatus 
externus  may  also  induce  it. ' 

'  Knapp  believes  that  there  is  always  either  a  hemorrhage  or  serous  or  purulent;  exudation  ii>to  the  semi- 
circular canals. — Archiv.  Ophth.  and  Otol.,  vol.  ii.,  No.  1. 


1068  DISEASES   OE   THE   NERVOUS   SYSTEM. 

III.  Gastric  vertigo  is  the  most  common,  and  is  an  almost  invariable 
attendant  on  dyspepsia.  Hepatic  disorders,  perhaps  cholsemia,  or  choles- 
tersemia  may  induce  it. 

IV.  Nervous  vertigo  is  induced  by  physical  or  nervous  excesses,  and 
Eamskill  ranks  vertigo  from  overwork  as  next  to  gastric  in  frequency. 
Those  who  are  ill-fed  and  overworked  are  predisposed  to  it.  It  is  also 
caused  by  excessive  use  of  tea,  coffee,  tobacco,  and  alcohol.  Vertigo  is 
commonly  present  in  megrim  or  sick  or  nervous  headache. 

V.  Epileptic  vertigo  precedes  an  epileptic  seizure,  and  usually  does  not 
occur  without  a  well-marked  paroxysm.  Vertigo  is  also  a  common  symp- 
tom in  many  diseases  of  the  nervous  system,  such  as  cerebral  tumors,  cere- 
bral apoplexy,  sclerosis,  tabes,  and  cerebellar  disease. 

VI.  Gouty  vertigo  is  due  to  the  blood-changes  which  characterize  the 
gouty  diathesis.  The  vertigo  of  the  aged  is  a  result  of  disordered  cerebral 
circulation,  produced  by  the  senile  condition  of  the  heart  and  vessels. 
Chronic  malarial  infection  frequently  induces  "  cachsemic  "  vertigo. 

Symptoms. — The  sensation  may  be  that  of  objects  moving  around  the  pa- 
tient, or  of  the  patient  moving  around  objects  which  remain  stationary. 
There  may  be  a  feeling  of  confusion  or  instability,  or  the  movements  may 
be  uncertain  and  unsteady.  More  or  less  suddenly  a  giddy  sensation  comes 
on,  objects  become  indistinct,  the  patient  staggers,  and  perhaps  falls,  un- 
less he  grasps  something  to  steady  himself.  There  is  no  loss  of  conscious- 
ness. Nausea  and  vomiting  are  not  infrequent,  and  there  is  ringing  in  the 
ears,  fluttering  in  the  heart,  and  external  sounds  are  greatly  magnified. 

The  first  symptoms  in  ocular  vertigo  will  be  running  together  of  the 
letters  on  the  page,  headache,  nausea,  and  pains  in  the  eyes.  In  Meniere^ s 
disease  slight  or  serious  tinnitus  aurium  accompanies  the  vertigo.  Sud- 
denly it  becomes  greatly  exaggerated,  and  the  patient  feels  as  if  he  were  in 
motion,  or  actually  moves  in  a  direction  opposite  to  the  side  on  wliich  the 
ear  is  affected.  The  motion  may  be  forwards  or  backwards,  to  one  side,  or 
about  a  vertical  axis.  These  patients  may  be  thrown  to  the  ground,  so  in- 
tense are  the  movements.  The  eyes  sometimes  oscillate.  Consciousness  is 
rarely  lost. 

After  the  attack  of  vertigo  passes  off  deafness  remains.  The  vertigo  and 
vomiting  may  continue  for  some  time,  and  are  increased  by  the  uiDright 
position.  One  attack  follows  another,  until  a  persistent  vertiginous  state 
is  reached.     When  permanent  deafness  occurs,  the  vertigo  ceases. 

Gastric  vertigo  is  accompanied  by  dyspeptic  symptoms,  nausea,  pyrosis, 
heartburn,  flatulence,  diarrhoea,  or  constipation  with  pain  and  fulness  in 
the  hypogastrium.  It  is  often  so  severe  and  sudden  in  its  onset  that  the 
patient  thinks  he  is  soon  to  have  a  stroke  of  paralysis.  The  mental  state 
is  often  deplorable,  and  true  melancholia  may  ensue. 

Nervous  vertigo  is  apt  to  occur  after  excessive  mental  effort :  the 
patient  while  standing  experiences  a  dizzy,  sick  sensation,  which  is  rarely 
severe  ;  objects  seem  to  whirl  for  a  moment,  and  there  is  a  slight  tendency 
to  fall.  This  form  of  vertigo  not  infrequently  precedes  softening  of  the 
brain  in  those  who  are  overworked  and  badly  nourished.     Irritability^ 


NEURALGIA.  1069 

restlessness  and  insomnia  often  accompany  it.  And  though  gastric  dis- 
turbances may  be  present,  their  relief  is  not  followed  by  a  relief  of  the 
vertigo.  Sick  headaches  are  frequently  accompanied  by  nausea,  vomiting 
and  this  form  of  vertigo. 

In  epileptic  vertigo  the  vertiginous  sensation  either  replaces  the  fit  or 
accompanies  it.  After  a  paroxysm  of  gouty  arthritis  an  attack  of  vertigo 
is  not  uncommon. 

Differential  Diagnosis. — The  vertigo  of  Meniere's  disease  may  be  distin- 
guished from  that  of  epilepsy,  apoplexy,  gastric  dera^igements  and  the  other 
causes  of  vertigo,  by  the  co-existence  of  tinnitus  aurium,  deafness,  com- 
bined with  syncope,  nausea  and  vomiting.  The  movements  are  in  a  uni- 
form direction  and  tingling  and  numbness  are  absent.' 

An  otoscopic  examination  should  be  made  in  all  cases  of  continued- 
vertigo,  and  the  tuning-fork  and  watch  test  should  be  employed. 

Prognosis. — Vertigo  in  the  adult,  unaccompanied  by  visceral  diseases,  is 
not  dangerous.  In  Meniere's  disease,  when  the  labyrinthine  affection  is 
due  to  some  remediable  defect,  the  disease  will  subside  on  removal  of  the 
cause — such  as  cerumen,  tympanic  catarrh,  etc.  When  the  lesion  is  pri- 
marily of  the  labyrinth,  a  certain  degree  of  deafness  and  tinnitus  always 
remains,  and  recurrence  of  the  attack  is  to  be  anticipated.  The  longer 
an  attack  has  existed  the  better  the  prognosis. 

Treatment. — Gastric  vertigo  demands  the  treatment  already  given  under 
the  head  of  dyspepsia.  When  disorders  of  vision  are  the  cause  of  vertigo, 
rest  for  the  eyes  and  properly  adjusted  glasses  will  remove  it.  In  Me- 
niere's disease  the  patient  should  be  placed  in  the  recumbent  jDOsture  and 
a  full  dose  of  bromide  of  potassium  or  ammonium  given,  followed  by  qui- 
nine in  full  doses.  Charcot  states  that  this  plan  is  attended  by  the  best 
results.  ^ 

In  nervous  vertigo,  iron,  quinine,  strychnine,  and  the  removal  of  the 
cause  are  sufficient.  In  the  overworked  and  under-fed,  wine,  hypophos- 
phites  and  a  nutritious  diet  are  indicated. 

The  vertigo  of  old  age  is  benefited  by  the  bichloride  of  mercury  and  the 
tincture  of  iron ;  a  highly  nutritious  diet  and  small  doses  of  Burgundy 
wine  are  also  of  service  in  such  cases. 

NEFEALGIA. 

The  term  neuralgia  is  applied  in  a  very  general  way  to  pain,  which  is 
either  of  idiopathic  origin  or  constitutes  the  principal  and  at  times  the 
only  symptom  of  some  obscure  lesion  of  functional  disturbance.  Neuralgia 
is  a  symptom  indicative  of  direct  injury  to,  or  altered  nutrition  of,  a  sen- 
sory nerve,  which  in  the  former  case  is  more  or  less  persistent,  but  in  the 
latter  is  usually  paroxysmal. 

Morbid  Anatomy. — It  may  be  functional  or  organic  ;  but  in  the  majority 

1  Woakes  states  that  aching  of  the  upper  extremities  and  discoloration  of  the  hands  may  occur  from 
irradiation  of  the  irritation  from  the  inferior  cervical  ganglion  to  the  brachial  plexus. 

"  Gowers  and  MacKenzie  recommend  gelsemium,  salicylate  of  soda,  counter-irritants,  or  even  the 
actual  cautery  applied  to  the  mastoid  region. 


1070  DISEASES    OF   THE   NEKVOUS   SYSTEM. 

of  instances  no  changes  can  be  found  after  death. '  When  neuralgia  is  a 
symptom  of  acute  neuritis  or  peri-neuritis,  the  nerve  trunk  is  hyperaemic 
and  swollen  or  degenerated  and  atrophied  ;  when  a  symptom  of  chronic  neu- 
ritis, the  nerve  has  undergone  sclerotic  processes,  and  compression  with 
degeneration  of  the  nerve-substance  follows. 

Neuritis  may  be  descending  or  ascending.  When  it  attacks  nerves  at 
various  points  it  is  called  disseminated  or  migrating  neuritis.  When 
neuralgia  is  a  symptom  of  pressure  from  tmnors,  either  in  brain,  cord  or 
at  any  jioint  along  the  nerve  trunks,  tlie  pain  will  be  confined  to  the  single 
nerve.  Gummata,  aneurisms,  and  osteomata  are  the  tumors  which  usually 
induce  such  compression. 

Etiology. — Neuralgia  is  often  an  hereditary  disease  in  those  of  a  neuro- 
pathic tendency.  Any  disease  causing  general,  or  local,  permanent  or 
transient  ancemia,  is  a  marked  predisposing  cause. 

Among  exciting  causes  are  cold  (especially  dmnp  cold),  lead,  mercurial 
and  other  states  of  chronic  blood  poisoning,  and  traumatism.  Disease  of 
the  genito-urinary  tract,  especially  in  women,  often  excites  reflex  or  sym- 
pathetic neuralgia  in  remote  nerve-trunks.  Reflex  neuralgia  is  also  induced 
by  decayed  teeth,  dyspepsia,  worms,  constipation,  etc.  Neuralgia  may 
follow  or  accompany  herpes  zoster,  and  occurs  very  frequently  in  convales- 
cence from  relapsing  fever. 

It  is  rare  before  puberty,  but  just  at  this  epoch  there  is  a  marked  predis- 
position to  it.  Those  between  twenty  and  fifty  years  of  age  suffer  most 
frequently.  Women  are  more  liable  than  men  ;  but  males  suffer  from 
sciatic  neuralgia  much  more  frequently  than  females.^ 

The  theory  that  neuralgia  often  depends  on  dilatation  of  the  venous 
plexuses  which  surround  a  nerve  at  its  exit  from  a  bony  canal,  is  supported 
by  the  fact  that  the  first  branch  of  the  trigeminus  suffers  far  oftener  than 
either  the  second  or  third,  or  both  combined.  ^ 

Symptoms. — Before  the  actual  pain  begins  in  a  nerve,  there  may  be 
numbness,  slight  cutaneous  hyperaesthesia,  or  some  peculiar  skin  sensation 
which  is  well-known  by  the  neuralgic  individual.  The  pain  is  at  first  in- 
termitting, later  it  is  continuous  with  slight  remissions.  The  character 
of  the  pain  varies  :  it  may  be  dull,  boring,  stabbing,  tearing  or  darting, 
and  is  confined  very  distinctly  to  the  course  and  distribution  of  the  af- 
fected nerve.  Indeed,  many  patients  trace  exactly  the  course  of  some 
nerve  when  pointing  out  the  locality  of  the  pain.  Sudden  movements,  as 
turning  and  coughing,  often  increase  the  pain. 

Increase  of  pain  on  pressure  is  an  important  point ;  the  exacerbation  is 
greatest  during  a  paroxysm,  and  greater  in  proportion  to  the  intensity  of 
the  original  pain.  Certain  points  are  markedly  sensitive  :  these  are  at  the 
exit  of  nerves  from  bony  canals,  or  foramina,  the  spot  where  they  pass 

1  It  is  claimed  that  the  acid  products  of  metamorphosis  of  nerve-tissue  acting  upon  the  nervous  system 
must  be  neutralized  by  the  blood,  before  pain  ceases.  Also,  that  nutritive  lesions  of  the  central  sensory 
tract  within  the  confines  of  the  gray  matter  are  the  essential  lesions.  Peripheral  pain  is  supposed  to 
originate  in  the  cord. 

2  Ilenle  states  that  the  left  side  is  predisposed  to  intercostal  neuralgia  on  account  of  the  arrangement 
of  the  venous  circulation. 

3  Allg.  Wien.  Med.  ZeiL,  1876,  pp.  24,  36. 


NEURALGIA.  1071 

through  a  muscular  aponeurosis,  at  their  bifurcation,  and  where  terminal 
branches  become  superficial.  These  pain-jjoints  are  better  marked  the 
longer  the  patient  has  suffered  from  neuralgic  attacks.  In  connection 
with  the  j)ain,  there  is  generally  associated  with  it  some  vaso-motor  dis- 
turbance, as  extreme  pallor  or  vivid  redness  and  reflex  movements  and 
twitchings  of  the  muscles.  Sliould  the  nerves  of  a  gland  be  attacked,  se- 
cretion will  probably  be  increased.  After  cessation  of  the  pain  the  part 
often  feels  sore  and  bruised,  and  there  is  a  general  sensation  of  exhaustion 
and  weariness. 

Actual  temporary  paralysis,  muscular  spasm,  herpetic  eruptions,  and 
ansesthesia  of  the  skin  may  complicate  or  follow  an  attack  of  neuralgia, 
and  later  the  muscles  supplied  by  the  affected  nerves  may  be  atrophied 
and  become  abnormally  weak.  During  a  prolonged  paroxysm  the  jiain 
may  extend  from  one  nerve  to  another  of  a  different  origin. '  In  a  few  rare 
cases  mental  effort  or  excitement  will  exacerbate,  or  even  excite,  a  parox- 
ysm of  neuralgia. 

If  neuralgia  be  caused  by  neuritis  the  pain  is  more  continuous,  and  the 
nerve  may  be  felt  as  a  hard  cord  beneath  the  skin,  which  latter  is  red  and 
cedematous.  With  neuritis  of  a  mixed  nerve,  twitching  and  contractions 
occur  with  the  pain.  In  neuralgia  of  functional  origin,  the  pain  is  more 
likely  to  shift  and  to  involve  corresponding  tracts  on  the  other  side  of  the 
body  or  head. 

One  of  the  most  common  forms  of  neuralgia  is  that  of  the  tri-facial 
nerve,  usually  attended  with  painful  spasm,  called  tic  douloureux.  One 
or  two,  rarely  all  the  divisions,  may  be  involved.  The  first  branch  is  its 
usual  seat,  when  it  is  termed  hrow-ague ;  the  third  is  rarely  attacked. 
When  the  ophthalmic  division  is  affected  the  neuralgia  is  called  hemi-crania 
or  migraine. 

Claris  hystericus  is  a  variety  of  tic  in  which  there  is  a  sensation  as  of  a 
nail  being  driven  into  the  skull.  It  is  usually  met  with  in  anaemic  females. 
The  hair  on  one  side  of  the  head  or  one  eyebrow  may  turn  white,  or  pig- 
mentation may  occur  along  the  course  of  the  pain,  and  the  tongue  on  the 
side  of  the  pain  may  exhibit  epithelial  overgrowth  in  long  standing  tic 
douloureux. 

Acute  glaucoma  and  recurrent  iritis  are  said  to  result  from  trophic 
changes  due  to  neuralgia.^ 

Pain  on  pressure  is  usually  best  marked  (1)  at  the  exit  of  the  frontal 
branch,  (2)  the  exit  of  the  inferior  maxillary  branch,  (3)  over  the  tempo- 
ral and  parietal  bones,  or  (4)  along  the  supra-orbital  ridges  (supra-orbital 
neuralgia). 

Sciatica  is  a  neuralgic  affection  of  the  sensory  nerves  of  the  sciatic  plexus. 

It  may  be  caused  by  the  pressure  of  tumors  and  inflammatory  exudation 
within  the  pelvis,  or  by  caries  or  carcinomatous  vertebrae  at  the  point  where 
the  nerves  pass  through  the  intervertebral  foramena.     Irritation  of  the  pe- 


J  Epileptiform  neural£?ia  is  that  variety  of  tic  doulonreux  where  the  seizures  are  very  abrupt  and  ac 
companied  by  spasm  of  the  facial  muscles. 

»  Anstie  states  tliat  near  the  painful  parts  ihe  periosteum  and  the  fibrous  tissue  are  thickened. 


1072  DISEASES    OF   THE   ISTERVOUS    SYSTEM. 

ripheral  branches  of  tlie  sciatic,  due  to  pressure  along  the  line  of  the  nerve, 
from  tun^ors,  etc.,  may  cause  sciatica,  but  in  the  majority  of  instances  the 
origin  is  rheumatic  and  the  direct  result  of  taking  cold.  Chronic  malarial 
infection  may  be  the  cause  of  sciatica.  It  is  most  frequently  met  with  in 
males  between  the  ages  of  twenty  and  sixty- 
It  is  usually  preceded  by  tingling  or  stiffness  in  the  buttock,  back  of  the 
thigh,  knee  and  leg.  The  pain  may  be  continuous  or  intermittent, 
and  its  most  frequent  seats  are  the  posterior  and  outer  part  of  the  thigh 
(particularly  near  the  tuberosity  of  the  ischium),  the  outer  side  of  the 
ankle,  and  the  dorsum  of  the  foot.  It  usually  comes  on  gradually,  the 
pain  becoming  more  intense  at  night.  The  patient  usually  lies  with  his 
legs  flexed.  In  walking  he  moves  the  affected  leg  slowly,  as  any  sudden 
motion  greatly  aggravates  the  pain.  The  pain  is  most  markedly  increased 
by  pressure  over  the  posterior  iliac  spine,  at  the  fold  of  the  buttock  and  the 
head  of  the  fibula.  Cramps  in  the  muscles  of  the  leg  are  common.  The 
limb  maybe  atrophied  and  the  patient  pass  into  a  semi-paralytic  condition, 
which  is  very  apt  to  be  chronic.  It  is  a  very  obstinate  affection,  lasting 
usually  from  six  weeks  to  two  months,  though  it  may  last  for  years.  Re- 
lapses are  not  uncommon. 

Intercostal  neuralgia  is  an  affection  of  any  of  the  dorsal  nerves  ;  the  an- 
terior branches  of  two  or  three  of  the  nerves  upon  the  left  side  are  those 
usually  affected.  It  occurs  in  women  as  a  rule.  Intermittent  pain  is  felt 
in  the  region  of  the  sixth,  seventh,  eighth  and  ninth  intercostal  nerves, 
tearing  or  stabbing  in  character,  increased  by  coughing  or  sneezing,  and 
perhaps  accompanied  by  a  dry  cough. 

There  are  three  diagnostic  points  of  tenderness  :  (1)  at  the  exit  of  the 
nerves  from  the  spine,  (2)  at  the  side  of  the  chest,  where  they  become 
subcutaneous,  and  (3)  near  the  sternum  or  median  line  at  the  terminal 
branches.  Cardiac  palpitation,  dyspnoea,  nausea  and  vomiting  are  fre- 
quent symptoms  of  this  ^o-coWq^  false  pleurisy .  Herpes  zoster,  intolerable 
itching,  and  attacks  of  angina  pectoris  often  complicate  it. 

Cervico-occipital  neuralgia  is  usually  attended  by  pain  along  the  course 
of  the  occipitalis  major,'  and  often  resembles  that  form  of  muscular  rheu- 
matism called  torticollis,  or  wry-neck.  (See  art.  Eheumatism.)  A  branch 
of  the  Iracliial  plexus  may  be  involved ;  the  ulnar,  however,  is  more  fre- 
quently affected  than  any  other. 

Coccyodynia  is  common  in  women,  and  is  due  to  neuralgia  of  the  coc- 
cygeal plexus. 

Headaclie. — Headache,  or  cephalalgia,  is  properly  a  form  of  neuralgia,  as 
it  can  only  be  referred  to  the  sensory  nerves  supplying  the  meninges  and 
scalp,  and  like  other  neuralgias  is  of  both  organic  and  functional  origin. 
It  is  a  frequent  symptom  of  cerebral  disease,  either  inflammatory  or  such 
as  produces  compression  of  the  cranial  contents,  and  is  especially  severe  in 
the  acute  forms  of  meningitis  and  some  cerebral  tumors.  It  results  from 
disturbance  of  the  cerebral  circulation,  which  causes  either  compression  of 
the  cranial  nerves  or  angemia,  and  consequent  disturbance  of  nutrition.    Its 

1  Gray's  Anatomy,  pp.  636-637. 


NEUKALGIA.  1073 

primary  cause,  however,  is  more  frequently  in  other  organs,  as  the  stomach 
or  genito-urinary  tract,  in  which  cases  the  headache  is  the  result  of  reflex 
disturbances,  frequently  of  the  circulation,  from  vaso-motor  irritation.  Of 
a  similar  nature  is  the  headache  resulting  from  the  strain  of  the  ciliary 
muscle,  consequent  upon  defects  of  refraction.  Again,  headache  is  fre- 
quently a  symptom  of  blood  poisons,  as  in  rheumatism,  gout  and  septic 
diseases. 

In  these  diseases,  as  probably  also  in  headache  with  high  temperature,  the 
condition  is  presumably  one  of  direct  irritation  of  nerve  centres,  or  of  de- 
fective nutrition.  Headache  assumes  a  great  variety  of  forms.  It  may  be 
limited  to  one  half  the  head,  to  the  forehead,  vertex,  occiput,  temporal  re- 
gion, or  any  point  on  the  cranium,  or  it  may  be  diffuse  and  extend  to  the 
eye,  face  and  neck.  In  character  and  severity  it  may  assume  any  of  the 
characteristics  of  neuralgia.  Headache  is  a  symptom  of  exceedingly  diffi- 
cult interpretation.  In  a  general  way,  however,  it  may  be  stated  that  head- 
ache of  gastric  or  hepatic  origin  is  commonly  frontal  and  throbbing  in 
character  and  associated  with  cerebral  congestion.  It  may  be  bilateral  or 
unilateral.  Headache  at  the  vertex  is  quite  constantly  symptomatic  of  cere- 
bral disturbances  of  local  origin,  or  due  to  reflex  irritation  starting  in  the 
pelvic  organs,  especially  the  genital  tract  of  the  female.  Pain  in  the  occip- 
ital region  is  mostly  an  accompaniment  of  disorders  of  circulation,  and  vaso- 
motor spasm  and  anaemia  in  particular.  The  pain  of  cerebral  compression 
or  tumor,  although  often  diffuse,  is  generally  localized,  persistent,  and  very 
intense. 

All  forms  of  cephalalgia  may  be  attended  by  hyperaesthesia,  especially  of 
the  optic  and  auditory  nerves,  with  subjective  sensations  of  light  and 
sound,  by  vertigo,  nausea,  drowsiness  or  wakefulness,  and  possibly  deliri- 
um. Visceral  neuralgias  have  been  considered  in  the  list  of  Visceral  Dis- 
eases. 

Differential  Diagnosis. — Neuralgia  may  be  mistaken  for  myalgia,  syphi- 
litic periostitis,  and  for  cerebral  abscess. 

Myalgia  is  distinguished  by  its  non-paroxysmal  character,  by  the  pain 
being  increased  by  motion,  and  by  the  fact  that  the  attachments  of  the 
muscles  are  the  points  chiefly  involved. 

SypMlitic  periostitis  \'s,  to  be  distinguished  from  neuralgia  by  the  pres- 
ence or  absence  of  other  symptoms  of  constitutional  syphilis. 

Cerebral  abscess  often  occurs  secondarily  to  caries  of  the  internal  ear  and 
after  otitis  in  childhood ;  neuralgia  rarely  appears  before  puberty.  Cere- 
bral abscess  frequently  follows  a  blow  or  injury  ;  neuralgia  comparatively 
seldom.  In  the  former  there  are  no  true  points  douloureux ;  these  are 
present  early  in  severe  neuralgia.  In  cerebral  abscess  the  pain  does  not 
completely  intermit ;  intermissions  of  pain,  complete,  and  of  considerable 
length,  occur  in  neuralgia.  The  pain  is  at  first  severe  in  cerebral  abscess ; 
in  neuralgia  it  is  slight  at  first  and  gradually  exacerbates.  Pain  in  cere- 
bral abscess  is  often  limited  in  situation,  seems  deep-seated,  though  often 
it  has  no  relation  to  the  site  of  the  abscess  ;  in  neuralgia  pain  is  superficial, 
and  follows  the  distribution  of  recognizable  nerve  branches  belonging  to 


1074  DISEASES   OF   THE   NEKVOFS   SYSTEM. 

the  trigeminus  or  great  occipital.  In  cerebral  abscess  there  are  no  well 
localized  vaso-motor  or  secretory  complications,  while  lachrymation  or 
congestion  of  the  conjunctiva  usually  occurs  in  neuralgia.  Cerebral  ab- 
scess is  rare  in  old  age,  and  then  generally  traumatic  ;  neuralgia  is  most 
common  at  that  period. 

Prognosis. — Life  is  rarely  compromised  by  neuralgia,  but  when  it  is  per- 
sistent the  general  health  may  be  seriously  affected.  When  occurring  in 
early  life  and  with  no  hereditary  predisposition  the  prognosis  is  the  most 
favorable. 

Treatment. — Neuralgia  has  been  well  said  to  be  the  cry  of  a  nerve  for  let- 
ter blood.  Should  anasmia  be  evidenced,  a  generous  diet,  cod-liver  oil,  the 
hypophosphites,  or  small  doses  of  phosphorus  and  the  appetizers,  along  with 
quinine,  iron  and  strychnine  should  be  ordered.  Neuralgia  due  to  syphilis 
demands  iodide  of  potash ;  to  rheumatism,  the  anti-rheumatics ;  to  gout, 
colchicum  ;  and  to  malaria,  quinine,  but  in  many  non-malarial  cases  also, 
especially  in  tic,  quinine  is  the  most  effectual  remedy.  A  patient  with 
neuralgia  should  be  removed  from  all  exposure  to  cold  and  irritations  of 
all  kinds. 

Locally,  blisters,  the  continuous  current,  chloroform,  opium,  belladonna 
and  veratria  liniments,  and  cold,  or  very  hot  water  may  be  applied,  and 
these  sometimes  afford  permanent,  nearly  always  temporary  relief.  Aco- 
nite enjoys  the  highest  reputation  at  the  present  day  among  local  remedies. 
Firing,  sinapisms  and  actual  cautery  are  frequently  beneficial.  Sometimes 
prolonged  residence  in  a  warm,  dry  climate  is  the  only  means  of  effecting 
a  permanent  cure. 

For  immediate  relief  of  pain,  morphine  is  the  most  effectual.  Neuralgic 
attacks  and  headache  that  are  accompanied  hj  flushing  of  the  face  are  often 
relieved  by  ergot.  But  when  the  face  is  very  pale,  nitrite  of  amyl  is  to  be 
preferred.  Gelsemium  is  sometimes  especially  effectual  in  the  treatment 
of  trigeminal  neuralgia.  This  and  croton  chloral  are  largely  employed. 
In  severe  chronic  neuralgias  a  portion  of  the  nerve  may  be  excised  (neu- 
rectomy), or  the  nerve  may  be  simply  cut  (neurotomy). 

Nerve-stretching  may  be  practised  upon  any  trunk  which  can  be  sur- 
gically reached.  The  sciatic  is  the  nerve  which  has  been  stretched  with 
most  success.  In  headache,  cold  to  the  head  and  heat  to  the  feet,  or  at 
times  the  persistent  application  of  heat  to  the  head  for  several  hours,  will 
afford  relief.  Guarana,  caffeine,  and  similar  remedies  are  often  very  useful 
in  sich  headache.  In  these  cases  a  purge  or  an  emetic  will  also  frequently 
bring  relief. 

In  all  severe  cases  of  sciatica,  in  addition  to  the  treatment  of  neuralgia 
in  general,  absolute  rest  is  essential  to  its  successful  management.  If  it  is 
caused  by  gout,  rheumatism,  or  syphilis,  treatment  appropriate  to  these 
conditions  must  be  employed.  If  there  be  a  chronic  malarial  taint,  quinine 
and  arsenic  must  be  given  in  full  doses.  The  hypodermic  injection  of 
morphine  gives  the  most  speedy  relief.  The  point  of  the  needle  should  be 
introduced  deep  into  the  tissues  over  the  exit  of  the  nerve.  In  many  in- 
stances its  daily  use  for  some  time  will  cure  sciatica,  even  of  long  standing. 


MEGRIM.  1075 

The  continuous  voltaic  current  is  often  palliative  and  sometimes  curative. 
The  systematic  treatment  with  baths  at  the  Hot  Springs  of  Arkansas  and 
Virginia,  I  have  found  especially  efficacious  in  sciatica  that  has  resisted  all 
other  remedial  measures.  The  apjolication  of  the  hot  iron  and  blisters 
along  the  course  of  the  nerve  have,  in  some  instances,  acted  remedially. 

MEGRIM. 

{Sick  Headache.) 

Sick  headache,  or  hemi-crania,  is  a  form  of  headache  attended  by  marked 
gastric  and  nervous  disturbances. 

Morbid  Anatomy. — Megrim  is  probably  due  to  disordered  cerebral  circu- 
lation, the  exciting  cause  of  which  is  vaso-motor  disturbance.  Changes 
similar  to  those  of  epilepsy  are  generally  considered  to  be  the  pathological 
condition,  that  is,  vaso-motor  irritation  with  arterial  sjoasm  and  consequent 
anaemia  of  the  cerebral  ganglia,  followed  by  relaxation  and  congestion. 
This  condition,  however,  still  demands  an  ultimate  cause,  which  is  prob- 
ably nervous  (cerebro-spinal)  exhaustion,  following  prolonged  irritation,  as 
indicated  in  its  etiology. 

Etiology. — Megrim  is  often  hereditary,  or,  more  exactly,  the  nervous 
weakness  and  instability  which  predispose  to  the  affection  are  hereditary. 
Whether  inherited  or  acquired,  it  commonly  develops  before  thirty,  and 
subsides  in  later  life.  Digestive  disturbances  are  frequent  exciting  causes, 
but  a  much  larger  proportion  of  cases  are  due  to  nervous  irritation  and 
exhaustion.  It  is  an  almost  unfailing  symptom  of  chronic  uterine  irrita- 
tion or  sexual  excesses,  and  is  frequently  due  directly  to  mental  labor, 
worry,  or  excitement.  In  neurasthenic  patients,  it  is  often  excited  by 
over-exertion,  or  the  lack  of  it,  by  too  much  or  too  little  sleep,  and  by 
irritation  of  the  nerves  of  special  sense — flickering  light  or  loud  noises — 
and  in  some  cases  the  slight  disturbance  of  co-ordination  attendant  upon 
the  use  of  the  stereoscope  or  opera-glass  is  sufficient  to  excite  an  attack. 

Symptoms. — As  the  term  indicates,  hemi-crania  is  almost  invariably 
confined  to  one  side  of  the  head,  and  is  generally  distinctly  localized  in  the 
frontal,  temporal,  or  occipital  region,  and  even  when  it  attacks  all  three 
places,  or  becomes  diffuse,  the  pain  is  still  most  intense  and  persistent  at  a 
small  circumscribed  point  in  each  region.  In  such  cases  there  is  often  a 
sensation  of  an  intra-cranial  cord  joining  the  painful  points. 

Frequently,  and  esjDecially  in  cases  due  to  ocular  strain,  the  eye  becomes 
the  seat  of  pain  and  is  tender  and  hypersesthetic.  Early  in  the  attack  the 
face  may  be  pale  and  the  cardiac  action  slow  and  weak.  Very  soon,  how- 
ever, the  head  becomes  hot  and  the  pulse  slow,  and  with  each  heavy  heart- 
beat the  carotids  pulsate  strongly  and  the  pain  is  greatly  increased.  Gen- 
erally within  a  few  hours  nausea  supervenes,  and  may  be  attended  by  dis- 
tinct recurring  chills  and  paleness  of  the  surface.  The  patient  is  greatly 
depressed  and  is  wretchedly  sick.  If  the  pain  is  not  too  severe  he  may  fall 
asleep,  to  wake  in  tlie  morning  with  only  a  soreness  about  the  scalp  and 
stiffness  of  the  muscles  of  the  neck  remaining.    More  frequently  the  nausea 


1076  DISEASES    OF   THE   2TERV0US    SYSTEM. 

increases  until  relieved  by  an  attack  of  vomiting.  A  few  hours  of  sleep 
then  restores  the  patient  to  his  usual  condition. 

Quite  characteristic  premonitory  symptoms  are  present  in  many  cases. 
The  most  common  are  disorders  of  vision  in  the  form  of  retinal  anaes- 
thesia or  irritation.  The  anesthetic  spot  may  be  located  in  any  part  of  the 
retina,  but  generally  affects  the  macula  lutea.  Eetinal  irritation  causes  the 
patient  to  see  variously  colored  lights  and  scintillations.  The  disturbance 
in  vision  may  commence  with  a  wavy  glimmering  at  the  outside  of  the 
field  of  vision  or  by  the  appearance  of  a  black  spot  close  to  its  centre.  Simi- 
lar disturbances  of  the  other  nerves  of  sense,  either  irritative  or  paralytic, 
may  be  present,  but  they  are  less  common  than  the  visual  disturbances. 

Hemi-crania  may  last  from  a  few  hours  to  two  or  three  days,  but  in  most 
cases  is  relieved  within  twenty- four  hours.  It  is  very  apt  to  recur  at  regu- 
lar intervals,  and  become  more  intractable  with  each  attack. 

Treatment. — By  way  of  prophylaxis,  the  patient  should  avoid  all  known 
causes  of  the  attack,  and  pursue  a  tonic  course  of  living.  At  the  beginning 
of  the  attack  full  doses  of  alcoholic  or  other  stimulants  may  prevent  its 
development.  Later,  the  bromides,  quinine,  strychnia,  belladonna,  canna- 
bis indica,  caffeine,  guarana,  and  chloral  at  times  afford  relief.  When 
nausea  is  present,  however,  an  emetic,  followed  by  a  few  hours'  sleep,  brings 
about  the  most  speedy  cure.  Morphia  hypodermically  is  the  best  and 
surest  means  for  the  relief  of  pain. 

During  the  interval  between  the  attacks  the  treatment  should  be  such  as 
will  as  far  as  possible  render  inoperative  its  cause.  No  two  cases  will  re- 
quire the  same  hygienic  or  therapeutic  measures.  The  main  thing  is  to 
overcome  the  acquired  or  hereditary  neurotic  tendencies  of  the  patient  by 
diet,  exercise  in  the  open  air,  and  cheerful  surroundings.  Drugs  accom- 
plish very  little  for  this  class  of  sufferers  except  to  give  temporary  relief. 

ECLAMPSIA    AND    INFANTILE    CONVULSIONS. 

Epileptiform  convulsions  are  of  frequent  occurrence  in  connection  with 
distinct  lesions  of  the  nervous  centres  as  well  as  with  various  reflex  disturb- 
ances. Indeed,  they  may  be  symptomatic  of  any  cerebral  disease,  as  com- 
pression from  fracture,  hemorrhage  and  tumors,  or  thrombosis,  embolism 
and  inflammatory  processes.  In  those  conditions  where  they  can  be, 
■ascribed  to  distinct  pathological  changes  they  are  termed  eclampsia.  Clini- 
cally such  convulsions,  as  well  as  those  from  uraemia  and  other  poisons,  are 
often  identical  in  appearance  with  epileptic  fits,  and  are  to  be  diagnosticated 
by  the  concomitant  symptoms. 

When  such  convulsions  occur  in  children,  as  they  often  do  from  reflex 
irritation  during  teething,  in  gastro-intestinal  disorders,  in  the  early  stages 
of  blood  poisoning,  and,  indeed,  in  any  condition  which  in  the  adult  pro- 
duces a  chill,  they  are  then  called  infantile  convulsions.  Although  fre- 
quently indistinguishable  from  epilepsy,  the  convulsions  of  eclampsia,  and 
more  particularly  infantile  convulsions,  may  present  only  a  portion  of  the 
true  epileptic  fit  or  even  be  very  slight.     They  are,  moreover,  less  regular 


SEASICKNESS.  1077 

in  their  occurrence  and,  until  the  cause  is  removed,  tend  to  increase  in  fre- 
quency and  intensity.  They  are  less  sudden  in  their  development  also, 
and,  although  much  more  fatal,  owing  to  their  frequent  dependence  upon 
an  irremediable  cause,  generally  cease  permanently  when  the  cause  is  re- 
moved. Infantile  convulsions  present  the  widest  range  of  intensity,  but  are 
always  a  cause  of  anxiety,  especially  when  the  respiratory  muscles  are  in- 
volved, as  is  frequently  the  case. 

The  indications  for  treatment  are,of  course,f ound  in  the  cause.  In  syphi- 
lis, uraemia,  ansemia,  gastro-enteritis,  etc.,  the  treatment  will  in  most  cases 
be  under  way  before  the  occurrence  of  convulsions.  When,  however,  they 
are  the  initiatory  symptoms,  all  possible  causes  must  be  carefully  sought. 
The  discovery  of  a  cause  will  indicate  the  treatment.  Infantile  convulsions 
often  arise  from  slight  causes  that  frequently  escape  detection.  In  such 
cases  the  general  health  must  be  improved,  the  alimentary  canal  freed  from 
a  possible  hidden  cause,  and  the  clothing  carefully  inspected  and  made 
loose  and  unirritating.  The  usual  anti-spasmodics,  belladonna,  the  bro- 
mides, etc.,  may  then  properly  be  used.  Hot  baths,  counter-irritants  to 
the  back  and  neck,  or  cold  to  the  head,  are  often  of  service.  Chloroform 
is  the  most  appropriate  agent  for  controlling  the  spasms  temporarily. 

SEASICKNESS. 

The  term  seasickness  is  applied  to  a  peculiar  form  of  functional  disturb- 
ance of  the  nervous  system  characterized  by  severe  depression  and  persistent 
nausea  and  vomiting. 

Morbid  Anatomy. — The  only  organic  changes  which  have  been  found, 
which  are  probably  secondary,  are  slight  hyperemia  of  the  gastric  mucous 
membrane,  due  to  the  prolonged  efforts  at  vomiting  and  the  presence  of 
abnormal  quantities  of  gastric  juice,  and  cerebral  anaemia  with  congestion 
of  the  spinal  centres.  The  primary  irritation  may  properly  be  considered 
as  a  form  of  shock  arising  from  the  unusual  combination  of  nervous  im- 
pressions calling  for  unaccustomed  action  on  the  part  of  the  nerve  centres. 
In  other  words,  the  nerve  centres  are  embarrassed,  and  the  resulting  nervous 
irritation  manifests  itself  through  vaso-motor  disturbances  in  precisely  the 
same  manner  as  is  seen  when  persons  blush  under  embarrassing  circum- 
stances or  pale  when  startled.  In  the  present  instance  this  disturbance, 
though  general,  is  most  marked  in  gastro-intestinal  and  cardiac  derange- 
ments. Paleness  of  the  surface  from  vaso-motor  irritation  is  probably  asso- 
ciated with  anaemia  of  the  brain  and  congestion  of  the  spinal  centres.'  As 
a  consequence  there  is  irritation  of  those  centres,  manifested  by  severe  gas- 
tric irritability,  with  nausea  and  vomiting  of  centric  origin. 

Etiology. — As  indicated  in  the  name,  seasickness  is  most  commonly  the 
result  of  the  motion  of  a  ship.  It  may,  however,  be  the  result  of  any  un- 
usual motions  to  which  the  person  is  unaccustomed,  and  especially  such  as 

'  Dr.  Clapham  reports  an  autoi)sy  made  four  hours  after  death  upon  a  man  accidentally  killed  while 
vomiting,  in  which  there  was  intense  congestion  of  the  spina!  cord  and  distention  of  the  vessels,  closely 
resembling  the  condition  found  in  an  epileptic  who  had  died  during  an  epileptic  seizure  —London  Lancet, 
1864. 


1078  DISEASES    OP   THE   JSTERVOUS    SYSTEM. 

raise  the  body  rapidly  or  suddenly  allow  it  to  fall,  as  the  motion  of  a  swing 
or  an  elevator.  Waltzing,  riding  backwards,  turning  a  somersault,  or  the 
sudden  jerk  of  a  railroad  train  as  it  starts  or  stops  or  goes  rapidly  around 
curves  in  the  track,  may  each  produce  a  precisely  similar  condition.  They 
are  not  usually  followed  by  the  full  development  of  the  disease,  solely  be- 
cause they  are  not  repeated  or  continued  sufficiently  long. 

Moreover,  it  is  not  always  necessary  that  the  patient  himself  should  be 
moved.  Frequently,  simply  watching  oscillating  objects  is  sufficient  to 
produce  a  mild  form  of  sickness.  Personal  idiosyncrasy  is  a  very  impor- 
tant factor  in  predisposing  to  seasickness.'  Some  persons  never  suffer,  even 
under  the  most  trying  circumstances,  while  others  are  unable  to  endure  the 
slightest  motion  on  the  water  or  elsewhere.  This  peculiar  susceptibility 
varies  also  in  the  same  person,  and  an  individual  who  has  resisted  through 
several  sea  voyages  may  finally  succumb  during  a  sail  on  some  small  inland 
lake. 

Habit  and  experience  are  generally  suffiicent  to  do  away  entirely  with  the 
susceptibility  to  the  disease,  but  occasionally  an  individual  suffers,  it  may 
be  with  increasing  severity,  whenever  he  is  on  rough  water. 

Symptoms. — Seasickness  usually  presents  the  two  stages  of  (1)  depression 
and  exhaustion,  and  (3)  reaction. 

It  begins  with  a  sense  of  weight  and  epigastric  oppression,  often  describei? 
as  a  feeling  of  coldness,  which  at  first  may  be  distinctly  intermittent,  oc- 
curring only  during  the  rapid  rise  and  fall  of  the  vessel.  It  may,  however, 
be  continuous  from  the  start,  and  even  at  first  be  a  distinct  nausea.  In  any 
event  it  speedily  becomes  so,  and  is  accompanied  by  vertigo  and  headache. 
INausea  is  quickly  followed  by  vomiting,  which  partakes  of  the  nature  of  both 
gastric  and  cerebral  vomiting.  N'ausea  is  always  most  intense,  and  at  the 
same  time  the  vomiting  is  often  sudden  and  projectile,  as  from  a  central 
cause.  As  the  vomiting  continues  the  ejected  matter  is  composed  of  in- 
tensely acid  gastro-biliary  secretions.  Constipation  is  the  rule,  and  all  the 
secretions  except  the  saliva  are  decreased.  The  appetite  is  entirely  lost,  and 
there  is  a  marked  repugnance  to  food,  and  especially  to  all  forms  of  fat.  In 
many  cases  the  simple  smell  or  thought  of  food  is  sufficient  to  excite  a 
paroxysm  of  vomiting.  In  this  stage  the  mental  depression  is  very  charac- 
teristic, the  patients  almost  exulting  in  the  thought  of  shipwreck  as  afford- 
ing relief  from  their  sufferings.  In  the  majority  of  cases  this  condition  con- 
tinues from  three  to  five  days,  provided  the  voyage  is  of  that  length,  during 
which  time  the  nausea,  vomiting  and  mental  depression  continue  with  vary- 
ing intensity,  and  is  then  followed  by  reaction  and  a  more  or  less  rapid  dis- 
appearance of  the  vomiting,  with  return  to  the  normal  condition. 

In  such  cases,  owing  to  the  enforced  abstinence,  there  is  for  a  time  a  rav- 
enous appetite  and  a  feeling  of  special  well  being. 

In  other  cases,  however,  the  stage  of  depression  continues  until  the  pa- 
tient is  again  on  terra  firma,  lasting  it  may  be  for  weeks,  or  it  may  in  a  few 
days  pass  into  a  stage  of  partial  collapse.     The  patient  is  sleepy  and  apa- 

1  Tn  some  instances  naval  officers  of  many  years'  experience  have  been  led  to  leave  their  profession  from 
their  inability  to  accustom  themselves  to  the  sea. 


SEASICKNESS.  1079 

tLetic,  the  surface  is  cold,  and  he  suffers  from  neuralgic  pains  or  general 
numbness.  Finally,  a  partial  coma  may  supervene  and  the  case  assume  a 
very  grave  aspect. 

Convalescence  is  generally  rapid,  and  the  patient  passes  from  a  state  of 
the  greatest  depression  to  one  of  comfort  and  entire  recovery  within  a  few 
hours ;  but  when  the  case  has  been  prolonged,  convalescence  may  be  de- 
layed and  be  attended  by  rise  in  temperature  and  other  febrile  conditions. 

Other  forms  of  seasickness  present  differences  of  degree  rather  than  of 
kind. 

Diagnosis. — Owing  to  the  peculiar  circumstances  under  which  it  is  devel- 
oped, seasickness  can  rarely  be  mistaken  for  any  other  condition.  It  may 
simulate  an  attack  of  gastro-enteritis  in  the  early  stages.  In  seasickness 
constipation  is  the  rule,  and  the  intense  nausea,  the  persistent  violent  vom- 
iting, and  the  loathing  of  food  are  much  more  marked.  Gastro-enteritis  is 
most  common  in  children,  while  they  seldom  suffer  severely  from  seasickness. 

Prognosis. — It  is  very  rarely  fatal,  but  occasionally  a  condition  of  collapse 
develops  which,  if  not  assiduously  treated,  may  pass  into  coma  and  death. 
A  general  irritability  of  the  gastro-intestinal  mucous  membrane  often  re- 
mains for  some  time  after  a  prolonged  sickness. 

Treatment. — The  remedies  proposed  and  tried  for  seasickness  are  innu- 
merable, but  as  most  of  them  are  only  palliative  or  worse  than  useless  it  is 
unnecessary  to  enumerate  them.  Two  general  plans  of  treatment  have  been 
adopted,  based  upon  the  accepted  pathology  of  vaso-motor  disturbance  and 
spinal  congestion,  (1)  the  sedative,  and  (2)  the  stimulant.  Among  the 
remedies  of  the  first  class  counter-irritation  to  the  spine,  or  ice  bags,  the 
bromides  and  nitrite  of  amyl  have  proved  the  most  useful.  The  applica- 
tion of  ice  to  the  spine  was  advocated  by  Dr.  Chapman  as  being  the  best 
means  for  controlling  spinal  congestion.  It  is  of  decided  value,  but  is  un- 
comfortable and  hardly  available  for  a  large  number  of  cases.  The  bro- 
mides are  often  used  successfully,  but  their  use  must  be  begun  some  time 
before  the  voyage  and  continued  in  large  doses  until  the  patient  is  fully  ac- 
customed to  the  motion  of  the  sea.  Amyl  nitrite,  both  from  the  rapidity 
with  which  it  acts  and  the  certainty  of  its  results,  seems  to  be  the  most  de- 
sirable and  efficacious  remedy  yet  proposed.  It  should  be  given  in  full 
doses  upon  the  first  appearance  of  epigastric  distress,  and  repeated  as  nec- 
essary. ' 

Under  the  class  of  stimulant  remedies  the  various  forms  of  alcohol  and 
the  diffusible  stimulants  are  most  used,  but  the  results,  though  good  in  some 
cases,  are  generally  far  from  satisfactory. 

In  some  cases  of  slight  disturbance,  any  device  which  controls  the  move- 
ments of  the  diaphragm  may  be  sufficient  to  prevent  the  development  of  vom- 
iting. Among  the  most  successful  of  these  is  a  prolonged  even  inspiration 
as  the  vessel  rises,  followed  by  a  similar  expiration  during  descent.  It 
must  be  confessed,  however,  that  in  many  instances  all  remedies  are  un- 
availing, and  only  time  and  experience  can  effect  a  cure. 

J  Dr.  Clapham  (Lancet,  vol.  ii.,  1875,  p.  376)  reports  121  successful  cases  out  of  a  total  of  124  in  which  amyl 
nitrite  was  used. 


INDEX. 


Abdominal  aneurism,  difEerential  diagnosis,  528. 
etiology,  527. 
morbid  anatomy,  527. 
physical  signs,  528. 
prognosis,  528. 
symptoms,  527. 
treatment,  538. 
Abdominal  dropsy.    See  Ascites,  333. 
Abortive  form  of  typhoid  fever,  630. 
Abortive  typhus,  730. 
Abscess,  3. 

Abscess,  bronchial,  129. 

Abscess  of  the  bralu.    See  Brain,  abscess  of,  975. 
Abscess  of  tlie  liver.  See  Hepatitis,  suppurative,  349. 
Abscess,  pericsecal.    See  Perityphlitis,  281. 
Abscess,  perinephritic.    See  Perinephritis,  600. 
Abscess,  retropharyngeal.    See  Ketropharyngeal  ab- 
scess, 223. 
Acholia.    See  Catarrh  of  the  bile-ducts,  397. 
Active  hypersemia  of  the  liver.    See  Liver,  hyperae- 

mia  of,  337. 
Acute  anterior  polio-myelitis.    See  Infantile  spinal 

paralysis,  1006. 
Acute  aortitis,  511. 

Acute  articular  rheumatism.  See  Kheumatism,  artic- 
ular, 858. 
Acute  ascending   paralysis.      See    Paralysis,  acute 

ascending,  1028. 
Acute  Bright's  disease  of  the  kidney.     See  Kidney, 

acute  Bright's  disease  of,  552. 
Acute  bulbar  paralysis.  See  Paralysis,  acute  bulbar, 

1001. 
Acute  capillary  bronchitis,  46. 
Acute  catarrhal  bronchitis,  42. 
Acute  catarrhal  laryngitis,  17. 
Acute  coryza,  9. 
Acute  croupous  laryngitis,  27. 
Acute  endarteritis.    See  Endarteritis,  acute,  511. 
Acute  exudative  endocarditis.      See  Endocarditis, 

acute  exudative,  431. 
Acute  gastric  catarrh.    See  Sub-acute  gastritis,  229. 
Acute  general  diseases,  classification  of,  610. 
definition  of,  609. 

theories  regarding  the  nature  of,  610. 
Acute  hydrocephalus.      See  Meningitis,  tubercular, 

943. 
Acute  intestinal  catarrh.    See  Enteritis,  257. 
Acute  meningitis.    See  Meningitis,  acute,  935. 
Acute  miliary  tuberculosis.    See  Tuberculosis,  acute 

miliary,  706 
Acute  myelitis.    See  Myelitis,  acute,  996. 
Acute  pancreatitis.    See  Pancreatitis,  acute,  410. 
Acute  parenchymatous  nephritis.   See  Kidney,  acute 

Bright's  disease  of,  .552. 
Acute  pericarditis.    See  Pericarditis,  acute,  420. 
Acute  phthisis.    See  Phthisis,  172. 
Acute  spinal   paralysis    of   adults.      See  Paralysis, 

acute  spinal  of  adults,  1009- 
Acute  ulcerative    endocarditis.      See  Endocarditis, 

acute  ulcei'ative,  433. 
Acute  uraemia.    See  Uraemia,  acute,  537. 
Acute  yellow  atrophy  of  liver.    See  Parenchymatous 

hepatitis,  356. 
Addison,  888. 

Addison's  disea-e,  difEerential  diagnosis,  899. 
etiology,  897. 
morbid  anatomy,  897. 
prognosis,  899. 
syra'ptoms,  899. 
treatment,  900. 


Adhesive  pleurisy.    See  Pleurisy,  162. 

Adhesive  pylephlebitis.  See  Pylephlebitis,  adhesive, 

362.  ,     , 

Adults,  acute   spinal  paralysis  of.    See  Paralysis, 

acute  spinal  of  adults,  1009. 
Albrecht,  740. 
Alcoholism,  differential  diagnosis,  915. 

etiology,  914. 

morbid  anatomy,  913. 

prognosis,  915. 

sj'mptoms,  914. 

ti  eatment,  915. 
"  Alcoholismus."    See  Alcoholism,  913. 
Allbutt,  445. 
Althaus,  867. 
Ammonaemia,  difEerential  diagnosis,  907. 

etiology,  900. 

morljid  anatomy,  900. 

prognosis,  907. 

symptoms,  900. 

treatment,  907. 
Amyloid  degeneratiim  of  artories,  513. 
Amyloid  degeneration   of   the   heart.     See  Heart, 

amyloid  degeneration  of,  494. 
Amyloid  degeneration  of  the  intestines.    See  Intes- 
tines, waxy  degeneration  of,  297. 
Amyloid  degeneration  of  the  spleen.    See  Spleen, 

waxy  degeneration  of,  417. 
Amyloid  form  of  Bright's  disease.    See  Waxy  kid- 
ney, 575. 
Amyotrophic  lateral  sclerosis,  difEerential  diagnosis, 
1026. 

etiology,  1025. 

morbid  anatomy,  1025. 

prognosis,  1026. 

symptoms,  1026. 

treatment,  1026. 
Anaemia,  difEerential  diagnosis,  884. 

etiology,  883. 

morbid  anatomy,  883. 

prognosis,  885. 

symptoms,  884. 

treatment,  885. 
Anaemia,  cerebral.    See  Cerebral  anaemia,  933. 
Anajmia  of  the  brain.    See  Cerebral  anaemia,  933. 
Anaemia  of  the  lungs,  129. 
Anagmia,  proL'ressive  pernicious.     See  Progressive 

pernicious  anaemia,  888. 
Anaemia,  pulmonary,  129. 

morbid  anatomy  of,  129. 

svmptoms  of,  129. 
Anse'^tliesia,  928. 
Anchylostomnm  duodenale,  309. 
Andejvoii,  Dr.  McCall,  178. 
Andral.  8S8. 

Aneurism  of  the  brain.    See  Cerebral  tumors,  977. 
Aneurism  of  the  heart.    See  Heart,  aneurism  of,  500. 
Aneurism,  valvular,  434. 
Angina  pectoris,  differential  diagnosis,  505. 

etiology,  504. 

prognosis,  505. 

symptoms,  504,  505. 

treatment,  506. 
Angiomata  of  the  brain.    See  Cerebral  tumors,  977. 
Aniniske,  982. 
Anstie,  171,  1071. 
Anterior  polio-myelitis,  acute.    See  Infantile  spinal 

paralysis,  1006. 
Anterior  polio-myelitis,  chronic.    /See Polio-myelitis, 
chronic  anterior,  1010. 


1082 


INDEX. 


A.ntbracosi8,  182. 

Antiseptic  treatment  of  phthisis,  203. 

Aortic  insufflciencj'.    See  Aortic  regurgitation,  448. 

Aortic  obstruction.    See  Aortic  stenosis,  444. 

Aortic  regurgitation,  differential  diagnosis,  452. 

etiology.  449. 

morbid  anatomy,  448. 

physical  signs,  450. 

symptoms,  449. 
Aortic  stenosis,  differential  diagnosis,  447. 

etiolog3%  445. 

morbid  anatomy,  444. 

physical  signs,  446, 447. 

symptoms,  444. 
Aortitis,  511. 

Aphasia.  See  Cerebral  thrombosis  and  embolism,  9.56. 
Apoplexy,  cerebral.    See  Cerebral  apoplexy,  964. 
Apoplexy,  circumscribed  pulmonarj',  120. 
Apoplexy,  diffuse  pulmonary,  etiology  of,  125. 

morbid  anatomy  of,  124. 

physical  signs  of,  125. 

prognosis  of,  125. 

symptoms  of,  125. 

treatment  of,  12.5. 
Apoplexy,  nodular  pulmonary,  120. 
Apoplexy,  spinal.    See  Spinal  apoplexy,  1029. 
Aphthous  stomatitis.    See  Follicular  stomatitis,  SIO. 
Arndt,  1053. 
Arteries,  cnncer  of,  513. 

classification  of  diseases  of,  513. 

fatty  degeneration  of,  513. 

guneral  dilatation  of,  514. 

syphilis  of,  513,  514. 

tuberculous  granules  in,  513. 

waxy  degeneration  of,  5.13. 
Arterio-capillary   filn-osis   with  contracted  kidney, 
diagnosis,  587. 

morbid  anatomy,  584,  585. 

symptoms,  586. 
Arterloma,  514. 
Arthritis  deformans,  differential  diagnosis,  867. 

etiology,  86"). 

morbid  anat<  >my,  865. 

prognosis,  867. 

symptoms,  866,  867. 

treatment,  8R7. 
Arthritis  rlieuiuatoid.     See  Arthritis  deformans,  865. 
Articular     rlicumatism,    acute.      See  Rheumatism, 
acute  articular,  858. 

chronic.     See  Rheumatism,  chronic  articular. 
Ascaris  Inmbricoides,  308. 
Ascending  paralysis,   acute.      See  Paralysis,  acute 

ascending,  1028. 
Ascites,  differential  diagnosis,  335. 

etiology,  3.33. 

morbid  anatomy,  333. 

physical  signs,  334. 

prognosis,  336. 

symptoms,  334.  ■ 

treatment,  336. 
Asthma,  bronchial,  59. 

differential  diagnosis,  62. 

etiology,  59. 

pliysical  signs,  61. 

prognosis,  62. 

symptoms,  60. 

treatment,  63. 
Ataxia,  locomotor.    See  Locomotor  ataxia,  1018. 
Atelectasis,  129. 
Atelectasis,  congenital,  129. 
Atelectasis,  pulmonary,  differential  diagnosis,  131. 

etiology  of.  130. 

morbid  anatomy  of,  129. 

physical  signs,  1.30. 

prognosis  of,  131. 

symotoms,  130. 

treatment,  131. 
Atheroma.    See  Chronic  endarteritis,  511. 
Atonic  dyspepsia  and  chronic  gastritis,  235. 
Atrophic  iiasal  catarrh,  13. 

difl  rential  diagnosis,  14. 

etiology,  13. 

niorb'd  anatomy,  13. 

prognosis,  14. 

symptoms,  14. 

treatment,  14. 
Atrophy  of  the  brain.     See  Brain,  atmptiy  of,  988. 
Atrophy  of  the  heart.    See  Heart,  atrophy  of,  496. 


Atrophy  of  the  liver.    See  Liver,  chronic  atrophy 

of,  370. 
Atrophy  of  the  lung,  144. 
Atrophy,    progressive    muscular.    See    Progressive 

muscular  atrophy,  1011. 
Autumnal  fever,    i'ee  Typhoid  lever,  611, 

Bacillus,  the  tubercle,  172,  174  175. 

Balfour,  455, 457. 

Bamberrier,  82,  434,  460. 

Bard,  669. 

Barloive,  471. 

Bartel,  557. 

Barthez,  913,  949. 

Barlholoiv.  578. 

Barton,  f,?A. 

Bar  well.  863.  866. 

Basedow's  disease,  differential  diagnosis,  510> 

etiology,  509. 

morbid  anatomy,  508, 509. 

prognosis,  510. 

symptoms,  509. 

treatment,  510. 
Bastian,  962,  964,  1011,  1030. 
Beard,  1064. 
Reck,  588. 
Beduar,  936. 
Begbie,  466.  467. 
Bellingham,  453,  467,  528. 
Bell's  palsy.    See  Facial  paralysis,  1059. 
Bell's  paralysis.    See  Facial  paralysis,  1059. 
Bence-.Join-».  1052. 
Benedict,  803. 
Beneke,  205. 
Benjamin,  980. 
Bennet,  95,891. 
Bergnumn,  1013. 
Berlin,  462,  466. 
Bernard,  265. 
Biermer,  889. 
Bile-ducts,  catarrh  of,  differential  diagnosis,  397, 

eti()loi;T,396. 

morbid"^  anatomy,  395. 

physical  signs.  397. 

prognosis,  397. 

symptoms,  396. 

treatment,  397. 
Biliary  calculi.    See  Gall-stones,  401. 
Biliiiry  colic,  404. 

Biliary  passages,  exudative  inflammation  of,  differ* 
ential  diagnosis,  399. 

etiology,  398. 

morbid  aniitomy.  398. 

phy^ical  signs,  398. 

prognosis,  399. 

symptoms,  398. 

treatment,  399 
Bilious  remittent  fever,  822. 
Biliousness.     See  Functional  derangements  of  livei^ 

406. 
Billroth,  696,  699,  701,  739. 
Binz,  802. 

Birch- Hirschf eld,  417,  910. 
Bii-d,  802. 

Black  measles.    See  Measles 
"Bleeders.'"    See  Haemophilia,  902. 
Bleeding  piles.    See  Hiemorrhoids,  304. 
Blood-vessels,  classification  of  diseases  of,  511. 
Bloody  flux.    See  Dysentery,  272. 
Bhrin.  821. 

Bothriocephalus  latus,  808. 
Bouchard,  965. 
Bouchut,  946. 
Bouillard,  85. 
Bouillaud,  441. 
Bourneville,  958. 
Brain,  abscess  of,  differential  diagnosis,  977. 

etiology,  976. 

morbid  anatomy,  975. 

prognosis,  977. 

symptoms,  976. 

treatment,  977. 
Brain,  aniemin  of.    See  Cerebral  anasmia,  933. 
Brain  and  meninges,  tumors  of,  differential  diagno- 
sis, 982-984. 

etiology.  981. 

morbid  anatomy,  978-981. 

prognosis,  984. 


INDEX. 


1083 


Brain  find  meningps,  tumors  of,  sj'mptoms,  981. 

treatment,  984,  985. 

varieties,  977. 
Brain,  aneurisms  of.    See  Cerebral  tumors,  977. 
Brain,  angiomata  of.     See  Cerebral  tumors,  977. 
Brain,  atropliy  of,  differential  diagnosis,  990. 

etiology,  989. 

morbid  anatomy,  988. 

prognosis,  990. 

symptoms,  989. 

treatment,  990. 
Brain,  cholesteatoma  of.    See  Cerebral  tumors,  977. 
Brain,  cysticerci  of.    See  Cerebral  tumors,  977. 
Brain,  cysts  of.    See  Cerebral  tumors,  977. 
Brain,  diseases  of,  930. 
Brain,  embolism  and  tlirombosis  of.      See  Cerebral 

thrombosis  and  embolism,  956. 
Brain,  fibromata  of.    See  Cc'rebral  tumors,  977. 
gliomata  of.    See  Cerebral  tumors,  977. 
hydatids  of.    *(?  Cerebral  tumors,  977. 
hyperajmia  of.    See  Cerebral  hypersemia,  930. 
Brain,  hypertrophy  of,  differential  diagnosis,  988. 

etiology,  987,  988. 

morbid  anatomy,  987. 

prognosis,  988. 

symptoms,  988. 
Brain,  lipomata  of.   See  Cerebral  tumors,  977. 
Brain,  localization  of  lesions  within,  970-972. 
Brain,  myxomata  of.    See  Cerebral  tumors,  977. 

osteomataof.    See  Cerebral  tumors,  977. 

pa))illomata  of.    See  Cerebral  tumors,  977. 

psammomata  of.     See  Cerebral  tumors,  977. 

sarcomata  of.    See  Cerebral  tumors,  977. 
Brain,  sclerosis  of.    See  Sclerosis  of  the  brain,  985. 
Brain,  softening  of.    See  Cerebral  softening,  959. 
Brain,  thrombosis  and  embolism  of.    See  Cerebral 

thrombosis  and  embolism,  956. 
Bramwell,  890. 
Brif/hf,  265,  551,  584,949. 

Bright's  disease,  amyloid  form  of.    See  Waxy  kid- 
ney, 575. 
Bright's  disease,  cirrhotic.    See   Kidney,  cirrhotic, 

Bright's  disease  of,  568. 
Bright's   diseases   of    the   kidneys.     See  Kidney, 

Bright's  diseases  of,  551. 
BHgidi.  889. 
Brimer,  798. 
Brinton,  293. 
Briquet,  1045. 
Bristowe,  294. 
Broadhent,  1051. 
Brodie,  1045. 
Bronchial  abscess,  129. 
Bronchial  a-thma,  59. 
Bronchial  hemorrhage,  65. 

differential  diagnosis,  68. 

etiology,  66. 

morbid  anatomy,  66. 

prognosis,  69. 

symptoms,  67. 

treatment,  69. 
Bronchiectasis,  55. 

differential  diagnosis,  57. 

etiology,  56. 

morbid  anatomy,  55. 

physical  signs,  56. 

symptoms,  ,56. 

treatment,  57. 
Bronchitis,  acute  capillary,  46. 

differential  diagnosis,  47. 

etiology,  46. 

morbid  anatomy,  46. 

physical  signs,  47. 

prognosis,  48. 

symptoms,  46. 

treatment,  48. 
Bronchitis,  acute  catarrhal,  42. 

differential  diagnosis,  45. 

etiology,  4.3. 

morbid  anatomy,  42. 

prognosis,  45. 

symptoms,  44. 

treatment,  45. 
Bronchitis,  chronic  catarrhal,  49. 

differential  diagnosis,  53. 

etiology,  51. 

morbid  anatomy,  ,50. 

physical  signs,  53. 


Bronchitis,  chronic  catarrhal,  prognosis,  54. 

symptoms,  52. 

treatment,  .54. 
Bronchitis,  clar-siflcation  of,  42. 
Bronchitis,  croupous,  ,57, 

■     differential  diagnosis,  58. 

etiology,  57. 

morbid  anatomy,  57. 

physical  signs,  58. 

prognosis,  59. 

symptoms,  57. 

treatment,  59. 
Broncliitis,  fetid.    See  Chronic  bronchitis,  51, 
Bronchitis,  vesicular,  129. 
Broncho-phthisis,  pulmonalis.    See  Chronic  phthisis, 

184. 
Broncho-pneumonia.    See  Lobular  pneumonia,  101. 
Brown  induration  of  the  lungs,  11.3. 
Brown  oedema  of  lungs,  Vircnow's,  115. 
Brown- Sequard,  897,  969,  995, 1036,  1039,  1043. 
Bi'undes,  95. 
Brunei,  654. 
Brvnton,  557. 
Buck,  751. 

Buhl,  144,  672,  800,  910. 

Bulbar  paralysis,  acute.    See  Paralysis,  acute  bulbar, 
1001. 

chronic.    /Sfee  Paralysis,  chronic  bulbar,  1002. 
Burns,  441. 
Buzzard,  1042-1044. 

Cascitis.     See  Typhlitis,  279. 

Calcification  of  arteries,  513.     - 

Calculi,  biliary.     See  Gall  stones,  401. 

Calculi  of  the  pancreas.  See  Pancreas,  calculi  of,  413. 

Calculi,  renal.    See  Eenal  calculi,  593. 

CalineU,  942. 

Cancani,  881. 

Cancer  of  arteries,  513. 

of  brain.    See  Cerebral  tumors,  977. 

of  gall-bliidder.    See  Gall-bladder,  cancer  of, 
399. 

of  heart,  501. 

of  intestine.    See  Intestine,  cancer  of,  298. 

of  kidney.    See  Renal  cancer,  596. 

of  larynx,  40. 

of  liver.    See  Liver,  cancer  of,  377. 

of  lungs.  140. 

of  oesophagus.     See   (Esophagus,  cancer   of, 
226. 

of  pancreas.    See  Pancreas,  cancer  of,  411. 

of  perioardinm,  502. 

of  pleura.    See  Pleura,  cancer  of,  164. 

of  ^pleen,  418. 

of  siomnch.     See  Stomach,  cancer  of,  241. 

of  tongue.    See  Tongue,  cancer  of,  216. 

pulmo'naiy,  140. 
Cancrum  oris.    See  Gangrenous  stomatitis,  211. 
Camtatf,  558,  910. 
Capillary  bronchitis,  acute,  46. 
Caput  MedusiB.  345. 
Cardiac  dilatation,  differential  diagnosis,  484. 

etiology,  4hl. 

morbid  anatomy,  480. 

physical  signs,  483. 

prognosis,  485. 

symptoms,  482. 

treatment,  486. 

varieties  of,  480. 
Cardiac  hypertrophy,  differential  diagnosis,  478. 

etiology,  474. 

morbid  anatomy,  473. 

physical  signs,  476. 

symptoms,  475. 

trcitment,  479. 

varieties  of,  472. 
Cardiac  murmurs  and  their  relation  to  valvular  dis> 
ease  of  the  heart,  441. 

murmurs.    /See  Murmur,  cardiac,  441. 
Cardiac  neuroses,  varieties  ol,  502. 
Cardiac  p.Upitation.  nervous,  differential  diagnosis, 
.503. 

etiology,  ,502. 

lU'OLTiiosis,  .504. 

symptoms,  .503. 
_  treatmi-nt,  504. 
Cardiac  thromliosis,  differential  diagnosis,  499. 

etiology,  498. 


1084 


INDEX. 


Cardiac  thrombo-'is,  morbid  anatomy,  497,  498. 

physical  signs,  499. 

prognosis,  499. 

symptoms,  499. 

tieaiment.  500. 
•'  Carditis."    See  Myocarditis,  487. 
Camificatioii  of  lung,  114. 
Carre,  1020. 
Carter,  740. 
Cary,  891. 

Casts  in  the  urine,  536. 
Catalepsy,  differential  diagnosis,  1049. 

etiology,   1048. 

prognosis,  1049. 

symptoms,  1048. 

treatment,  1049. 
Cs<arrh,  acute  gastric.    See  Sub-acute  gastritis,  229. 
Catarrh,  atrophic  nasal.  See  Atrophic  nasal  catarrh, 

13. 
Catarrh,  chronic  nasal.     See  Chronic  coryza,  10. 
Catarrh,  chronic  naso-pharyngeal.   See  Hypertrophic 

nasal  catarrh,  11. 
Catarrh,  dry  nasal.    See  Atrophic  nasal  catarrh,  13. 
Catarrh,  epidemic.    See  Influenza,    797. 
Catarrh,  fetid  nasal.    See  Ozaena,  15. 
Catarrh,    hypertrophic    nasal.     See    Nasal  catarrh, 

hypertrophic,  11. 
Catarrh,  intestinal.     See  Enteritis,  257. 
Catarrh  of  the  bile-ducts.      See  Bile-ducts,  catarrh 

of,  395. 
Catarrh  of  the  larynx,  chronic  phthisical,  23. 
Catarrhal  bronchitis,  acute.    See    Bronchitis,  acute 

catarrhal,  42. 
Catarrhal  bronchitis,  chronic.    /See  Bronchitis,  chron- 
ic catarrhal,  49. 
Catarrhal   laryngitis,   acute.    See  Laryngitis,  acute 

catarrhal,  17. 
Catarrhal  laryngitis,  chronic  syphilitic.    See  Laryn- 
gitis, chronic  catarrhal  syphilitic,  21. 
Catarrhal  laryngitis,   simple  chronic.       See  Laryn- 
gitis, chronic  catarrhal,  21. 
Catarrhal  pharyngitis.    See  Pharyngitis,  catarrhal, 

221. 
Catarrhal  pneumonia.    See  Pneumonia,  lobular,  101. 
Catarrhal  stomatitis.    See  Stomatitis,  208. 
Cavalie,  906. 

Cavities  in  phthisis,  180. 
Cayley,  980. 
Celborne,  975. 

Cerebral  abscess.    See  Brain,  abscess  of,  975. 
Cerebral  ansemia,  differential  diagnosis,  934. 

etiology,  933. 

morbid  anatomy,  933. 

prognosis,  934. 

symptoms,  934. 

treatment,  934. 
Cerebral  .ipoplexy,  differential  diagnosis,  972,  973. 

etiology,  966,  967. 

morbid  anatomy,  964,  966. 

prognosis,  973,  974. 

symptoms,  967,  972. 

treatment.  974,  975. 
Cerebral  hyperaemia,  differential  diagnosis,  932. 

etiology,  9.30. 

morbid  anatomy,  930. 

prognosis,  932. 

symptoms,  931. 

treatment,  932. 
Cerebral  lesions,  localization  of,  970.  971,  973. 
Cerebral  softening,  differential  diagnosis,  963. 

etiology,  961. 

morbid"  anatomy,  959-961. 

prognosis,  963 

symptoms,  962. 

treatment,  963.  964. 

varieties  of.  959. 
Cerebral  thrombosis  and  embolism,  differential  diag- 
nosis, 958. 

morbid  anatomy,  956,  957. 

prognosis,  959. 

symptoms,  9.57. 

treatment,  959. 
Cerebral  tumors.   See  Brain  and  meninges,  tumors  of, 

Cerebro-spinal  fever.   See  Cerebro-spinal  meningitis, 

684. 
Cerebro-sninal    meningitis,    differential   diagnosis, 

690,  691.  I 


Cerebro-spinal  meningitis,  etiology,  686. 
morbid  anatomy,  684,  686. 
prognosis,  691,  692. 
symptoms,  686-690. 
treatment,  692-694. 
Cerebro-spinal  sclerosis,  differential  diagnosis,  1017. 
etiology,  ]i)16. 
morbid  anatomy,  1015. 
prognosis,  1017. 
symptoms,  1016. 
treatment,  1017. 
Chalicosis,  182. 
Chalmeil,  659. 
Chapman,  1077,  1079. 
Charcot,  179,  484,  463,  865,  866,  876,  961,  965,  969, 98T, 

999,  1003,  1019,  1021,  1030,  1047,  1061,  1069. 
Charcot  and  Loomis,  858,  966. 
Chauveau,  441. 

Chicken-pox.   See  Varicella,  764. 
Chlorosis,  differential  diagnosis,  887. 
etiology,  886. 
morbid  anatomy,  886. 
prognosis,  887. 
symptoms,  886. 
treatment,  887,  888. 
Cholera,  English.    See  Cholera  morbus,  266. 
Cholera  epidemic,  differential  diagnosis,  666,  667. 
etiology,  663. 
morbid  anatomy,  660. 
prognosis,  667. 
symptoms,  663. 
treatment,  667,  668. 
variiHies  of,  665^ 
Cholera  infantum,  differential  diagnosis,  269. 
etiology,  268. 
morbid  anatomy,  268. 
prognosis,  270. 
symptoms,  269. 
treatment,  270,  271. 
Cholera  morbus,  differential  diagnosis,  267. 
etiology,  266. 
morbid  anatomy,  266. 
prognosis,  268. 
symptoms,  266. 
treatment,  268. 
Cholera  nostras.    See  Cholera  morbus,  266. 
Cholera  sporadic.    See  Cholera  morbus,  266. 
Cholesteatoma  of  the  brain.    See  Cerebral  tumors, 

977. 
Chamel,  108. 

Chorea,  differential  diagnosis,  1052. 
etiology,  1051. 
morbid  anatomy,  1050. 
prognosis,  1052. 
symptoms,  1051. 
treatment,  1053. 
Chronic  anterior  polio-myelitis.    See  Polio-myelitis, 

chronic  anterior,  1010. 
Chronic  articular  rheumatism.     See   Kheumatism, 

chronic  articular,  863. 
Chronic  atrophy  of  the  liver.    See,  Liver,  chronic 

atrophy  of,  370. 
Chronic    Bright's,   of    the    kidney.     See    Kidney, 

chronic  Bright's  disease,  of,  562. 
Chronic  bulbar  paralysis.  *See  Paralysis,  chronic  bul- 
bar, 1002. 
Chronic  catarrhal  bronchitis,  49. 
Chronic  catarrh  of  the  larynx  in  phthisis,  23. 
Chronic  catarrh  of  the  stomach.    See  Chronic  gas- 
tritis, 231. 
Chronic  coryza,  10. 
Chronic  endarteritis,  511. 
Chronic  endocarditis.    See  Endocarditis,  interstitial, 

431. 
Chronic  endophlebitis,  514. 
Chronic  general  diseases,  classification,  857. 
Chronic  hydrocephalus.  See  Hydrocephalus,  chronic, 

948. 
Chronic  inflammatory  dj'spepsia.    See  Chronic  gas- 
tritis, 231. 
Chronic  laryngitis,  21. 
Chronic  laryngitis  of  syphilis,  25. 
Chronic  lead  poisoning.  See  Lead  poisoning,  chronic, 

317,  319. 
Chronic   malarial  infection,  differential  diagnosis. 
854 
etiology.  853. 
morbid  anatomy.  853. 


INDEX. 


1085 


Chronic  malarial  infection,  prognosis,  855. 

symptoms,  853. 

treatment,  855. 
Chronic  meningitis.    See  Meningitis,  chronic,  941. 
Chronic  mercurialism.     See  Mercurial  ism,  chronic, 

1066. 
Chronic  myelitis.    See  Myelitis,  chronic,  999. 
Chronic  myocarditis.    See    Fibroid  disease  of  the 

heart,  490. 
Chronic  nasal  catarrh.    See  Chronic  coryza,  10. 
Chronic  naso-pharyngeal  catarrh.    See  Hypertrophic 

nasal  catarrh,  11. 
Chronic  pancreatitis.    See  Pancreatitis,  chronic,  411. 
Chronic  pericarditis.     See  Pericarditis,  cbronic,  429. 
Chyluria,  etiology,  604. 

morl)id  anatomy,  604. 

prognosis,  605. 

symptoms,  605. 

treatment,  605. 
Cicatrization  in  inflammation,  3. 
Giniselli,  52?. 

Circumscribed  pulmonary  apoplexy,  120. 
Circumscribed  pulmonary  gangrene,  125. 
Circum^^cribed  suppurative  hepatitis.    See  Hepatitis 

circumscribed  suppurative,  349. 
Cirrhosis,  4. 

Cirrhosis  of  the  liver.    See  Interstitial  hepatitis,  342. 
Cirrhosis  of  the  Inng,  108. 
Cirrhotic  Bright's  disease.     See  Kidney,  cirrhotic 

Bright's  disease  of,  568. 
Clapham,  1077, 1079. 
Clark,  184,  330,  908,  991,  1015,  1019,  1023. 
Climatic  treatment  of  phthisis,  203. 
Clonston,  104. 

Cloutly  swelling  of  the  heart.    See  Heart,  parenchy- 
matous degeneration  of. 
Coagulation-necrosis  in  phthisis,  174. 
Coal-miner's  lung,  182. 
Cobbokl,  501. 
Oohnheim,  79,  118,  174,  175,  187,  518,  553,  557,  556, 

558,  739,  748,  888,  916,  918,  946,  1026. 
Cold  bath,  rules  for,  in  acute  pneumonia,  99. 
Cold,  rules  for  use  of,  in  acute  pneumonia,  99. 
Colic,  biliary,  404. 

Colic,  copper.    See  Intestinal  colic,  319. 
Colic,  gall-stone,  404. 
Colic,  intestinal,  differential  diagnosis,  319. 

etiolog}',  317. 

jjrognosis,  320. 

symptoms,  318. 

treatment,  320. 

varieties  of,  318,  319. 
Colic,  lead.    See  Intestinal  colic,  317,  319. 
Colic,  nephritic,  594. 
Colic,  renal,  594. 

Colica  pictonum.    See  Lead  colic,  317,  319. 
Colitis.    See  Enteritis,  257. 
Collapse  of  the  lungs,  129. 
Collapse,  pulmonary,  129. 
Collie,  756. 
Colloid  caseous  pneumonia.    See  Chronic  phthisis, 

179. 
Coma,  causes  of,  929. 
Coma  vigil,  718. 

Compensatory  liypersemia  of  the  lungs,  113. 
Confluent  variola.    See  Small-pox,  745. 
Congestion,  hypostatic,  113. 
Congestion  of  the  brain.    See  Cerebral  hyperaemia, 

9.30. 
Congestion  of  tlie  kidneys.    See  Renal  hypereemia, 

543. 
Congestion  of  the  liver.    See  Liver,  passive  hyperse- 

miaof,  .339. 
Congestion  of  the  lungs,  113. 
Constipation,  differential  diagnosis,  316. 

etiology,  314,  315. 

morbid  anatomy,  314, 

prOiinosis,  316. 

symptoms,  315. 

treatment,  316. 
Consumption  of  the  lungs.    See  Phthisis,  171. 
Contagion,  definition  of,  609. 

Continued    malarial    fever,    dififerential   diagnosis, 
8.34. 

etiology,  828. 

morbid  anatomy,  827. 

prognosis,  835. 

symptom.-',  829. 


Continued  malarial  fever,  treatment,  8-36. 
Contracted    kidney^  arterio-capillary  Jibrosis.     See 

Arterio-capillary  fibrosis,  584. 
Convulsions,  927. 

Convulsions,  infantile,  and  eclampsia,  1076. 
Cooper,  1045. 

Coordination,  disorders  of,  929. 
Cojilarid,  799. 

Copper  colic.     See  Intestinal  colic,  317. 
Uorlies,  510. 

Cwnil,  349,  368,  473,  487. 

Corrdl&nA  Hanvier,  110,  113,  516,  518,  548,  569,  570, 
575,  588,  650,  892,  898,  903,  979,  980,  981,  1016. 
1019. 
Corrigan,  110,  441,  450. 
Cm'Visari,  441,  445. 
Coryza,  acute,  9. 

differential  diagnosis,  10. 

etiology,  9. 

morbid  anatomy,  9. 

prognosis,  10. 

symptoms,  li. 

treatment,  10. 
Coryza,  chronic,  10. 

differential  diagnosis,  11. 

etiology,  10. 

morbid  anatomy,  10. 

symptoms,  10. 

treatment,  11. 
Croup,  27. 
Croup,  membranous.  See  Acute  croupous  laryngitis, 

27. 
Croupous  bronchitiSj  57. 
Croupous  inflammation,  6. 
Croupous  laryngitis,  acute,  27. 
Croupous  pharyngitis,  223. 
Croupous    stomatitis.      See    Follicular    stomatitis, 

210. 
Crudeli,  809. 

Cmveilhier,  964,  966,  981. 
CurHe,  641. 
Ciirshmann,  751 

Cysticerci  of  the  brain.    See  Cerebral  tumors,  977. 
Cystic  kidneys,  etio.ogy  and  morbid  anatomy,  591^ 

592. 
Cystitis,  differential  diagnosis,  607. 

etiology,  606. 

morbid  anatomy,  606. 

prognosis,  608. 

symptoms,  607. 

treatment,  608. 

varieties,  606. 
Cysts  in  the  heart,  502. 

Cysts  in  the  pancreas.    See  Pancrea?,  cysts  of,  413. 
Cysts  of  the  brain.    See  Cerebral  tumors,  977. 
Cysts  of  spleen,  418. 

Da  Costa,  87. 

Dejeriae,  828 . 

Delano's  atomizer,  10. 

Belasiaure,  1089. 

Delirium  tremens.    See  Alcoholism,  913. 

Dengue  fever,  differential  diagnosis,  851. 

etiology,  849. 

morbid  anatomy,  849. 

prognosis,  853. 

syniptouis,  850. 

treatment,  852. 
Dermoid  cysts  in  the  lung,  143. 
Desgranqea.  883 
Diabetes  insipidus,  differential  diagnosis,  882. 

etiology,  882. 

morbid  anatomy,  882. 

prognosis,  882. 

symptoms,  882. 

treatment.  883. 
Diabetes  mellitus,  differential  diagnosis,  880. 

etiology,  878. 

morbiii  anatomy,  877. 

prognosis,  880. 

symptoms,  878-880. 

treatment,  880,  881. 
Diarrhoea,  acute,  differential  diagnosis,  265. 

prognosis,  265. 

symptoms,  264. 

treatment,  265. 

varieties  of,  263. 
Diarrhoea,  chronic,  265. 


1086 


IlS^DEX. 


Diathesis,  the  hemorrhagic.    See  Haemophilia,  902, 
JJickensoa,  471,  5ia,  u8:i.  o.3. 

DifEiise  catarrhal  ulcers  of  the  intestine.    See  Intes- 
tinal ulcers,  'Mb. 
Diffuse  parenclij'matous    hepatitis.    See  Hepatitis, 

parenchymatous,  350. 
Diffuse  pulmonary  apoplexy,  124. 
Diffuse  pulmonary  gangrene,  125 
Digestive  system,  diseases  of,  208. 
Dilatation  of  ihe  heart.    See  Cardiac  dilatation,  480. 
Dilatation  of  the  stomach     See  Stomach,  dilatation 

of,  254. 
Diphtheria,  definition,  668. 

differential  diagnosis,  678. 

etioogy,  6i'2,  Ocj. 

morbid-anatomy,  669-672. 

prognosis,  68U. 

seqiiehe,  677. 

symptoms,  constitutional,  675-678. 

symptoms,  local,  673-675. 

treatment,  6ol-684. 
Diphtheritic  intiammation,  7. 
Diphtheritic  paralysis,  677. 
Diphtheritic  pharyngitis,  223. 
Discrete  variola.    See  Small-pox,  745. 
Diseases,  ciironic  generi.l,  857. 

of  larynx,  17. 

of  nasal  passages,  9. 

of  respiratory  organs,  9. 

of  the  blood-vessels,  classification  of,  511. 

of  the  brain,  classification  of,  930. 

of  the  gall-bladder,  cl  issification  of.  395. 

of  the  gall-duct-:,  classification  of,  395. 

of  the  heart,  cla-siflcadon  of,  420. 

of  the  kidneys,  529. 

of  the  liver,  classification  of,  337. 

of  the  nrrvous  system,  general  symptomatol- 
ogy of,  924. 

of  tne  pancreas,  classification  of,  410. 

of  the  spinal  cord,  classification  of,  990. 

of  the  spleen,  classification  of,  413. 
Disseminated  sclerosis.  See  Cerebro-spinal  sclerosis, 

1015. 
Dobell's  solution,  11. 
Dochmius  duodeualis,  309. 
I)m±iu.  881. 
Dover's  powder,  45. 
Brachman II ,  8ii7. 
Drake,  826,  829. 
Draper,  879. 

Dropsy,  abdominal.   See  Ascites,  333. 
Dropsy  of  the  abdomen.    See  Ascites,  333. 
Dropsy  of  the  gall-bladder     See  Enlarged  gall-blad- 
der, 3'J9. 
Dropsy  of  the  kidnev.     See  Hydronephrosis,  580. 
Dropsy  of  the  pericardium.    See  Hydropericardiiim, 

506. 
Dry  nasal  catarrh.    See  Atrophic  nasal  catarrh,  13. 
Duchenne,  1003,  1005,  1009,  1026,  1027,  1062. 
Duchenne's  disease.     See  Locomotor  ataxia,  1018. 
Diijardin-Beavvietz,h7A. 
Duodenitis.    See  Enteritis,  257. 
Duodenum,  nicer  of.  etiology,  284. 

morbid  anatomy,  284. 

prognosis,  285. 

symptoms,  284. 
DuponU  349. 

Dvrancl- Fardel,  961.  962,  973,  989. 
Dysentery,  acute,  differential  diagnosis,  877. 

etiology,  273. 

morbid  anatomy,  272,  273. 

proei'osis,  277. 

symptoms,  275. 

treatment,  278,  279. 
Dj'sentery,  chronic,  277. 
Dy-^eiitery,  varieties  of,  272. 
Dyspepsia.  238. 

differential  diagnosis,  240. 

etiology,  238,  239. 

morbid  anatomy,  238. 

prognosis,  240. 

symptoms,  239. 

treatment.  240,  241. 
Dj'spepsia,  inflammatory,  231. 
Dyspepsia,  intestinal,  etiology,  271. 

symptoms,  271. 

t'-eatment,  271. 
Dysphagia,  inflammatory.    See  CEsophagitis,  224. 


Echeverria,  1036,  1041. 

Echinococci  in  the  lungs.    See  Hydatids,  154. 

Echinococci  of  lung  and  pulmonary  infarction,  123. 

Ecliiuucocci  of  the  liver.  Ste  Li\  er,  hydatids  of,  385. 

Eclampsia  and  infantile  convulsions,  1076. 

J^cker,  930. 

E/uiic/i,  888. 

Eicli.boni,  659. 

Eu-lilwrst,  888. 

Electrical  irritability,  925. 

Ely's  powder  l)lov\er,  11. 

Embolic  pneumonia.  See  Pulmonary  infarction,  130. 

Embolic  pneumonitis,  120. 

Embolism,  definition  of,  517. 

morbid  anatomy,  518, 
Embolism  of  lung,  fat,  122. 
Embolism  of  the  brain.    See  Cerebral  thrombosis 

and  embolism,  956. 
Embolism  of   the  kidney.    See  Renal  hemorrhage, 
548. 

pulmonary  fat,  122. 
Ernerson,  828. 
Emphysema,  interlobular,  131. 

differential  diagnosis,  137. 

etiology  of,  134. 

morbid  anatomy,  132,  134. 

physical  signs,  136. 

prognosis,  138. 

symptoms,  135. 

treatment,  138. 
Emphysema  of  the  lungs,  131. 
Emphysema,  pulmonary,  131. 
Emphysema,  vesicular,  131. 

differential  diagnosis,  161. 

etiology,  159. 

morbid  anatomy,  158. 

physical  signs,  161. 

Ijrognosis,  161. 

symptoms,  160. 

treatment,  161. 
Enchondromata  in  the  lungs,  142. 
Endarteritis,  acute. 

etiology,  511. 

morbid  anatomy,  511. 

symi)toms.  511. 
Endarteritis,  chronic,  differential  diagnosis,  513. 

etiologv,  512. 

moriiid  anatomy,  511. 

prognosis,  513. 

symptoms   512. 
Endarteritis,  deformans.     See  Chronic  endarteritis, 

511. 
Endemic  hsematuria,  601,  603. 
Endocardial  murmurs.    See  Murmurs,  endocardial, 

443. 
Endocarditis,  acute  exudative,  431. 

differential  diagnosis,  427. 

etiology,  434. 

morbid  anatomy,  432. 

physical  signs, 435. 

prognosis,  438. 

symptoms,  435, 

treatment,  438,  439. 
Endocardii is,  chronic.  See  Endocarditis,  interstitial, 

439. 
Endocarditis,  interstitial,  etiology,  441. 

morbid  anatomy,  439. 

symptoms,  441. 

varieties  of,  431. 
Endocarditis,  ulcerative,  etiology,  434. 

morbid  anatomy,  433. 

prognosis,  438. 

symptoms,  435. 

treatment,  483. 
Endophlebitis,  514. 

English  cliolera.     &e  Cholera  morbus,  266. 
Enlarged  gall-bladder.    See  Gall-bladder,  enlarged, 

399. 
Enlarged  spleen.    See  Spleen,  hypertrophy  of.  416. 
Enteric  fever.     See  Typhoid  fever,  611. 
Enteritis,  acute,  260 

differential  diagnosis,  261. 

etiology,  259. 

morbid  anatomj'',  257. 

prognosis,  262. 

symptoms,  259. 

treatment,  263. 
Enteritis,  varieties  of,  257. 


INDEX. 


1087 


Enteritis,  chronic,  261.  ,     ,.     ,    ,  not 

Enteritis,  follicular.    See  Intestinal  ulcers,  285. 
Enteritis,  niembranous,  260. 
BnteritiH,  phlegmonous,  261. 
Enteriti.s,  strumous.    See  Intestinal  ulcers,  285. 
Enteroliths.    See  Intestinal  obstruction,  292. 
Epidemic  catarrh.    See  Influenza,  797.    ^,      ^      , 
Epidemic  cerebro-spinal   meningms.    See  Cerebro 

spinal  meninsiiis,  epidemic,  684. 
Epidemic  cholera.    See  Cholera,  epidemic  660. 
Epidemic  roseola.    &><?  German  measles   .91. 
Epilepsy,  differential  diagnosis,  1039,  1040. 
etiology,  1035,  1036. 
morbid  anatomy,  1034,  1035. 
prognosis,  1040. 
symptoms,  10:^6,  1039. 
treatment,  1(140,  1042. 
Epithelioma  of  the  lung,  143. 
Epithelioma  of  tongue.   See  Cancer  of  tongue,  216. 
Erb  996,  1000,  100471006,  1007,  1010,  1016,  1019,  1021, 

1023,  1024,  1026,  1030,  1049. 
Erichsen,  588. 

Erlancier,  906.  . 

Ervcipelas,  differential  diagnosis,  706. 
etiology,  703. 
morbid  anatomy,  701. 
prognosis,  705. 
symptoms,  704. 
treatment,  705,  706. 
Erythism  of  the  stomach.     See  Gastric  neuroses, 

252. 
Esmarch  ice-bag,  99.  ^„„^ 

Eulenberg,  510,  1021,  1026,  1048,  1049,  1062. 
Ewart,2T:8.  „      ^      ,    j.  ►«□ 

Exophthalmic  goitre.    See    Basedow's  disease,  508. 
External    pachymeningitis.      See   Pachymeningitis 

externa,  951. 
Exudation,  inflammatory,  3.  _  ,  I 

Exudative  endocarditis.  See  Endocarditis,  acute  ex- 
udative, 431. 
Exudative  inflammation  of  the  biliary  passages.  See 
Biliary  passages,  etc.,  398. 

Eabra,991.  ,     .     ,    .  ,   ^„,,„ 

Facial  paralysis.    See  Paralysis,  facial,  1059. 
Fseces,  retention  of,  and  diarrhoea,  265. 
Eagge,  454,  471. 
Ea>re,  904. 

Pat  embolism  of  the  lungs,  122. 
Fate  of  pus,  8. 

Fatty  degeneration  of  arteries,  513. 
Fatty  degeneration  of  the  heart.  See  Heart,  fatty  de- 
generation of,  491. 
Fatty  degeneration  of  the  pancreas.    See  Pancreas, 

fatty  degeneration  of,  411. 
Fatty  hypertrophic  cirrhosis'  of  the  liver,  i'49. 
Fatty  infiltration  of  liver.    See  Fatty  liver,  372. 
Fatty  liver,  differential  diagnosis,  374. 

etiolosy,  373. 

morbid  anatomy,  372. 

physical  signs.  374. 

prognosis,  374. 

symptoms,  373. 

treatment,  .374.  375. 
Fatty  metamorphosis  of  the  liver.    See  Fatty  liver, 

372. 
Eaulkner,  65. 
Eay?r,r,  1056. 
Eede,  888. 

FeMing's  test  for  sugar  in  the  urine,  879. 
Eeinberg,  992. 

Fermentation  test  for  sugar  in  the  urine,  879. 
F«>tid  bronchitis.    5de  Chronic  bronchitis,  57. 
Fetid  nasal  catarrh.    See  Ozsena,  15. 
Fever,  continued  malarial.    See  Continued  malarial 
fever,  827. 

dengue.    See  Dengue  fever,  849. 

enteric.    See  Typhoid  lever,  611. 

infantile  remittent,  260. 

intermittent.    See  Intermittent  fever,  810. 

malarial.    See  Malarial  fever,  810. 

milinry.    See  Miliary  fever,  794. 

peniicious  malarial.    See  Pernicious  malarial 
fever,  839. 

relapsing.     See  Relnpsing  fever,  7-38. 

remittent.    See  Remittent  fever,  818. 

rheumatic.    See  Rheumatism,  acute  articular, 
857. 


Fever,  scarlet.    See  Scarlet  fever,  765. 

spotted.    ,S'««  Cerebro-spinal  meningitis,  bai. 
typhoid.     See  Typhoid  fever,  611. 
typho-malarial.    See  Continued  malaria!  fever, 

827 
typhus.    See  Tyi^hns  lever,  710. 
tongue  in,  and  catarrhal  stomatitis,  209. 
Fibroid  disease  of  the  heart.    See  Heart,  fibroid  dis- 
ease of,  490. 
Fibroid  induration  of  the  lung  and  cancer  of  the 

lung,  142. 
Fibroid  pneumonia,  108. 
Fibromata  in  lungs,  142. 

Fibromata  of  the  brain.    See  Cerebral  tumors,  977. 
Fibromata  of  the  heart,  501. 
Fibromata  of  the  kidney,  598. 

Fibrous  phthisis.   See  Phthisis,  chronic  fibrous,  181. 
Eitz,  803. 
Eletchei',  984. 
Eliclisiq,  1025. 

Flint,  loo,  899.  „     ,. 

Floating  or  movable  kidney.  See  Kidney,  floating  or 

movable,  601. 
Flux,  the  bloody.    See  Dysentery,  272. 
Follicular  enteritis.    See  Intestinal  ulcers,  285. 
Follicular  pharyngitis.    See  Catarrhal  pharyngitis, 

221. 
Follicular    stomatitis.     See    Stomatitis,    follicular, 

210. 
Follicular  ulcers  of  the  intestine.    See   Intestinal 

ulcers,  285. 
Forster.  953.  966,  978. 
Foster,  557,  882,  892,  941,  942,  975,  1004. 
Fotherqili.  885 

Fox,  79,  95,  108,  109,  174,  190,  978. 
Frank,  878. 
Frankel,  175. 
Franklin,  207. 

Free  surfaces,  mflammation  of,  4. 
Freiich,  538. 
Friedreich,  887,  1019. 
Eriedrich,  510. 
Enedrichs,  441. 
Frarmnann.  1016. 

Functional  derangements  of  the  liver,  406. 
Functional  diseases  of  the  intestines,  314. 
Functional  diseases  of  the  nervous  system,  1034. 

Ocdezoivski,  946. 

Gall-bladder,  cancer  of,  etiology,  399. 

morbid  anatomy,  399. 

physical  signs,  399. 

symptoms,  399. 
Gall-bladder,  diseases  of,  395. 
Gall-bladder,  dropsy  of.    See  Enlarged  gall-bladder, 

399. 
Gall-bladder,  enlarged,  differential  diagnosis,  400. 

etiology,  400. 

morbid  anatomy,  400. 

physical  signs,  400. 

prognosis,  401. 

symptoms,  400. 

treatment,  401. 
Gall-ducts,  diseases  of,  395. 
Gall-stone  colic,  404. 
Gall-stones,  differential  diagnosis,  405. 

etiology,  403. 

morbid  anatomy,  401, 

prognosis,  405. 

symptoms,  403. 

treatment,  406. 
Gangrene,  125. 

Gangrene,  circumscribed  pulmonary,  125. 
Gangrene,  diffuse  pulmonary,  125. 
Gangrene  of  the  lungs,  125. 

Gangrene,    pulmonary,    differential    diagnosis    of, 
127. 

etiology  of,  126. 

morbid  anatomy  of,  126. 

physical  signs,  127. 

])rognosis  of,  128. 

symptimis  of,  126. 

treatment  of,  128. 
Gangrenous  stomatitis.    See  Stomatitis,  gangrenous, 

211. 
Crctrdner.  888. 
aarrod.  858,  860,  874. 
Gastric  catarrh,  acute.    See  Sub-acute  gastritis,  229. 


1088 


ISTDEX. 


Gastritis,  ncnto,  228. 

dilieieulial  diagnosis,  229. 

etiol()c;y,  S-^8. 

morljid  anatomy,  228. 

\>v  t'liosis,  229. 

tiymptoms,  2a8,  229. 

tieatmi'iit,  2;Jil. 
Gastritis,  chronic,  231. 

ditt'ereuuiil  diagnosis,  235. 

.•tioiosy,  233. 

morbid  iuiatomy,  231. 

prognosis,  ■i'io. 

sympioms,  233. 

treatment,  235. 
Gastritis,  piilegmonous,  differential  diagnosis,  237. 

etiology.  237. 

morbid  anatomy,  236. 

symptom^,  237'. 

prognosis,  237. 

treatment,  237. 
Gastritis,  sub-acuie,  differential  diagnosis,  231. 

etiology,  230. 

morbid  anatomy,  229. 

prognosis,  231. 

symptoms,  230. 

treatment,  231. 
Gastritis,  toxic.    See  Acute  gastritis,  228. 
Geigel,  457. 

Gelatiniform  infiltration.    See  Chronic  phthisis,  179. 
Getulrin,  441,  978. 
General  dilatation  of  arteries,  514. 
General  pnralysis,  925. 
GerboreU,  952. 
Qerhnrdt,  124. 
German  measles,  differential  diagnosis,  793. 

etiology,  729. 

morbid  anatomy,  791 . 

prognosis,  793. 

symptoms,  792. 

treatment,  793. 
Gihh,  829. 
Gibney,  601. 
Gill,  100. 

Gliomata  of  the  brain.    See  Cerebral  tumors,  977. 
Glossitis,  214. 

differential  diagnosis,  215. 

etiology,  215. 

morbid  anatomy,  214. 

pro'jnosis.  216. 

symptoms,  214. 

treatment,  216. 

vsirieties  of,  214. 
Glosso-labio-laryngeal  paralysis.    /Sije  Chronic  bulbar 

paralysis,  1002. 
Glottis,  dropsy  of,  25. 
Glottis,  oedema  of,  25. 
Glucosnria.    See  Diabetes  mellitus,  877. 
Glycohfemia.    See  Diabetes  mellitus,  877. 
Glycosuria.     See  Diabetes  mellitiis,  877. 
Goitre,  exophthalmic.    See  Basedow's  disease,  508. 
Golgi,  933. 
Golis,  949. 
Goodhart,  885. 
Good3'ear's  atomizer,  10. 
Gougoiienheim,  970. 
Gout,  differential  diagnosis,  874. 

etiology,  872. 

morbid  anatomy,  870-873. 

prognosis,  875. 

symptoms  873. 

treatment,  875,  876. 
Gouty  kidney.    See  Kidney,  cirrhotic  Bright's  dis- 
ease of,  .568. 
Gonty  liver     S-'e  Interstitial  hepatitis,  342. 
Gotuers,  1035,  1036,  1042,  1049,  1060,  1069. 
(?/««/e,669. 

Grariular  liver.    See  Interstitial  hepatitis,  342. 
Gravel,  hepatic,  403. 

Graves'  disease.    See  Basedow's  disease,  608. 
Graves,  735. 
Gray.  1072. 

Gray  infiltration.    (S'fg  Chronic  phthisis,  179. 
Greene,  87. 
Greenhorv,  900. 

Griexinger.  6.52,  727,  931,  952, 1043. 
GrlfoJe,  79,  88,  95,  108. 
Growitz,  888. 
Gubkr,  538,  968,  971. 


Gull,  475,  90P,  1030. 

Gull  and  Sutton,  490,  513,  538,  569,  584,  587,  862,  975i 

976. 
Gummata  of  spleen,  418. 

Gummata  of  the  br.dn.    See  Cerebral  tumors,  977. 
Gummata  of  the  heart,  ,508. 
Gummy  rumor  ot  the  liver.    See  Liver,  gummata  of, 

Gusferoa ,  889. 
Guttmuii,  457,  465. 

Hsematemesis  and  bEeniopty.«is,  254. 
Hsematemesis,  differential  diagnosis,  254 

etiology,  2.53. 

prognosi.'^,  254. 

symptoms,  2,53. 

treatment,  254. 
Hsemntinuria,  604. 
Usemntomata  in  the  lungs,  142. 
Hsematiiria,  differential  diagnosis,  604. 

etiology,  602. 

sj'uipioms,  603. 
Hsematnriii,  endemic,  603. 
Haemoglobinuria,  604. 
HEemopericardium.  507. 
Hsemopliilia,  differential  diagnosis,  903. 

etiol.  gy,  902. 

morbid  anatomy,  903. 

prognosis,  903. 

symptoms,  902. 

treatment,  903. 
Haemoptysis  and  hsematemesis,  254. 
Haemoptysis,  f^pnnou:^,  69. 
Hsemothorax,  171. 

etiology,  171. 

symptoms,  171. 

treatment,  171. 
TToimsch,  650. 
Hall,  1041. 
Hamilton,  183. 

Hammond.  970,  975,  987, 1056. 
Hanof,  349. 
Hardie,  654. 
Hare,  1046. 
Harkin,  903. 
Harley,  603  1053. 
Harvard,  122. 

Hay  den,  454,  460,  462,  471,  528. 
Hayem,  960. 

Headache,  sick.    See  Megrim,  1075. 
Heart,  amyloid  degeneration  of,  etiology,  495. 

morbid  anatomy,  494. 

sympfoms,  495. 

treatment,  495. 
Heart,  aneurism  of,  440. 

etiology,  500. 

morbid  anatomy,  500. 

physical  signs,  501. 

prognosis,  501. 

symptoms,  ,500. 

treatment,  501. 
Heart,  atrophy  of,  etiology,  496. 

morbid  anatomy,  496. 

prognosis,  497. 

symptoms,  496. 

treatment.  497. 
Heart,  cancer  of,  501. 
Heart-clots.    See  Cardiac  thrombosis,  497. 
Heart,  cysts  of,  502. 

Heart,  dilata'ion  of.    See  Cardiac  dilatation,  480. 
Heart  disease,  pneumonia,  114. 
Heart,  diseases  of.  420. 

Heart,  fatty  degeneration  of,  differential  diagnosis, 
494. 

etiology,  493. 

morbid  anatomy,  491. 

physical  signs,  493. 

prognosis,  494. 

symptoms,  493. 

treatment,  494. 

varieties,  491. 
Heart,  tibroid  disease  of,  differential  diagnosis,  491. 

etiology.  490. 

morbtd  anatomy,  490. 

prognosis,  491. 

symptoms,  490. 

treatment,  491. 
Heart,  flbrou.a  of,  501. 


INDEX. 


1089 


Heart,  gummata  of,  508.      „     „     ,.      ,  .       , 

Heart,  hypertrophy  of.      See  Cardiac  hypertrophy, 

273. 
Heart,  lipoma  of,  .501. 
Heart,  lymphoma  of,  501. 
Heart,  myoma  of,  501.   _  . 

Heart,  new  formations  in,  varieties,  501. 
Heart,  parasites  of,  501. 

Heart,  parenchymatous  degeneration  of,  diiEerential 
diagnosis,  495. 

etiology,  49.i. 

morbid  anatomy,  495. 

prognosis,  495. 

symptoms,  495. 

treatment,  495. 
Heart,  rupture  of,  etiology,  497. 

morbid  anatomy,  497. 

prognosis  of,  497. 

symptoms,  497. 

treatment,  497. 
Heart,  sarcoma  of,  501. 
Heart,  syphilitic  disease  of,  etiology,  508. 

morl)id  anatomy,  508. 

symptoms,  508. 
Heart,  tubercle  in,  501.  . 

Heart,  valvular  disease  of,  prognosis  of,  467. 

valvular  diseases  of,  treatment,  470. 
Heart-burn,  333. 
Heidenham,  78. 
Heller,  865. 

Helmholtz,  65.  -r       -,. 

Hematogenous  jaundice.    See  Jaundice,  393. 
Hemiplei;ia.  causes  of,  936. 

definition  of,  936. 
Hemorrhage  from  the  kidney.     See  Kenal  hemor- 
rhage, 54S. 
Hemorrha"-e,  intestinal,  differential  diagnosis,  289. 

etioloay,  288. 

morbid  anatomy,  288. 

prounosis,  289. 

symptoms,  288. 

treatment,  289. 
Hemorrhagic  diathesis.    See  Haemophilia,  903. 
Hemorrhagic  nodular  infarction,  120. 
Hemorrhagic  variola.    See  Small-pox,  745. 
Hemorrhoids,  differential  diagnosis,  306. 

etiology,  305. 

morbid  anatomy,  304,  305. 

prognosis,  306. 

symptoms,  305. 

treatment,  306. 

varieties  of,  304. 
Eenle,  898,  1070. 
Hepatic  gravel.  403. 

Hepatitis,   circumscribed    suppurative,  differential 
diagnosis,  353. 

etiology,  351. 

morbid  anatomy,  349. 

physical  signs,  353. 

prognosis,  354. 

symptoms,  351,  352. 

treatuient,  355. 
Hepatitis,  diffuse  parenchymatous,  differential  diag- 
nosis, 359 

etiology,  357. 

morbid  anatomy,  356. 

physical  signs,  358. 

prognosis,  360. 

symptoms,  3,57. 

treatment,  360. 
Hepatitis,  interstitial,  diagnosis,  346. 

etiologv,  .344. 

morbid  anatomy,  342. 

physical  signs,  346. 

prognosis,  347. 

symptoms,  344. 

treatment,  348. 
Hepatization,  white,  143. 
Hepatogenous  jaundice.    See  Jaundice,  393. 
Hernia,  internal.    See  Intestinal  obstruction,  294. 
Hertz,  125. 
Him,  997. 
Hirgch,  78,  686. 
Hirschberrj,  9a3. 

Hob-nailed  liver.    See  Hepatitis,  342. 
Hodgkin's  disease,  differential  diagnosis,  896. 

etiology,  896. 

morbid  anatomy,  895. 

69 


Hodgkin's  disease,  prognosis,  897. 

symptoms,  896. 

treatment,  897. 
Holmes,  698. 
Hoppe,  949. 
Hoppe-Seyler,  605. 
Hubner,  766. 
Hugwian,  9.36,  953,  954. 
Huidenlanrj,  429. 
Hunter,  44. 
Huss,  79. 
Hutchinson,  967. 
Hater,  800. 

Hydatids  of  the  brain.    See  Cerebral  tumors,  797. 
Hydatids  of  the  kidney.    See  Kidney,  hydatids  of, 

599. 
Hydatids  of  the  liver.    See  Liver,  hydatids  of,  385. 
Hydatids  of  the  lung,  144. 
Hydatids  of  the  spleen,  418. 
Hydremia.    See  Anaemia,  883. 
Hydrocephalus,  acute.    See  Meningitis,  tubercular, 

943. 
Hydrocephalus,  chronic,  differential  prognosis,  950. 

etiology,  949. 

morbid  anatomy,  948. 

prognosis,  950. 

symptoms,  949. 

treatment,  950,  951. 
Hydronephrosis,  differential  diagnosis,  590. 

etiology,  590. 

morbid  anatomy,  589. 

prognosis,  591. 

symptoms,  590. 

treatment,  591. 
Hydropericardium,  etiology,  506,  507. 

morbid  anatomy,  506. 

prognosis,  507. 

symptoms,  507. 

treatment,  507. 
Hydro-peritoneum.    See  Ascites,  333. 
Hydrophobia  and  (Esophagitis,  226. 
Hydrophobia,  differential  diagnosis,  805. 

etiology,  803. 

morbid  anatomy,  803. 

prognosis,  805. 

symptoms,  804. 

treatment,  805. 
Hydrops  cystidis  fellae.    See  Enlarged  gall-bladder, 

399. 
Hydrothorax,  169. 

differential  diagnosis,  170. 

etiology,  170. 

morbid  anatomy,  169, 170. 

prognosis,  iTO. 

symptoms,  170. 

treatment,  170. 
Hygroma  of  the  dura  mater,  953. 
Hypersemia,  cerebral.    See  Cerebral  hj^persemia,  930. 
Hyperaemia,  inflammatory,  1. 
Hypersemia  of  the  kidneys.    See  Renal  hyperaemia, 

543. 
HyperEemia  of  the  liver,  acute.    See  Liver,  hyperae- 
mia of,  337. 
Hyperaemia  of  the  lungs,  113. 

Hyperaemia  of  the  spinal  cord  and  meninges.    See 
Spinal  cord  and  meninges,  hyperaemia  of, 
991. 
Hypertemia  of  the  spleen.  See  Spleen,  hyperaemia  of, 

413. 
Hyperaesthesia,  928. 

Hypertrophic  cirrhosis  of  the  liver,  343. 
Hypertrophic  cirrhosis  of  the  liver,  fatty,  349. 
Hypertropliic  nasjil  catarrh,  differential  diagnosis,  13. 

etiology,  12. 

morbid  anatomy,  11. 

prognosis,  12. 

symptoms,  13. 

treatment,  13. 
Hypertrophy  of  the  brain.  See  Brain,  hypertrophy  of, 

987. 
Hypertrophy  of  the  heart.    See  Cardiac  hypertrophy, 

472. 
Hypertrophy  of  the  spleen.  See  Spleen,  hypertrophy 

of,  416. 
Hypostatic  congestion,  113. 
Hypostatic  pneumonia,  114. 
Hysteria,  differential  diagnosis,  1045,  1046. 

etiology,  1042. 


1090 


INDEX. 


Hysteria,  morbid  anatomy,  1042. 

prognosis,  1046. 

symptoms,  1043-1045. 

treatment,  104fi,  1047. 
Hystero-epilepsy,  difEerential  diagnosis,  1047. 

etiology,  1047. 

prognosis,  1047. 

symptoms,  1047. 

treatment,  1048. 

Icterus.    See  Jaundice,  393. 

Beitis.    See'Eu  teritis,  357. 

Jmmerman,  886. 

"India  liver,"  341. 

Induration,  brown,  113. 

Induration,  inflammatory,  4. 

Induration  of  lung,  brown,  114, 

Induration,  pigment,  114. 

Infantile  convulsions  and  eclampsia,  1076. 

Infantile  remittent  fever.  260,  823. 

Infantile  spinal   paralysis.    See  Paralysis,  infantile 

spinal,  10U6. 
Infarction,  liemorrhagic  nodular,  120. 
Infarction  of  the  kidney.     See  Kenal  hemorrhage, 

.548. 
Infarction  of  tlie  lungs,  120. 
Infarction,  pulmonary,  differential  diagnosis,  123. 

etiology,  122. 

morbid  anatomy,  120. 

physical  signs,  123. 

prognosis,  123. 

symptoms,  123. 

treatment,  124. 
Inflammation,  adhesions  in,  5. 

cellular  elements  in,  3. 

cicatrization  in,  2. 

croupous,  6. 

definition  of,  1. 

diphtheritic,  7. 

exudation  in,  2. 

fate  of  pus  in,  8. 

hypersemia  in,  1. 

interstitial,  4,  8. 

mucous,  5. 

of  free  surfaces,  4. 

of  mucous  surfaces,  5. 

of  serous  membranes,  4. 

parenchymatous,  8. 

resohttion  in,  3. 
Inflammation,  scrofulous.  See  Chronic  phthisis,  179. 

serous,  4. 

suppuration  in,  2. 

ulceration  in,  7. 
Inflammation  of  the  spleen.    See  Spleen,  inflamma- 
tion of,  414. 
Influenza,  differential  diagnosis,  799. 

etiology,  798. 

morbid  anatomy,  797. 

prognosis,  79!t. 

symptoms,  798. 

treatment,  799. 
Inherit  ed  syphilis.    See  Syphilis,  918. 
Inoculation,  759. 
Insolation.    /S«e  Sunstroke,  1053. 
Insufficiency  at  the  aortic  orifice.    See  Aortic  regur- 
gitation, 448. 
Insufficiency  at  the  mitral  orifice.    See  Mitral  re- 
gurgitation, 457. 
Insufficiency  at  the  pulmonary  orifice.   /Sfe«  Pulmonic 

regurgitation,  467. 
Insufficiency  at  the  tricuspid  orifice.     See  Tricuspid 

regurgitation,  462. 
Interlobular  emphysema,  131. 
Intermittent  fever,  differential  diagnosis,  815. 

etiolosy,  811. 

morbid  anatomy,  810. 

prognosis,  815. 

symptoms,  811. 

treatment,  815. 

varieties,  811. 
Intermittent  fever,  masked,  817. 
Internal  hernia.    See  Intestinal  obstruction,  294. 
Interstitial  endocarditis.     See  Endocarditis,  inter- 
stitial, 439. 
Interstitial  hepatitis.   See  Hepatitis,  interstitial,  341. 
Interstitial  inflammation,  8. 

Interstitial  nephritis,  acute.    See  Surgical  kidney, 
588. 


Interstitial  nephritis,  chronic.    See  Gouty  kidney, 

568. 
Interstitial  pneumonia,  108. 
Intestinal  catarrh.    (S'ee  Enteritis,  257. 
Intestinal  colic.    See  Colic,  intestinal,  317. 
Intestinal  dyspepsia.    See  Dyspepsia,  intestinal,  271. 
Intestinal  hemorrhage.    See  Hemorrhage,  intestinal, 

287. 
Intestinal  obstruction,  definition  of,  289. 

diff'erential  diagnosis,  294. 

etiology,  290,  291,  292. 

morbid  anatomy,  290,  291. 

prognosis,  295. 

symptoms,  292,  293,  294. 

treatment,  296,  297. 

varieties  of,  290. 
Intestinal  parasites,  description  of,  306. 

differential  diagnosis,  312. 

etiology,  310. 

morbid  anatomy,  306-310. 

prognosis,  312. 

symptoms,  310,  311. 

treatment,  312,  313. 

varieties  of,  306,  307,  308,  309,  310. 
Intestinal  ulcers,  difftise  catarrhal,  etiology,  285. 

morbid  anatomy,  285. 
Intestinal  ulcers,  follicular,  symptoms,  285. 
Intestinal  ulcers,  tuberctdous,  differential  diagnosis, 
287. 

etiologj',  286. 

morbid  anatomy,  285. 

physical  signs,  2ti7. 

prognosis,  287. 

symptoms,  286. 

treatment,  287. 
Intestinal  ulcers,  varieties  of,  284. 
Intestine,  cancer  of,  differential  diagnosis  of,  30O. 

etiology,  299. 

morbid  anatomy,  298. 

prognosis,  301. 

symptoms,  299-300. 

treatment,  301. 
Intestines,  classification  of  diseases  of,  257. 
Intestines,  functional  diseases  of,  314. 
Intestines,  waxy  degeneration  of,  differential  diag- 
nosis, 298. 

etiology,  297. 

morbid  anatomy,  297. 

prognosis,  298. 

symptoms,  297. 

treatment,  298. 
Intra-thoracic  tumors  and  sub-acute  pleurisy,  155. 
Intussusception.    See  Intestinal  obstruction,  290. 
Irritability,  electrical,  925. 
Irritation,  spinal.    See  Spinal  irritation,  1055. 

Jaccoiid,  85,  433,  529. 

Jackson,  654.  967,  971,  976,  1035,  1044. 

Jacobsori,  538. 

Jarvis'  ecraseur,  13. 

Jaundice,  differential  diagnosis,  394. 

etiology,  394. 

morbid  anatomy  of,  398. 

varieties  of,  393. 
Jaundice,  malignant.  ^S'ee  Parenchj'matous  hepatitis, 

356. 
Jeiunitis.    See  Enteritis,  257. 
Jenner,  191,  490,  759,  978. 
Johnson,  569. 
Jolhj,  1042,  1044. 
Jones,  915,  1062. 
Jurgensen,  97,  101,  104,  107,  134. 

Kahler,  1020. 
Kdsch,  5.53 
Ketley,  1028. 

Key,  475.  ,    ,._       i_.  .  ji 

Kidney,  acute  Bright's  disease  of,  dmerential  olag. 
nosis,  559. 

etiology,  554,  555. 

morbid  anatomy,  552. 

prognosis,  559. 

symptoms,  555-559. 

treatment,  560-562. 
Kidney,  amyloid  form  of  Bright's  disease  of.    See 

Waxy  kidney,  575. 
Kidney,  amyloid.    See  Waxy  kidney,  575. 
Kidney,  Bright's  diseases  of,  classification  of,  552. 


INDEX. 


1091 


Kidney,  Bright' s  diseases  of,  varieties  of,  551. 
Kidney,  calculi  in.    See  Renal  calculi,  592. 
Kidney,  cancer  of.    8ee  Renal  cancer,  596. 
Kidney,  chronic  Bright's  diseases  of,  562. 
Kidney,  chronic  parenchymatous  inflammation   of. 
See  Nephritiri,  chronic  parenchymatous,  562. 
Kidney,  cirrhotic  Brighi's  diseases  of,  differential 
diagnosis,  573. 

etiology,  571. 

morbid  anatomy,  568. 

prognosis,  573. 

symptoms,  571. 

treatment,  574. 
Kidney,  classification  of  diseases  of,  543. 
Kidney,  congestion  of.    See  Renal  hypermmia,  543. 
Kidney,  contracted  and  arterio-capillary  fibrosis.   See 

Arterio-capillary  fibrosis,  584. 
Kidney,  cystic.    See  Cystic  kidney,  591. 
Kidney,  cy.sts  in.    See  Cystic  kidney,  591. 
Kidney,  diseases  of,  529. 
Kidney,  dropsy  of.    See  Hydronephrosis,  589. 
Kidney,  embolism  of.    See  Renal  hemorrhage,  548. 

fibromata  of,  598. 
Kidney,  floating  or  movable,  differential  diagnosis, 
602. 

etiology,  601. 

morbid  anatomy,  601. 

prognosis,  602. 

syniptoms,  602. 

treatment,  602. 
Kidney,  gummaia  of,  597. 

Kidney,  hemorrhage  of.   See  Renal  hemorrhage,  548. 
Kidney,  hydatids  of,  morbid  anatomy,  599. 

prognosis,  599 

symptoms,  599. 

treatment,  600. 
Kidney,  hyperaemia  of.    See  Renal  hyperisemia,  543. 
Kidney,  infarction  of.      See  Renal  hemorrhage,  548. 
Kidney,  lar^e  white,  564. 
Kidney,  leukaemic  tumors  in,  597. 
Kidney,  lipomata  of,  598. 
Kidney,  lymphadenomata  of,  597. 
Kidney,  new  growths  in,  596. 
Kidney,  parasites  in,  599. 
Kidney,  sarcomata  of,  598. 
Kidney,  small  granular,  fatty,  564. 
Kidney,  surgical.    See  Nephritis,  suppurative  inter- 
stitial, 588. 
Kidney,  tuberculosis  of,  differential  diagnosis,  599. 

etiology,  598. 

morbid  anatomy,  598. 

prognosis,  599. 

symptoms,  598. 

treatment,  599. 
Kidney,  waxy  degeneration  of,  dtfEerential  diagno- 
sis, 578. 

prognosis,  578. 

treatment,  578,  579. 
Kidney,  waxy.    See  Waxy  kidney ,'575. 
Kirchof,  1004. 

Klebs,  101,  483,581,  588,  809,  853. 
Klein,  767. 
Klob,  936. 
Knapp,  1067. 
Knecht,  751. 
Koch,  174,  175. 
Koehler,  993. 
Kolliher,  897. 
KoBter,  1053. 
Kreizlnrj,  439. 
Kuhn,  79. 
Kuvze,  1042. 
KuUner,  121. 
Kuasmaul,  513. 

LaMnnec,  55,  179,  203,  204,  441. 

Laennec's  rale,  i,37. 

Lancereaux,  .349,  961. 

Lardaceous  degeneration  of  the  intestines.  See  In- 
testines, waxy  degeneration  of,  297. 

Lardaceous  degeneration  of  the  liver.  See  Amyloid 
degeneration  of  liver,  .366. 

Large  white  kidney.  See  Nephritis,  chronic  paren- 
chymatous, 562. 

La  Roche,  6.50. 

Laryngeal  paralysis.  See  Neuroses  of  the  larynx,  .34. 
spasm  hysterical  and  acute  catarrhal  laryngi- 
tis, 19. 


Laryngisums  stridulus,  .37. 
Laryngitis,  acute  catarrhal,  17. 

differential  diagnosis,  19. 

etiology,  18. 

morbid  anatomy,  17. 

prognosis,  19. 

symptoms,  18. 

treatment,  20. 
Laryngitis,  acute  croupous,  27. 

differential  diagnosis  of,  30. 

etiology  of,  28. 

morbid  anatomy  of,  27. 

prognosis  of,  30. 

symptoms  ol,  28. 

treatment  of,  31. 
Laryngitis,  chronic  catarrhal,  differential  diagnosis 
of,  22. 

etiology  of,  21. 

morbid  anatomy,  21. 

prognosis,  22. 

symptoms,  21. 

treatment,  22. 
Laryngitis,  chronic  catarrhal  in  phthisis,  23,  24. 
Laryngitis,  chronic  catarrhal  in  syphilis,  25. 
Larynx,  cancer  of,  40. 

catarrhal  ulcer  of,  32, 

chronic  catarrh  of,  in  phthisis,  23. 

classification  of  diseases  of,  17. 

cystic  tumors  of,  40. 

diseases  of,  17. 

fibro  cellular  growths  of,  40. 

fibromata  of,  40. 

follicular  ulcer  of,  32. 

glandular  growths  of,  40. 
Larynx,  neuroses  of,  differential  diagnosis,  96. 

etiolog}'',  35. 

morbid  anatomy,  34. 

prognosis,  36. 

symptoms,  35. 

treatment,  37. 
Larynx,  oedema  of,  25. 

papilloma  of,  39. 

phthisical  ulcers  of,  32. 
Larynx,  spasmodic  affections  of,  37. 

differential  diagnosis,  38. 

etiology,  37. 

morbid  anatomy,  37. 

prognosis,  .38. 

syniptoms,  38. 

treatment,  38. 
Larynx,  syphilitic  ulcers  of,  33. 
LarynXj  tumors  of,  39. 

differential  diagnosis,'41. 

etiology,  40. 

morbid  anatomy,  39. 

prognosis,  41. 

symptoms,  40. 

treatment,  41. 
LarjTix,  typhous  ulcers  of,  32. 
Larynx,  ulcers  of,  differential  diagnosis,  34. 

etiology,  33. 

morbid  anatomy,' 32. 

prognosis,  34. 

symptoms,  33. 

treatment,  34. 

varieties  of,  32. 
Larynx,  variolus  ulcer  of,  32. 
Lasegue,  1045. 

Lateral  sclerosis,  amyotrophic.  /Stee  Amyotrophic  lat- 
eral sclerosis,  1025. 
Laycock,  883. 

Lead  colic.    See  Intestinal  colic,  317,  319. 
Lead  palsy.   See  Chronic  lead  poisoning,  1064. 
Lead  poisoning,  319. 
Lead  poisoning,  chronic,  differential  diagnosis,  1065. 

etiology,  1064. 

morbid  anatomy,  1064. 

prognosis,  1065. 

symptoms,  1064. 

treatment,  1065. 
Lebert,  79,  95,  437,  .529,  712, 713,  715,  716,  740, 863,  888, 

977,  984, 1061. 
Lego,  902. 
Leicblenstem.  195. 

Lenitis.    See  Phlegmonous  gastritis,  236 
Leo,  7'51. 

Leptothrix  buccalis.    See  Thrush,  213. 
Leiulle,  898. 


1092 


IlifDEX. 


Letzreich,  800. 

Leucocythsemia,  differential  diagnosis,  895. 

etiology,  893. 

morbid  anatomy,  891. 

prognosis,  894. 

symptoms,  iS93. 

treatment,  895. 
Leulcaemiii,  pseudo.    See  Hodgliin's  disease,  894, 
•'Leukismia."    See  Leucocytlisemia,  891. 
Leiiksemic  tumors  of  the  kidney,  597. 
Lewinsky,  475. 
Ley  den,  461),  997,  1012. 
Lichtheim,  130. 
Liebermeister,  100. 
Lientery.    See  Diarrtioea,  264. 
Lipomaita  in  the  lungs,  142. 

Lipomata  of  the  brain.    See  Cerebral  tumors,  977. 
Lipomata  of  the  heart,  501. 
Lipomata  of  the  kidney,  598. 
LiouvUle,  10.30. 
Litten,  518,  888. 

Liver,  abscess  of.     See  Suppurative  hepatitis,  349. 
Liver,  active  hyperemia  of,  difEerential  diagnosis, 
338. 

etiology,  338. 

morbid  anatomy,  337. 

physical  signs,  338. 

prognosis,  339. 

symptoms,  338. 

treatment,  339. 
Liver,  acute  yellow  atrophy  of.     See  Parenchyma- 
tous hepatitis,  356. 
Liver,  amyloid   degeneration   of,  differential  diag- 
nosis, 369. 

etiology.  368 

morbid"  anatomy,  366. 

physical  signs,  369. 

prognosis,  369. 

symptoms,  368. 

treatment,  369. 
Liver,  cancer  of,  differential  diagnosis,  381. 

etiology,  380. 

morbid  anatomy,  378. 

physical  signs,  381. 

prognosis,  382. 

symptoms,  380. 

treatment,  382. 

varieties,  377. 
Liver,  chronic  atrophy  of,  differential  diagnosis,  371. 

etiology,  371. 

moi'bid  anatomy,  370. 

physical  signs,  371. 

prognosis,  371. 

symptoms,  371. 

treatment,  372. 
Liver,  cirrhosis  of.    See  Interstitital  hepatitis,  342. 
Liver,  congestion  of.    See  Passive  hyperemia  of  the 

liver,  .339. 
Liver,  diseases  of,  337. 

Liver,  fatty  degeneration  of.    See  Fatty  liver,  372. 
Liver,  fatty  hypertrophic  cirrhosis  of,  349. 

etiology,  349. 

morbid  anatomy,  349. 

symptoms,  349. 
Liver,  fatty  infiltration  of.    See  Patty  liver,  372. 
Liver,  fatty  metamorphosis  of.     See  Patty  liver,  372. 
Liver,  functional  derangements  of,  differential  diag- 
nosis, 409. 

etiology,  406. 

prognosis,  409. 

symptoms,  407,  408. 

treatment,  409. 
Liver,  gouty.    See  Interstitial  hepatitis,  342. 
Liver,  granular.    See  Interstitial  hepatitis,  342. 
Liver,  gummata  of,  differential  diagnosis,  384. 

etiology,  384. 

morbid  anatomy,  383. 

physical  signs,  384. 

prognosis,  384. 

symptoms,  384. 

treatment,  384. 
Liver,  hydatids  of,  differential  diagnosis,  388. 

etiology,  387. 

morbid  anatomy,  385. 

physical  signs,  388. 

prognosis,  389. 

symptoms,  .387. 

treatment,  389. 


Liver,  hypertrophic  cirrhosis  of,  343. 
Liver,  melanotic  sarcoma  of,  378. 
Liver,  multilocular  hydatids  of,  differential  diagno> 
sis,  391. 

etiology,  391. 

morbid  anatomy,  390. 

physical  signs,  391. 

prognosis,  392. 

symptoms,  .391. 

treatment,  392. 
Liver,  passive  hyperemia  of,  differential  dia^osis, 
341. 

etiology,  340. 

morbid  anatomy,  339. 

physical  signs,  341. 

prognosis,  341. 

symptoms,  341. 

treatment,  341. 
Liver,  pigment  degeneration  of,  differential  diagnO' 
sis,  377. 

etiology,  376. 

morbid  anatomy,  375. 

physical  signs.  377. 

prognosis,  377. 

symptoms,  376. 

treatment,  377. 
Liver,  rare  tumors  of,  393. 
Liver,  torpid.  See  Punciional  derangements  of  liver» 

406. 
Liver,  tuberculosis  of,  etiology,  393. 

morbid  anatomy,  39:2. 

symptoms,  393. 
Liver,  waxy.    See  Amyloid  degeneration  of,  366. 
Livingstone,  825. 

Lobular  pneumonia.    See  Pneumonia,  lobular,  101. 
Localization  of  cerebral  lesions,  970,  971,  972. 
Localized  spasm  and  paralysis,  differential  diagno- 
sis,  1064. 

etiology,  1063. 

morbid  anatomy,  1063. 

prognosis,  1064. 

symptoms,  1063. 

treatment,  1064. 
Lock-jaw.    See  Tetanus,  1058. 
Locomotor  ataxia,  differential  diagnosis,  1022. 

etiology,  1019. 

morbid  anatomy,  1018. 

prognosis,  1022. 

symptoms,  1020. 

treatment,  1023. 
Louis,  79. 
Lung,  atrophy  of,  144. 

etiology,  144. 

morbid  anatomy,  144. 

physical  signs,  144. 

symptoms,  144. 
Lungs,  active  hypersemia  of,  113. 
Lungs,  anaemia  of,  129. 
Lungs  and  pleura,  diseases  of,  70. 
Lungs,  brown  cedema  of,  115. 
Lungs,  cancer  of.  140. 

differential  diagnosis,  141. 

etiology,  141. 

physical  signs,  141. 

prognosis,  142. 

symptoms,  141. 

treatment,  142. 

varieties  of,  140. 
Lungs,  carniftcation  of,  114. 

cirrhosis  of,  109. 

coal-miner's,  182. 

compensatory  hypercemia  of,  113. 

compression  of.    See  Atelectasis,  19. 

congestion  of,  113. 

dermoid  cysts  in,  142. 

echinococci.    See  Hydatids,  144. 

enchondromata  in,  142. 

epithelioma  of,  143. 

fat  embolism  of,  122. 

fibromata  in,  142. 

gangrene  of,  125. 

hfematomata  in,  142. 
Lungs,  hydatids  of  j  144. 

differential  diagnosis,  145, 

etiology,  145. 

morbid  anatomy,  145. 

prognosis,  145. 

syrnptoms,  145. 


INDEX. 


1093 


Lungs,  hydatids  of,  treatment,  146. 
Lungs,  hypenieinia  of,  113. 

ditlerential  diagnosis,  116. 

etiology,  115. 

morbid  anatomy,  113. 

physical  sigus,  116. 

prognosis,  116. 

symptoms,  115 

treatment,  116. 
Lungs,  infarction  of,  120. 
Lungs,  lipomata  in,  143. 

melanotic  tumors  in,  142. 

myxomata  in,  142. 
Lungs,  non-malignant  growths  in,  142. 

differential  diagnosis,  143. 

symptoms,  143. 
Lungs,  ijeduma  of.    See  (Edema,  puhnonary,  117. 

osteomata  in,  142. 

passive  hyperasmia  of,  113. 

sarcomata  in,  142. 

scirrhus  of,  108. 

sclerosis  of,  103. 

splenization  of,  113. 
Lungs,  syphilitic  disease  of,  143. 

morbid  anatomy,  143. 

symptoms  of,  143. 
Lumbas^o,  860. 
L^l.ys,  970,  971,  1049. 
Lymphndenomata  of  the  kidney,  597. 

heart,  501. 

Mackenzie,  1069. 

Mackrill,  659. 

Maclean,  349,  828. 

Magnan,  991. 

Mahomed,  538,  573,  584,  587,  908. 

Maiei',  513. 

Malarial  fever,  continued.    See  Continued  malarial 

fever,  827. 
Malarial  fever,  introduction,  806-810. 
Malarial  fever,  pernicious.    See  Pernicious  malarial 

lever,  839. 
Malarial  infection,  chronic.    See  Chronic  malarial 

infection,  853. 
Malassez,  192. 
Malignant  jaundice.    See  Parenchymatous  hepatitis, 

356. 
Malignant    pustule    and    gangrenous     stomatitis, 

211. 
Manassein,  739. 
Mannkopf,  693. 

Masked  intermittent  fever,  817. 
Maumene's  test  for  sugar  in  the  urine,  879. 
Maw-worm.    See  Intestinal  parasites,  306. 
Mayer,  851,  931. 
Measles,  complications,  787. 

differential  diagnosis,  788. 

etiology,  783. 

morbid  anatomy,  782. 

prognosis,  789. 

sequelae,  788. 

symptoms,  784. 

treatment,  790,  791. 
Measles,  German.    See  German  measles,  791. 
Meckel,  441. 
Mediastinal  tumors,  etiology,  529. 

physical  signs,  529. 

progno^^is,  529. 

seat  of,  529. 

symptoms,  529. 

treatment,  529. 

varieties  of,  528. 
Megrim,  etioiogy,  1075. 

morbid  anatomy,  1075. 

symptoms,  1075. 

treatment,  1076. 
Meir/s,  802. 
Melanotic  liver.    See  Liver,  pigment  degeneration 

of,  375. 
Melanotic  timiors  in  the  lungs,  142. 
Melasma  saprarenalis.    See  Addison's  disease,  897. 
Melier,  659. 

Mellituria.    See  Diabetes  mellitus,  877. 
Membranous  croup.     See  Laryngitis,  acute  croup- 
ous, 27. 
Memltraiious  fjesophagitis.    See  (Esophagitis,  224. 
Membranous  pharyngitis,  223. 
Vniere's  disease.    See  Vertigo,  1067. 


Meninges,    hyperaemia   of.     See   Spinal   cord   and 

meninges,  hyperaemia  of,  991. 
Meninges,  tumors,   etc.    See  Brain  and  meninges 

tumors  of,  97'8. 
Meningitis,  acute,  differential  diagnosis,  939. 

etiology,  936. 

morbid  anatomy,  935. 

prognosis,  939. 

symptoms,  937. 

treatment,  93'.^. 
Meningitis,  cerebro-spinal.    See  Cerebro-spinal  men- 
ingitis, 684. 
Meningitis,  chronic,  differential  diagnosis,  942. 

etiology,  942. 

morbid  anatomy,  941. 

prognosis,  943. 

symptoms,  942. 

treatment,  943. 
Meningitis,  epidemic  cerebro-spinal.    See  Meninglp 

tis,  epidemic,  684. 
Meningitis  foudroyante,  690. 
Meningitis,  spinal,  differential  diagnosis,  994. 

etiology,  993. 

morbid  anatomy,  992,  993. 

prognosis,  994. 

symptoms,  9H3. 

treatment,  995. 
Meningitis,  sub-acute,  differential  diagnosis,  941. 

etiology,  940. 

morbid  anatomy,  940. 

prognosis,  941. 

symptoms,  940. 

treatment,  941. 
Meningitis,  varieties,  935. 
Meningitis,  tubercular,  differential  diagnosis,  947. 

etiology,  944. 

morbid  anatomy,  943. 

prognosis,  947. 

symptoms,  944. 

treatment,  949. 
Menjaud,  1013. 

Mental  disturbances  in  nervous  diseases,  929. 
Merbach,  195. 
Mercurialism,  chronic,  differential  diagnosis,  1067. 

etiology,  1066. 

morbid  anatomy,  1066. 

prognosis,  1067. 

symptoms,  1066. 

treatment,  1067. 
Mercurial  tremor.    See  Chronic  mercurialism,  1066. 
Merkel,  685,  898. 
Meschede,  685. 
Meyer,  1007,  1009. 
Miasm,  definition  of,  609. 
Miclull,  656. 
Miliary  fever,  differential  diagnosis,  796. 

etiology,  794. 

morbict  anatomy,  794. 

prognosis,  796. 

symptoms,  795. 

treatment,  797. 
Miliary  tuberculosis,  acute.    See  Tuberculosis,  acute 

miliary,  706. 
Mitchell,  987,  1053. 

Mitral  obstruction.    See  Mitral  stenosis,  453. 
Mitral  regurgitation,  differential  diagnosis,  461. 

etiology,  459. 

morbid  anatomy,  457. 

physical  signs,  460. 

symptoms,  459. 
Mitral  stenosis,  differential  diagnosis,  457. 

etiology,  455. 

morbid  anatomy,  453. 

physical  signs.  456. 

symptoms,  455. 
MOller's  oil  in  chronic  phthisis,  200. 
Montague,  Lady  Ma.ry^  759. 
Moore's  test  for  sugar  m  the  urine,  879. 
Morbid  sensibility  of  the  stomach.    See  Chronic  gas- 
tritis, 231. 
Morbus  Addisonii.     See  Addison's  disease,  897. 
Morbus  macnlosus  Werlhofii.    See  Purpura,  905. 
Moslei;  417,  902. 
Motor  paralysis,  924. 
Movline,  984. 
Mouth,  diseases  of,  208. 

Movable  or  floating  U-idney.     See  Kidney,  floating 
or  movable,  601 . 


1094 


INDEX. 


Moxon,  557,  898,  1000. 

Mucous  menibiane,  croupous  inflammation  of,  6. 

Mucous  surfaces,  inflammatiou  of,  5. 

Mucous  surfaces,  ulceration  of,  7. 

"  Muguet."    See  Thrush,  213 

Multliocular  hydatids  of  )iver.    See  Liver,  multiloc- 

ular  hydatids  of,  390. 
Mumps.    See  Parotitis,  ai7. 
Murvhison,  407,  40s,  715,  727,  729. 
Murmurs,  cardiac,  liistory  of,  441. 

mechanism  of,  441,  442. 

theories  of,  441. 
Murmurs,  endocardial,  characteristics  of,  443. 

classiticaTion  of,  444. 

combination  of,  443. 

relative  frequency  of,  443. 

table  of,  443. 
Muscular  atrophy,  progressive.    See  Progressive  mus- 
cular atropny,  1011. 
Muscular  uuuition,  !)25. 
Muscular  rheumatism.    See  Rheumatism,  muscular, 

868. 
Myalgia.    See  Muscular  rheumatism,  868. 
"Mycosis  endocardii,"  433. 
Myelitis,  acute,  differential  diagnosis,  998. 

etiology,  996. 

morbid  anatomy,  996. 

prognosis,  998. 

symptoms,  997. 

treatment,  998. 

varieties  of,  995. 
Myelitis,  chronic,  difEerential  diagnosis,  1000. 

etiology,  999. 

morbid  anatomy,  999. 

prognosis,  1000. 

symptoms,  999. 

treatment,  1000. 
Myocarditis.  difEerential  diagnosis,  489, 

etiology,  488. 

morbid  anatomy,  487. 

prognosis,  489. 

symptoms,  488. 

treatment,  489. 

varieties  of,  487. 
Myocarditis,  chronic.    See  Fibroid  diseases  of  the 

heart,  490. 
Myomata  of  the  heart,  501. 
Myxoedema,  differential  diagnosis,  908. 

etiology,  908. 

morbid  anatomy,  907. 

prognosis,  909. 

symptoms,  908. 

treatment,  909. 
Mjrsomata  in  lungs,  142. 
Myxomata  of  the  brain.    See  Cerebral  tumors,  977. 

Nasal  catarrh,  atrophic,  13. 

Nasal  catarrh,  chronic.    See  Chronic  coryza,  10. 

Nasal  catarrh,  dry.     See  Atrophic  nasal  catarrh,,  13. 

Nasal  catarrh,  fetid.    See  Ozasna,  15. 

Nasal  catarrh,  hypertrophic,  11. 

Nasal  passases,  classification  of  diseases  of,  9. 

Nasal  passages,  diseases  of,  9. 

Naso-pharyngeal  catarrh,  chronic.  See  Hypertrophic 

nasal  catarrli,  11. 
Necrosis,  3. 
Nephritic  colic,  594. 

Nephritis,  acute  suppurative  interstitial,  differential 
diagnosis,  589. 

etiology,  588. 

morbid  anatomy,  588. 

prognosis,  589. 

symptoms,  .588. 

treatment,  589. 
Nephritis,  chronic  parenchymatous,  differentiaVdiag- 
nosis,  566. 

etiology,  565. 

moibid anatomy,  562. 

prognosis,  566.  — 

symptoms,  565. 

treatment,  567. 

varieties  of,  562. 
Nephritis,  strumous,  598. 

Nervous  cardiac  palpitation.    See  Cardiac  palpita- 
tion, nervous,  ,502. 
Nervous  system,  functional  diseases  of,  1034. 
Nervous  system,  general    symptomatology  of  the 
diseasee  of,  924. 


Neuman,  893. 

Neuralgia,  differential  diagnosis,  1073. 
etiology,  1070. 
morbid  anatomy,  1069. 
prognosis,  1074. 
symptoms,  1070. 
treatment,  1074. 
varieties,  1071. 
Neurasthenia,  differential  diagnosis,  1050. 
etiology,  1049. 
prognosis,  1050. 
symptoms,  1049. 
treatment,  1050. 
Neuroses  of  the  heart,  varieties  of,  502. 
Neuroses  of  the  larynx,  34. 
Neuroses  of  the  stomach.  See  Stomach,  neuroses  of 

252. 
New  formations  in  the  heart.  See  Heart,  new  forma- 
tions in,  501. 
New  growths  in    the   kidney.      See  Kidney,  new 

growths  in,  596. 
Niemeyer,  108,  111,  186,  418,  434,  467,  472,  476,  607, 
861,  886,  903,  912,  930,  948,  967,  975,  979,  990, 
1060. 
Nodular  infarction,  pulmonary,  120. 
Nodular  pulmonary  apoplexy,  120. 
Noma.    See  Ulcerative  stomatitis,  212. 
Non-inflammatory  softening  of  the  spinal  cord.    See 
Spinal  cord,  non-inflammatory  softening  of, 
1000. 
Non-malignant  erowths  in  the  lungs,  141. 
Nothnarjel,  930,  931,  934,  957,  968,  1040,  1042. 
Nutrition,  muscular,  925. 

Obenneir,  739,  751,  979,  981. 

Obstruction  at  the  pulmonary  orifice.    See  Pulmonic 

obstruction.  465. 
Obstruction  at  the  tricuspid  orifice.   See  Trictispid 

stenosis,  462. 
Obstruction,  intestinal.    See  Intestinal  obstruction, 

289. 
Obstruction  of  the  mitral  valve.    See  Mitral  stenosis, 

453. 
(Edema  glottidis,  25. 

differential  diagnosis  of,  26. 

etiology  of,  26. 

morbid  anatomy  of,  26. 

prognosis  of.  27. 

symptoms  of,  26. 

treatment  of,  27. 
(Edema  of  the  larynx,  25. 
(Edema,  pulmonaiy,  differential  diagnosis,  118. 

etiology,  117. 

morbid  anatomy,  117. 

physical  signs,  118. 

prognosis,  119. 

symptoms,  118. 

treatment.  119. 
(Edema,  Virchow's  brown,  115. 
Oertel,  672,  800. 
(Esophagitis,  differential  diagnosis,  836. 

etiology,  224. 

membranous,  224. 

morbid  anatomy,  224. 

prognosis,  226. 

symptoms,  225. 

treatment,  226. 
(Esophagus,  cancer  of,  differential  diagnosis,  9St 

etiology,  226. 

morbid  anatomy,  226. 

prognosis,  227. 

symptoms,  227. 

treatment,  227. 
(Esophagus,  diseases  of,  224. 
(Esophagus,  stricture  of,  225. 
Oqle,  958. 

OVdium  albicans.    See  Thrush,  313. 
Oinomania,  915. 
Oligsemia,  883. 
Olhvier,  997. 
Oppolzer,  334,  1061. 
Ord,  907. 
Ormerod,  466. 

Osteomata  in  the  lungs,  143. 

Osteomata  of  the  brain.    See  Cerebral  tumors,  ^f. 
Otto,  950. 

Oxyuris  vermicularis,  309. 
Ozsena,  15. 


INDEX. 


1095 


Ozsena,  differential  diagnosis,  16. 
etiology,  15. 
morbid  anatomy,  15. 
progiioi?is,  16. 
symptoms,  15. 
treatment,  Iti. 

Pachymeningitis  externa,  differential  diagnosis,  952. 

etiology,  951. 

morbid  anatomy,  951. 

prognosis,  953. 

symptoms,  9.52. 

treutment,  9.52. 
Pachymeningitis  interna,  differential  diagnosis,  955. 

etiology,  954. 

morbid  anatomy,  953-954. 

prognosis,  955. 

symptoms,  954. 

treatment,  955. 
Pachymeningitis  syphilitica,  differential  diagnosis, 
956. 

morbid  anatomy,  955,  956. 

prognosis,  956. 

symptoms,  956. 

treatment,  956. 
Paget,  408. 

Palpitation  of  the  heart,  nervous.    See  Cardiac  pal- 
pitation, nervous,  503. 
Pancreas,  calculi  of,  morbid  anatomy,  413. 

etiology  of,  413. 

symptoms,  413. 
Pancreas,  cancer  of,  differential  diagnosis,  413. 

etiolOLfy,  412. 

morbid  anatomy,  411,  413. 

prognosis,  413. 

symptoms,  412. 
Pancreas,  cysts  of,  etiology,  413. 

morbid  anatomy,  413. 

symptoms,  413. 
Pancreas,  diseases  of,  410. 
Pancreas,  fatty  degeneration  of,  etiology,  411. 

morbid  anatomy,  411 

varieties,  411. 
Pancreas,  round  worms  in,  413. 

small-celled  sarcoma  of,  413. 

syphilitic  gnmmata  of,  413. 

tuberculosis  of,  413. 

vi'axy  degeneration  of,  411. 
Pancreatitis,  acute,  differential  diagnosis,  410. 

etiology,  410. 

morbid  anatomy,  410. 

prognosis,  410. 

symt)toms,  410. 

treatment,  410. 
Pancreatitis,  chronic,  etiology,  411. 

morbid  anatomy,  411. 

symptoms,  411. 
Panum,  698. 
Papillomata  of  the  brain.    See  Cerebral  tumors,  977. 

of  the  larynx,  40. 
Paralysis,  acute  ascending,  differential   diagnosis, 
1028. 

etiology,  1028. 

prognosis,  1029. 

symptoms,  1028. 

treatment,  1029. 
Paralysis,  acute  bulbar,  etiology,  1001. 

morbid  anatomy,  1001. 

prognosis,  1003. 

symptoms,  1001. 

treatment,  1003. 
Paralysis,  acute  spinal  of  adults.  drEEerential  diag- 
nosis, 1009. 

etiology,  1003. 

morbid  anatomy,  1009. 

prognosis,  11)10. 

symptoms,  1009. 

treatment,  1010. 
Paralysis  agitans,  differential  diagnosis,  1063. 

etiology,  1061. 

morbid  anatomy,  1061. 

prognosis,  1062. 

symptoms,  1061. 

treatment,  1062. 
Paralysis,  Bell's.    See  Facial  paralysis. 
Paralysis  and  spasm,  localized.  See  Localized  spasm 

and  paralysis,  1063. 
Paralysis,  chronic  bulbar,  differential  diagnosis,  1005. 


Paralysis,  chronic  bulbar,  etiology,  1004. 

morbid  anatomy,  1003. 

prognosis,  1005. 

symptoms,  1U04. 

treatment,  1005. 
Paralysis,  facial,  differential  diagnosis,  1060. 

etiology,  10.59. 

prognosis,  1060. 

symptoms,  1060. 

treatment,  1060. 
Paralysis,  general,  925. 
Paralysis,  glosso-labio-laryngeal.  See  Chronic  bulbar 

paralysis,  1003. 
Paralysis,   infantile    spinal,  differential   diagnosis, 
1008. 

etiology,  1007. 

morbid  anatomy,  1006,  1006. 

prognosis,  1008. 

symptoms,  1007. 

treatment,  1009. 
Paralysis,  lead.    See  Chronic   lead-poisoning,  317, 

319. 
Paralysis,  motor,  934. 
Paralysis  of  the  abductors  of  the  vocal  cords,  34. 

of  the  adductors  of  the  vocal  cords,  34. 

of  the  tensors  of  the  vocal  cords,  3 1. 
Paralysis,  pseudo-hypertrophic.    Bee  Pseudo-hyper- 
trophic  paralysis,  1026. 
Paralysis,  recurrent  laryngeal,  34. 
Paralysis,  sensory,  938. 

Paralysis,  spastic.    See  Amyotrophic  lateral  sclero- 
sis, 1025. 
Paraplegia,  causes  of,  937. 

definition  of,  937. 
Parasites,  intestinal.    See  Intestinal  parasites,  306. 
Parasites  in  the  heart,  501. 
Parasites  in  the  kidney,  599. 
"  Parasitic  nephritis."    See  Surgical  kidney,  588. 
Parchaj^pe,  989. 

Parenchymatous  degeneration  of   the   heart.     See 

Heart,  parenchymatous  degeneration  of,  493. 

Parenchymatous  hepatitis,  diffuse.    See  Hepatitis, 

parenchymatous,  356. 
Parenchymatous  inflammation,  8. 
Parenchymatous  nephritis,  acute.  See  Kidney,  acute 
Bi'ight's  disease  of,  5.52. 

nephritis,  chronic.    See  Nephritis,  chronic  pa- 
renchymatous, 563. 
Parkes,  860. 
Parotitis,  differential  diagnosis,  219. 

etiology,  218. 

metastatic,  318. 

morbid  anatomy,  217. 

prognosis,  219. 

symptoms,  218. 

treatment,  219. 
^varieties  of,  317. 
Parrot,  1045. 
Passive  hyperemia  of  the  liver.    See  Liver,  passim 

hyperemia  of,  339. 
Pasteur,  804,  900. 
Peacock,  445. 
Penzoldt,  906. 
Pepper,  303,  888. 
Periarteritis,  etiology,  513. 

morbid  anatomy,  513. 
Pericecal  abscess.    See  Perityphlitis,  281. 
Pericarditis,  acute,  differential  diagnosis,  426. 

etiologv.  422. 

morbid  anatom^y,  430. 

physical  signs,  424. 

prognosis,  427. 

symptoms,  423. 

treatment,  428. 

varieties  of,  421. 
Pericarditis,  chronic,  differential  diagnosis,  430. 

etiology,  429. 

morbid  anatomy,  429,  430. 

physical  signs,  430. 

prognosis,  430. 

symptoms,  430. 

treatment,  430. 
Pericardium,  cancer  of,  502. 

dropsy  of.    See  H  ydropericardium,  506. 

tuberculosis  of,  503. 
Pereira,  1066. 
Perihepatitis,  differential  diagnosis,  ,361. 

etiology,  361. 


1096 


INDEX. 


Perihepatitis,  morbid,  anatomy,  360. 

prognosis,  362. 

symptoms,  361. 

treatment,  363. 

syphilitica,  360. 
Peri  nephritic  abscess.    See  Perinephritis,  600. 
Perinephritis,  differential  diagnosis,  601. 

etiology,  600. 

morbid  anatomy,  600. 

physical  signs,  601. 

prognosis,  601. 

symptoms,  600. 

treatment,  601. 
Periplilebitis,  515. 
Periproctitis,  diflferential  diagnosis,  304. 

etiology,  302. 

morbid  anatomy,  303. 

prognosis,  304. 

symptoms,  304. 

treatment,  304. 
Peritoneal  dropsy.    See  Ascites,  333. 
Peritonitis,  321. 

difEerential  diagnosis,  339. 

etiology,  32-1,  325. 

morbid  anatomy,  331. 

prognosis,  330. 

symptoms,  .326,  327,  328,  829. 

treatment,  330,  331,  333,  333. 
Peritonitis,  cancerous,  334. 
Peritonitis,  chronic,  333. 
Peritonitis,  hemorrhagic,  333. 
Peritonitis,  tubercular,  333. 
Peritonitis,  varieties  of,  331. 
Perityplilitis,  difEerential  diagnosis,  282. 

etiology,  283. 

morbid  anatomy,  281. 

physical  signs,  382. 

prognosis,  283. 

symptoms,  233. 

treatment,  283. 
Pernicious  aniemia.    /Sfee  Progressive  pernicious  an- 

eemia,  888. 
Pernicious    malarial    fever,  differential   diagnosis, 
845. 

etiology,  849. 

morbid  anatomy,  839. 

prognosis,  846. 

sj^mptoms,  840. 

treatment.  847. 
Pertussis.    See  Whooping-cough,  800. 
FMger,  1004. 
Pharyngitis  catarrhal,  morbid  anatomy,  221. 

etiology,  333. 

symptoms,  233. 

differential  diagnosis,  223. 

prognosis,  323. 

treatment,  233. 
Pharyngitis,  croupous,  223. 
Pharyngitis,  diphtheritic,  223. 
Pharyngitis,  follicular.    See  Catarrhal  pharyngitis, 

221. 
Pharyngitis,  membranous,  233. 
Pharyngitis,  phlegmonous.    See  Quinsy,  219. 
Pharynx,  classification  of  diseases  of,  219. 

diseases  of,  319. 
Phlebitis,  difEerential  diagnosis,  515. 

etiology,  514. 

morbid  anatomy,  514. 

prognosis,  515. 

symptoms,  514. 

treatment,  515. 
Phlegmonous  gastritis.   See  Gastritis,  phlegmonous, 

236. 
Phlegmonous  pharyngitis.     See  Quinsy,  219. 
Phthisis,  catarrh  of  larynx  in,  23. 

cavities  in,  180. 

classification  of,  172. 

diiierential  diagnosis,  196. 

different  names  of,  172. 

etiology  of,  185,  186,  187. 

antihygienic  surroundings  in,  185. 

climate  in,  186. 

heredity  in,  185. 

local  causes  in,  186,  187. 

Koch's  experiments  concerning,  174, 175. 

physical  signs  of,  193,  196. 

prognosis,  197. 

quiescent  cavities  in,  184. 


Phthisis,  symptoms,  187-193. 
cough,  188. 
emaciation,  190. 
fever,  190. 
haemoptysis,  189. 
pulse,  191. 
respirations,  191. 
sputa,  189. 

theories  of ,  i71. 

treatment,  19S. 

antiseptic,  203. 
climatic,  203-207. 
hygienic,  303. 
medicinal,  199,  200. 
prophylactic,  198,  199. 
Phthisis,  acute,  171. 

difEerential  diagnosis,  177. 

etiology,  174,  175. 

morbid  anatomy,  172,  173, 174. 

physical  signs,  177. 

prognosis,  178. 

symptoms,  175. 

treatment  of,  178. 
Phthisis,  catarrhal,  cavities  in,  180. 

morbid  anatomy,  178-181. 
Phthisis,  chronic,  178 
Phthisis,  fibrous,  181. 

morbid  anatomy,  181,  182, 183,  184. 
Phthisis,  hemorrhagic,  206. 
Phthisis,  infective.  187. 
Phthisis,  stone-cutter's,  182. 
Phthisis,  tubercular  183, 

morbid  anatomy,  183,  184 

sputa  in,  175. 
Phthisis,  tuberculo-pneumonic,  174. 
HcJc,  1020,  1025. 
Pietres,  970. 

Pigment  induration  of  lungs,  114. 
Pigment,  liver.    See  Liver,  pigment  degeneration  <A 

375. 
Piles.    See  Hemorrhoids,  304. 
Pleura,  cancer  of,  etiology,  164. 

prognosis,  165. 

symptoms,  164. 

treatment,  165. 
Pleurisy,  acute,  146. 

differential  diagnosis,  149. 

etiology,  147. 

morbid  anatomy,  146. 

physical  signs,  148. 

prognosis,  150. 

symptoms,  147. 

treatment,  150. 
Pleurisy,  adhesive,  etiology,  163. 

morbid  anatomy,  162. 

physical  signs,  163. 

prognosis,  164. 

symptoms,  163. 

treatment,  104. 
Pleurisy,  dry,  146. 
Pleurisy,  sub-acutej  151. 

difEerential  diagnosis,  155. 

etiology,  1.52. 

morbid  anatomy,  151. 

physical  signs,  153. 

prognosis,  155. 

symptoms,  152. 

treatment,  156. 
Pleurisy,  varieties  of,  146. 
Pleurisy  with  a  sero-fibrinous  and  purulent  efEusion. 

See  Empyema,  158. 
Pleurisy,  with  efEusion.   See  Sub-acute  pleurisy,  151, 
Pleurodynia,  86S. 
Pneumonia,  acute  lobar,  70. 

complications,  96. 

definition.  70. 

differentiii!  diagnosis,  93. 

etiology,  76. 

morbid  anatomy,  70. 

physical  signs,  89. 

prognosis,  95. 

rules  for  administration  of  quinine  in,  VXL 

rules  for  use  of  cold  baths  in,  99. 

stages,  70,  72,  73. 

symptoms,  79. 

terminations,  87. 

treatment,  97. 

varieties,  88. 


INDEX. 


1097 


Pneumonia,  broncho.    See  Lobular  pneumonia,  101. 

Pneumonia,  catari'lial.    Hee  Lobular  pneumonia,  101. 

Pneumonia,  cbronic  fibroid,  108. 

Pneumonia,  chronic  interstuial,  108. 

Pneumonia,  chronic  lobular,  105.  _       ,    ,  -  . 

Pneumonia,  colloid  caseous.    See  Chronic  phthisis, 

179. 
Pneumonia,  desquamative.    See  Chrome  phthisis, 

179. 
Pneumonia,  embolic,  120. 

fibroid,  108. 

hypostatic,  114. 
Pneumonia,  heart  disease,  114. 
Pneumonia,  interstitial,  108. 

diflferential  diagnosis  of,  111. 

etiology  of,  110. 

morbid  anatomy  of,  108. 

physical  signs  of.  111. 

prognosis  of,  112 

symptoms  of,  110. 

treatment  of,  112.  . 

Pneumonia,  lol)ular,  differential  diagnosis  or,  106. 

etiology  of,  103. 

morbid  anatomy  of,  101. 

physical  signs  of,  105. 

prognosis  of,  107. 

symptoms  of,  103. 

temperature  in,  104. 

terminal  ions  of,  102. 

treatment  of,  107. 
Pneumonia,  syphilitic  of  the  new-bom,  143. 
Pneumonia,  tubercular.    See  Fibrous  phthisis,  181. 
Pneumopericardium,  507. 
Poisoning,    chronic    lead.       See   Lead    poisoning, 

cbronic,  1064. 
Poison,  iri'itant,  and  cholera  morbus,  367. 
Polio-myelitis,  acute    anterior.      See  Lifantile  pa- 
ralysis, 1006. 
Polio-myelitis,  chronic  anterior,  differential   diag- 
nosis, 1010. 

etiology,  1010. 

morbid  anatomy,  1010. 

prognosis,  1010. 

symptoms,  1010. 

treatment,  1011. 
Pollock,  193. 
Polycholia,  356. 

Polydipsia.    See  Diabetes  insipidus,  883. 
Polyuria.    See  Diabetes  insipidus,  888. 
Port,  954. 

Ponfick,  708,  739,  888. 
Poore,  1063. 
Porcher,  660. 

"  Portal  thrombosis."    See  Pylephlebitis,  363. 
Poivell,  116. 
Power,  tioi. 
Primavera,  881. 
Proctitis,  difterential  diagnosis,  303. 

etiology,  302. 

morbid  anatomy,  301. 

prognosis,  303. 

symptoms,  302. 

treatment;  303. 
Proctitis,  chronic,  302. 

Prognosis  in  valvular  disease  of  the  heart,  467. 
Progressive  muscular  atrophy,  differential  diagnosis, 
1014. 

etiolo-;y,  1012. 

morbid  anatomy,  1011. 

prognosis,  1014. 

symptoms,  1013. 

treatment,  1015. 
Progressive  pernicious   anaemia,  differential   diag- 
nosis, 890. 

etiology,  889. 

morbid  anatomy,  888. 

prognosis,  890. 

symptoms,  889,  890. 

treatment,  891. 
Psammomata  of  the  brain.  See  Cerebral  tumors,  977. 
Pseudo-hypertrophic  paralysis,  etiology,  1026. 

morl)id  anatomy,  1026. 

prognoj^is,  1027. 

symptoms,  1027. 

treatment,  1027. 
Pseudo-leukieinia.    See  Hodgkin's  disease,  895. 
Pulmonary  anwmia,  129. 
Pulmonary  apoplexy,  diffuse,  124. 


Pulmonary  cancer,  140. 
Pulmonary  collapse,  129. 
Pulmonary  embolism,  fat,  122. 
Pulmonary  emphysema,  31. 
Pulmonary  gangrene,  125. 
Pulmonary  infarction.    See  Infarction,  120. 
Pulmonary  cedema.    See  CEdema,  jjulmonary,  117. 
Pulmonic  insufficiency.     See  Pulmonic  regurgita- 
tion, 467. 
Pulmonic  obstruction,  differential  diagnosis,  466. 

etiology,  466. 

morbid  anatomy,  465. 

physical  signs,  466. 

symptoms,  466. 
Pulmonic  regurgitation,  differential  diagnosis,  467. 

morbid  anatomy,  467. 

physical  signs,  467. 
Pulmonic  stenosis.    See  Pulmonic  obstruction,  465. 
Purpura,  differential  diagnosis,  907. 

etiology,  9U6. 

morbid  anatomy,  905. 

prognosis,  907. 

symptoms,  906. 

treatment,  907. 
Purpura  hemorrahgica.    See  Purpura,  905. 
Purulent  infection.    See  Septicaemia,  694. 
Pus,  fate  of,  8. 

theory  of  formation  of,  3. 
Pustule,  malignant,  and  gangrenous  stomatitis,  311. 
Putrid  fever.    See  Septicaemia,  694. 
Pyaemia,  differential  diagnosis,  700. 

etiology,  698. 

morbid  anatomy,  697. 

prognosis,  700. 

symptoms,  699. 

treatment,  701. 
Pyelitis,  differential  diagnosis,  583. 

etiology,  580. 

morbid  anatomy,  579. 

prognosis,  583. 

symptoms,  581. 

treatment,  584. 
Pylephlebitis,  adhesive,  differential  diagnosis,  363. 

etiology,  363. 

morbid  anatomy,  362. 

physicnl  signs,  363 

prognosis,  364. 

sjTnptoms,  363. 

treatment,  364. 
Phylephlebitis,  suppurative,  differential  diagnosis, 
365. 

etiology,  364. 

morbid  anatomy,  364. 

physical  signs,  365. 

prognosis,  366. 

SjTnptoms,  364. 

treatment,  366. 
Pyonephrosis,  582. 
Pyopneumothorax,  165. 

differential  diagnosis,  168. 

etiology,  l65. 

morbid  anatomy,  165. 

physical  signs,  167. 

prognosis,  168. 

symptoms,  166. 

treatment,  169. 

Quain,  462,  473,  475,  491,  494,  506,  768,  789. 

"  Quain's  fatty  heart,"  491. 

Quincke.  751,  878,  889. 

Quinine,  rules  for  administration  of,  in  acute  lobar 

pneumonia.  100. 
Quinsy.    See  Tonsilitis,  219. 


Rabies.    See  Hydrophobia,  803. 

Rachitis.     See  Rickets,  911. 

PadcUfe,  993,  1000. 

Balfe,  903. 

Ramsklll,  941,  955,  1037,  1068. 

Panvier,  473,  487. 

Rawson,  865. 

Payer,  548,  588,  883. 

Recklinqhausen,  697. 

Rectitis.    See  Enteritis,  257  :  Proctitis,  3M. 

Recurrent  laryngeal  paralysis,  34. 

Recurrent  scarlatina,  769.  ■ 

Reflex  action,  924. 


1098 


INDEX. 


Eegurgitatinn  at  the  aortic  orifice.    See  Aortic  re- 
gurgitation, 448. 
Kegurgitation  at  the  mitral  orifice.    /Sfee  Mitral  re- 
gurgitation, 457. 
Regurgitation  at  the  pulmonary  orifice.     See  Pul- 
monic regurgitation,  467. 
Eegurgitatioii  at  the  tricuspid  orifice.    /Sise  Tricuspid 

regurgitation,  462. 
Behn,  912. 
Reinhardt,  553. 
Reitz,  78. 
Eelapsin^  fever,  complications,  743. 

difitereutial  diagnosis,  744. 

etiologj',  739,  740. 

morbid  anatomy,  738,  739. 

prognosis,  744. 

symptoms,  740-744. 

synonyms,  738. 

treatment,  745. 
Remak,  866,  867, 1015. 
Eemittent  fever,  infantile,  360. 

differential  diagnosis,  823. 

etiology,  819. 

morbid  anatomy,  818. 

prognosis,  824. 

symptoms,  820. 

treatment,  824. 

varieties,  822,  823. 
Renal  calculi,  diii'erential  diagnosis,  595. 

etiology,  .593. 

morbid  anatomy,  592,  593. 

prognosis,  595. 

symptoms,  594. 

treatment,  595. 
Renal  cancer,  differential  diagnosis,  596. 

etiology,  596. 

morbid  anatomy,  596. 

prognosis,  597. 

symptoms,  596. 
Renal  colic,  594. 
Renal  hemon-bage,  etiology,  549. 

morbid  anatomy,  548. 

prognosis,  550. 

symptoms,  550. 

treatment,  550,  551. 
Renal  hypersemia,  differential  diagnosis,  546. 

etiology,  545. 

morbid  anatomy,  543. 

prognosis,  546. 

symptoms,  545. 

treatment,  547. 

varieties,  543. 
Benan,  349. 

Resolution,  inflammatory,  3. 
Respiratory  organs,  diseases  of,  9. 
Eetropharyngeal  abscess,  differentia  Idiagnosis,  224. 

etiology,  223. 

morbid  anatomy,  223. 

prognosis,  224. 

symptoms,  223. 

treatment,  224. 
Reynolds,  962,  964,  1035,  1036,  1063. 
Eheumatic  fever.    See  Rheumatism,  acnte  articular, 

858. 
Rheumatism,  acnte  articular,  differential  diagnosis, 
860. 

etiology.  858. 

morbid  anatomy,  857. 

prognosis,  860. 

symptoms,  858. 

treatment,  861. 
Rheumatism,  chronic  articular,  differential    diag- 
nosis, 864. 

etiology,  863. 

morbid  anatomy,  863. 

prognosis,  864. 

symptoms,  863. 

treatment,  864,  865. 
Rheumatism,  muscular,  differential  diagnosis,  869. 

etiology,  868. 

morbid  anatomy,  868. 

prognosis,  869. 

symptoms,  868. 

treatment,  869. 

sub-acute,  863. 

varieties  of,  8.57. 
Rheumatoid  arthritis.    See  Arthritis  deformans,  865. 
Richardson,  858. 


Richardson's  atomizer,  10. 
Rickets,  diflerential  diagnosis,  913. 

etiology,  912. 

morbid  anatomy,  911. 

prognosis,  913. 

symptoms,  913. 

treatment,  913. 
Riesel,  898. 
RiUier,  669. 
Rilliet  949. 
Rinflelsch,'  66,  103, 173,  179,  183,  437,  494,  975,  976, 

979. 
Ringer,  61,  100,  883. 
Roberts,  429,  1014. 
Rohre,  596. 

Rolcitanskij,  110, 121,  122,  248,  412,  417,  950,  953,  961, 
965,  979. 

HOSSTl'Stf'Z'il    *^00 

Rosenthal,'  962,  970,   976,  988,  991,  1000,  1025,  1042, 

1049,  1061. 
Roseola.    See  German  measles,  791. 
Rostan,  412. 

Rotheln.    See  German  measles,  791. 
Round  worm.    See  Intestinal  parasites,  306. 
Rozes,  880. 

Eubeola.    See  Measles,  783. 
Ruhle,  491. 
Rullier,  1046. 
Runeherg,  557. 

Eupture  of  the  heart.    See  Heart,  rupture  of,  497. 
Russell,  79. 
Rutherfm-d,  409. 
Rutty,  738,  745. 

Sabounn,  349. 

Sago-spleen .   See  Spleen,  waxy  degeneration  of,  417, 

"  St.  Vitus'  dance."    See  Chorea,  1050. 

Salter,  491. 

Sanderson,  663,  694. 

Sarcinfe  ventriculi,  234. 

Sarcomata  in  lungs,  142. 

Sarcomata  of  the  brain.    See  Cerebral  tumors,  977. 

Sarcomata  of  the  heart,  501. 

Sarcomata  of  tlie  kidney,  598. 

Saturnismus.    See  Lead  poisoning,  319. 

Scarlatina.    See  Scarlet  fever,  765. 

Scarlet  fever,  compjlications,  774. 

diflerential  diagnosis,  776. 

etiology,  767,  769. 

irregularities,  773. 

morbid  anatomy,  765-767. 

prognosis,  778,  779. 

sequelas,  774,  775. 

symptoms,  769-777. 

treatment,  779. 

varieties,  765. 
Schloz,  976. 
Schmidt,  498. 
Schneeniann,  1013. 
Sckottelins,  175. 
ScMippel,  909,  1032. 
Scirrhus  of  the  lungs,  108. 
Sclerosis,  amyotrophic   lateral.      See  Amyotrophic 

lateral  sclerosis,  1025. 
Sclerosis,  cerebro-spinal.    See  Cerebro-spinal  sclero- 
sis, 1015. 
Sclerosis  of  the  brain,  differential  diagnosis,  987. 

etiology,  986. 

morbid  anatomy,  985,  986. 

prognosis,  987. 

symptoms,  986. 

treatment,  987. 
Scorbutus.    See  Scurvy,  903. 

Scriveners'  palsy.    See  Localized  spasm  and  paraly- 
sis, 1063. 
Scrofula,  differential  diagnosis,  911. 

etiology,  909. 

morbid  anatomy,  909. 

prognosis,  911. 

symptoms,  910. 

treatment,  911. 
"  Scrofulosis."    See  Scrofula,  909. 
Scrofulous  inflammation.    See  Chronic  phthisis,  ITO. 
Scurvy,  morbid  anatomy,  903. 

diflerential  diagnosis,  904. 

etiology,  904. 

prognosis,  905. 

symptoms,  904. 


INDEX. 


1099 


Scurvy,  treatment,  905. 

Seasickness,  differential  diagnosis,  1079. 

etiolof,'y,  1077. 

morbid  anatomy,  1077. 

prognosis:,  1079. 

symptoms,  1078. 

treatment,  1079. 
Seat-worm.     See  Intestinal  parasites,  306. 
SeeligmuUcr,  1009. 
Sensory  paralysis,  928. 
Septicemia,  differential  diagnosis,  696. 

etiology,  694,  695. 

morbid  anatomy,  694. 

prognosis,  696. 

symptoms,  695,  696. 

treatment,  696. 
Serous  membranes,  inflammation  of,  4. 
Shand,  907. 
Shaituck,  803. 
Shubert,  659. 
Sibson,  519. 

Sick-headache.    See  Megrim,  1075. 
Siderosis,  182. 

Simple  chronic  catarrhal  laryngitis,  31. 
SUyl,  78. 

Skoda,  96,  460,  1061.  .      , 

Small  granular  fatty  kidney.    See  Nephntis,  cnronic 

parenchymatous,  562. 
Small-pox  complications,  756. 

differential  diagnosis,  754,  755. 

etioloa;v,  747,  748. 

morbid  anatomy,  745-747. 

prognosis,  755-757. 

symptoms,  748-754. 

treatment,  7.57,  758. 

varieties,  745. 
Softening  of  the  brain.    See  Cerebral  softening,  959. 
Southey,  558,  574. 
Spanaemia.    See  Antemia,  883. 
Spasm  and  paralysis,  localized.    See  Localized  spasm 

and  paralysis,  1063. 
Spasmodic  affections  of  the  larynx,  37. 
Spasmodic  tabes  dorsalis,  differential  diagnosis,  1025. 

etiology,  1023. 

morbid  anatomy,  1023. 

prognosis,  1025. 

syrdptoms,  1024. 

treatment,  1025. 
Spasms,  927. 
Spastic  paralysis.    See  Amyotrophic  lateral  sclerosis, 

1025. 
Spina-bifida,  etiology,  1033. 

morbid  anatomy,  1033. 

prognosis,  1033. 

symptoms,  1033. 

treatment,  1033. 
Spinal  apoplexy,  differential  diagnosis,  1030. 

etiology,  1030. 

morbid  anatomy,  1029. 

prognosis,  1031. 

symptoms,  1030. 

treatment,  1031. 
Spinal  cord  and  meninges,  hypersemia  of,  differential 
diagnosis;  992. 
-     etiology.  991. 

morbid  anatomy,  991. 

prognosis,  992. 

symptoms,  991. 

treatment,  992. 

varieties,  991. 
Spinal  cord,  diseases  of,  990. 
Spinal  cord,  classification  of  diseases  of,  990. 
Spinal  cord,    hypersemia  of.    See  Spinal  cord  and 

meninges,  hyperemia  of,  991. 
Spinal  cord,  non-inflammatory  softening  of,  differ- 
ential diagnosis,  1001. 

etiology,  1000. 

morbid  anatomy,  1000. 

prognosis,  1001. 

symptoms,  1001. 

treatment,  1001. 
Spinal  cord,  tumors  of,  difi'erential  diagnosis,  1032. 

prognosis,  1032. 

symptoms,  1031. 

tre>itment,  1032. 
Spinal  irritation,  differential  diagnosis,  1057. 
etiology,  10.55. 
prognosis,  1057. 


Spinal  irritation,  symptoms,  1056. 

treatment,  1057. 
Spinal  meningitis.    See  Meningitis,  spinal,  992. 

paralysis,  infantile.     See  Paralysit^,  infantile 
spinal,  1006. 
Spinal  paralysis  of  adults,  acute.  /See Paralysis,  acute 

spinal  of  adults,  1009. 
Spleen,  cancer  of,  418. 
Spleen,  cysts  of,  418. 
Spleen,  diseases  of,  413. 

Spleen,  enlarged.    See  Spleen,  hypertrophy  of, 416. 
Spleen,  gummata  of,  418. 
Spleen,  hydatids  of,  418. 
Spleen,  hyperajmia  of,  etiology,  413. 

morbid  anaiomy,  413. 

prognosis,  414. 

symptoms,  413. 

treatment,  414. 
Spleen,  hypertrophy  of,  etiology,  417. 

morbid  anatomy,  416. 

symptoms,  417. 

treatment,  417. 

varieties,  416. 
Spleen,  inflammation  of,  differential  diagnosis,  415, 
416. 

etiology,  415. 

morbid  anatomy,  414. 

physical  signs,  415. 

prognosis,  416. 

sj'mptoms,  415. 

treatment,  416. 
Spleen  morbid  growths  in,  418. 
Spleen  the  sago.    &e  Spleen,  waxy  degeneration  of, 

417. 
Spleen,  tubercles  in,  418. 
Spleen,  waxy  degeneration  of,  etiology,  417. 

morbid  anatomy,  417. 

symptoms,  418 

treatment,  418. 
Splenitis.     See  Spleen,  inflammation  of,  414. 
Splenization  of  the  lungs,  113,  129. 

pulmonary,  129. 
Sporadic  cholera.    See  Cholera  morbus,  266. 
Spotted  fever.    See  Cerebro-spinal  meningitis,  684. 
"  Sprue."    See  Thrush,  213. 
Squire,  802. 

Stasis,  inflammatory,  3. 
Sleiner,  991. 

Stenosis  at  the  mitral  orifice.    See  Mitral  stenosis, 
453. 

at  the  pulmonary  orifice.    See  Pulmonic  ob- 
struction, 465. 

at  the  tricuspid  orifice.    See  Tricuspid  steno- 
sis, 462. 

of  aortic  valve.    See  Aortic  stenosis,  444. 
Stewart,  601. 
Stiemer,  757. 
Stokes,  4,50,  613.  735. 
Stomach,  acidity  of,  from  hypersecretion,  and  from 

fermentation,  240. 
Stomach,  cancer  of,  300. 

differential  diagnosis,  345. 

etiology,  243. 

morbid  anatomy,  241. 

physical  signs,  245. 

prognosis,  246. 

symptoms,  244. 

treatment,  246. 

varieties,  241. 
Stomach,  dilatation  of,  differential  diagnosis,  356. 

etiology,  255. 

morbid  anatomy,  254. 

physical  signs,  256. 

prognosis,  256. 

symptoms,  255. 

treatment,  256. 
Stomach,  diseases  of,  228. 
Stomach,  erythism  of.    See  Stomach,  neuroses  of, 

252. 
Stomach,  hemorrhagic  erosion  in,  234. 
Stomach,  morbid  sensibility  of.    See  Chronic  gastri- 
tis. 231. 
Stomach,  neuroses  of,  differential  diagnosis,  253. 

etiology,  252. 

prognosis,  2.53. 

symptoms,  252. 

treatment,  253. 
Stomach,  ulcer  of,  differential  diagnosis,  250. 


1100 


IlfDEX. 


Stomadi,  ulcer  of,  etiology,  248. 
morbid  anatomy,  247. 
prognosis,  250. 
symptoms,  249. 
treatment,  251. 
varieties,  246. 
Stomatitis,    aplitboiis.      See   Follicular   stomatitis, 

210. 
Stomatitis,  catarrhal,  208. 

differential  diagnosis,  209. 
etiology,  208. 
morbid  anatomy,  208. 
prognosis,  209. 
symptoms,  209. 
treatment,  209. 
Stomatitis,  croupous.    See  Follicular  stomatitis,  210. 
Stomatitis,  foihcular,  difiereutial  diagnosis,  210. 
etiology,  210. 
morbid  anatomy,  210. 
prognosis,  210. 
symptoms,  210. 
treatment,  210. 
Stomatitis,  gangrenous,  differential  diagnosis,  Sll. 
etiology,  211. 
morbid  anatomy,  211. 
prognosis,  211. 
symptoms,  211. 
treatment,  211. 
Stomatitis,  ulcerative,  differential  diagnosis,  212. 
etiology,  312. 
morbid  anatomy,  212. 
prognosis,  213. 
symptoms,  212. 
treatment,  213. 
Stone-cutter's  phthisis,  182. 
"  Stony  kidney."    See  Renal  hypersemia,  543. 
SiracMns,  79. 
Strieker.  876,  935. 
Stricture  of  the  oesophagus,  225. 
Strumous  enteritis.    See  Intestinal  ulcers,  285. 
Strumous  nephritis,  598. 
Stumpell,  1024. 
Siurges,  78. 

Sub-acute  meningitis.  See  Meningitis,  sub-acute,  940. 
rheumatism .    Set  Rheumatism,  sub-acute,  863. 
Summer  complaints.    See  Cholera  infantum,  268. 
Sunstroke,  differential  diagnosis,  1055. 
etiology,  1054. 
morbid  anatomy,  1053. 
prognosis,  1055. 
symptoms,  1054. 
treatment,  1055. 
Suppuration,  2. 

Suppurative  hepatitis,  circumscribed.    <S^ee  Hepatitis, 
suppitrative,  349. 
pylephlebitis.    See  Pylephlebitis,  suppurative, 
364. 
Surgical  fever.     See  Septicaemia,  694. 

kidney.      See   Acute   suppurative   interstitial 
nephritis,  588. 
Sutton,  475. 

Syphilis,  chronic  catarrhal  laryngitis  in,  25. 
differential  diagnosis,  923. 
etiology,  919. 
inherited,  921. 
morbid  anatomy,  918,  919. 
prognosis,  922. 
symptoms,  primary,  919. 

secondary,  920. 
tertiary,  921. 
treatment.  922.  923. 
Syphilitic  disease  of  arteries,  513,  514. 

of  the  heart.    See  Heart,  syphilitic  disease  of, 

508. 
of  (he  liver.     Si'.e  Liver,  gummata  of,  383. 
of  the  lung,  143. 
gummata  of  the  kidney,  597. 
pneumonia  of  the  new-born,  143. 

Tabes  dorsalis.    See  Locomotor  ataxia,  1018. 
Tabes  dorsalis,   spasmodic.    See   Spasmodic  tabes 

dorsalis.  1023. 
Tabes  mesenterica.    'Bee  Intestinal  ulcers,  286. 
Taenia  medlocannellata,  807. 
Taenia  saginata,  307. 
Taenia  solium,  307. 
Tanner,  949. 
Tape-worm.    See  Intestinal  parasites,  306. 


Teale,  701. 

Tests  for  saccharine  urine,  879. 

Tetanus,  differential  diagnosis,  1059. 

etiology,  1058. 

morbid  anatomy,  1058. 

prognosis,  1059. 

symptoms,  10.58. 

treatment,  1059. 
Thcwn,  179. 

The  germ  theory  of  disease,  610. 
Theory  of  organisms  of  disease,  610. 
Thomas,  769, 850. 
ThomiKOh,  Reginald,  187. 
Thoracic  aneurism,  differential  diagnosis,  534, 

definition,  519. 

etiology,  520. 

morbid  anaiomy,  519. 

physical  signs,  523. 

prognosis,  525. 

symptoms,  521. 

treatment,  medical,  526. 
surgical,  527. 

varieties,  519. 
Thread-worm.     See  Intestinal  parasites,  306. 
Thrombi  in  the  heart.      See  Cardiac  thrombosis, 

497. 
Thrombosis,  etiologj',  517. 

morbid  anatomy,  515. 

symptoms,  517. 
Thrombosis  of  the  brain.    See  Cerebral  thrombosis 

and  embolism,  956. 
Thrush,  213. 

differential  diagnosis,  214. 

etiology,  214. 

morbid  anatomy,  213. 

prognosis,  214. 

symptoms,  214. 

treatment,  214. 
Todd,  874. 
Tongue,  cancer  of,  differential  diagnosis,  217. 

etiology,  216. 

morbid  anatomy,  216. 

prognosis,  217. 

symptoms,  216. 

treatment,  217. 
Tonsilitis,  differential  diagnosis,  220. 

etiology,  220. 

morbid  anatomy,  219. 

prognosis,  220. 

symptoms,  220. 

treatment,  221 . 
Torpid  liver.    See  Functional  derangements  of  liver, 

406. 
Torticollis.    See  Wry-neck,  868. 
Toxic  gastritis.    See  Acute  gastritis,  228. 
Traube,  90,  128,  553,  1002. 
Traumatic  fever.    See  Septicaemia,  694. 
Treatment  of  valvular  disease  of  the  heart,  470. 
Tremor,    mercurial.        See   Chronic  mercurialism, 

1066. 
Trichina  spiralis,  309. 
Trichinae  poisoning.    See  Trichinosis,  916. 
Trichinosis,  differential  diagnosis,  918. 

etiology,  917. 

morbid  anatomy,  916. 

prognosis,  918. 

symptoms,  917. 

treatment,  918. 
Trichocephalus  crenatus,  309. 
Trichocephalus  dispar,  309. 
Tricuspid  regurgitation,  differential  diagnosis,  465. 

etiology,  463. 

morbid  anatomy,  468. 

physical  signs,  464. 

sj'fnptoms,  464. 
Tricuspid  stenosis,  etiology,  462. 
morbid  anatomy,  462. 
physical  signs,  462. 
Trismus  nascentiiim,  1058. 
Trojanoivsky,  769. 

Trommer's  test  for  sugar  in  the  urine,  879. 
Trophic  changes  in  nervous  diseases,  929. 
Trousseau,  64,  79,  408,  510,  6G9,  750,  874,  883,  895,  931, 

948,  968,  971,  1018,  1041. 
Tubercle  bacillus,  Koch's  experiments  concerning, 

174.  175. 
Tubercles  in  splee",  418. 
Tubercles  in  the  heart,  501. 


INDEX. 


1101 


Tubercular  disease  of  the  kidney.    See  Kidney,  tu- 

Ijerculosis  of,  598. 
Tubei'cniiir  meningitis.    See  Meningitis,  tubercular, 

943. 
Tubercular  phthisis,  chronic,  183. 
Tubercular  piieuinonia,   interstitial.      See   Fibrous 

phthisis,  ]81. 
Tuberculosis,  acute  miliary,  difEerential  diagnosis, 
709. 

etiology,  707. 

morbid  anatomy,  706. 

physical  signs,  709. 

prognosis,  709. 

symptoms,  708. 

treatment,  710. 
Tuberculosis  of  the  liver.    See  Liver,  tuberculosis 

of,  392. 
Tuberculosis  of  the  pericardium,  502. 
Tuberculous  granules  in  arteries^  513. 
Tuberculous  ulcers  of  the  intestines,     ^'ee  Intestinal 

ulcers,  285. 
Tufnell,  526,  528. 
Tully's  powder,  45. 
Tumors  of  the  brain  and  meninges.     See  Brain  and 

meninges,  tumors  of,  981. 
Tumors  of  tiie  spinal  cord.    See  Spinal  cord,  tumors 

of,  1031. 
Tilrck,  9(i9 

Tiirck,  degeneration  of,  1025. 

Tyndall's  experiments  concerning  vegetable  organ- 
isms.   See  Phthisis,  204. 
Typhlitis,  difEerential  diagnosis,  280. 

etiology,  279. 

morbid  anatomy,  279. 

physical  signs,  280. 

prognosis,  280. 

symptoms,  279. 

treatment,  281. 
Typnoniiilarial  fever.    See  Continued  malarial  fever, 

827. 
Typhoid  fever,  abortive  form,  630. 

complications,  635. 

differential  diagnosis,  631-633. 

etiology,  618-620. 

morbid  anatomy,  611-618. 

prognosis,  633-638. 

relapses,  637. 

symptoms,  620-631. 

treatment,  638-650. 
Typhus  fever,  complications,  728,  739. 

differential  diagnosis,  723-73?. 

etiology,  714-716. 

morbid  anatomy,  710-714. 

prognosis,  727-731. 

symptoms,  716-723. 

synonym?,  710. 

trealment,  731-737. 
Typhus  siderans,  730. 

Ulceration,  3. 

Ulceration  of  mucous  surfaces,  7. 

Ulcerative  stomatitis.     See  Stomatitis,  ulcerative, 

212. 
Ulcers  of  the  bowel.    See  Intestinal  ulcers,  284. 
Ulcers  of  the  intestine.    See  Intestinal  ulcers,  284. 
Ulcers  of  the  stomach,  varieties  of,  246. 
Urtemia,  acute,  differential  diagnosis,  539. 

etiology,  537,  538. 

prognosis,  540. 

symptoms,  539. 

theories  of,  537,  538. 

treatment,  541,  542.  543. 
Urinary  casts,  varieties  of,  536. 
Urinary  sediments,  532. 
Urine,  animal  organisms  in,  537. 

blood  in,  534,  535. 

casts  in,  535,  536. 

inorganic  constituents  of,  530. 

normal  constituents  of,  529. 

pus  in,  535. 

sediments  in,  .532. 

tests  for  sugar  in,  879. 

vegetable  organisms  in,  537. 

Vaccination,  759-764. 
Vaccinia,  760-762. 
Vullender,  1042. 


Valvular  aneurisms,  434. 

Valvular  disease  of  the  heart,  and  cardiac  murmurs, 

441. 
Valvular  disease  of  the  heart,  prognosis  in,  467. 
Valvular  disease  of  the  heart,  treatment  of,  470. 
Varicella,  differential  diagnosis,  764. 

etiology,  764. 

progn(;sig,  764. 

symptoms,  764. 

treatment,  764. 

varieties,  764. 
Variola  confluens,  752. 
Variola  discreta,  749. 
Variola  hemorrhagica,  7.53,  754. 
Variola.    See  Small-pox,  745. 
Varioloid,  morbid  anatomy,  763. 

prognosis,  763. 

symptoms,  762,  763. 

treatment,  763. 
V'arix,  morbid  anatomy,  515. 
Verdeil,  82. 
Vertigo  differential  diagnosis,  1069. 

etiology,  1067. 

morbid  anatomy,  1067. 

prognosis,  1069. 

symptoms,  106S. 

treatment,  1069. 

varieties,  1067. 
Vertigo,  stomachic  and  cerebral,  340. 
Vesicular  bronchitis,  129. 
Vesicular  emphysema,  131. 
Vievssens,  441. 
Vigla,  938. 

Yirchow,  72  ,78,  114,  187,  248,  305,  325,  407,  413,  441, 
445,  449,  518,  519,  669,  685,  702,  886,  891,  909, 
942,  952,  953,  979,  987.  1012. 
Virchow's  brown  oedeniii  of  lungs,  115. 
Vocal  cords,  paralysis  of  abductors  of.  See  Neuroses 
of  the  larynx,  34. 

paralysis  of  adductors  of.   See  Neuroses  of  the 
larynx,  34. 

paralysis  of  tensors  of.    See  Neuroses  of  the 
larynx,  34. 
Vogel,  76. 
Voison,  1013. 

Volvulus.    See  Intestinal  obstruction,  290. 
Von  &raefe,  510. 
Von  Briimi,  898. 
Vulpian,  987. 

Waffmr,  132,  334,  553,  888,  979. 

"Walking  tvphus,"  730. 

Walshe,  82,  95,  169,  468,  470. 

Warburg's  tincture,  848. 

Warfynge,  897. 

Warren's  test  for  sugar  in  the  urine,  879. 

Waterhovse,  759. 

Watson,  603,  930,  949,  1058. 

Waxy  degeneration  of  the  heart.  See  Heart,  amyloid 

degeneration  of,  494. 
Waxy  degeneration  of  the  intestines.  See  Intestines, 

waxy  degeneration  of,  297. 
Waxy  degeneration  of  the  pancreas.    See  Pancreas, 

waxj^  degeneration  of,  411. 
Waxy  kidney,  etiology,  576. 

morbid  anatomy,  575. 

symptoms,  576. 
Waxy    liver.     See  Amyloid  degeneration  of  liver, 

366. 
Weber's  nasal  douche,  11. 
WeigeH.  121,  1^4,  697,  746,  748. 
Weldon,  891. 
Werlhof,  906. 
Westp/ial,  756,  979,  1036. 
Whip-worm.     See  Intestinal  parasites,  306. 
White  hepatization,  143. 
Whooping-cough,  differential  diagnosis,  801. 

etiolosry.  800. 

moi'bid  anatomy,  800. 

prognosis,  801. 

symptoms,  800. 

treatment.  802. 
Wilkx,  888,  898,  968. 
Williams,  174,  186. 
Wilson,  733. 
WoaA-es,  1069. 
Wood,  826,  828,  838. 
Worms.    See  Intestinal  parasites,  306. 


1L02 


IKDEX. 


Wry  neck,  868. 
Wunderlich,  434.  861, 1046. 

Yellow  fever,  diflerential  diagnosis,  658, 659. 
etiology,  653-654. 
morbid  anatomy,  650-652. 
prognosis,  659. 


Yellow  fever,  symptoms,  654-657. 
treatment,  659,  660. 

Zahn,  670. 
Zenker,  132,  711. 
Ziemssen,  95. 
Zvizer,  733,  757o 


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